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Gene Information
Gene symbol: CD2
Gene name: CD2 molecule
HGNC ID: 1639
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 35126185 | Serum and glucocorticoid-inducible kinase 3 (SGK3) is involved in maintaining podocyte function by regulating the protein levels of podocin and CD2-associated protein. |
| 2 | 35126185 | Nephrin is also one of the slit diaphragm proteins of podocytes, but whether SGK3 participates in podocyte injury by regulating the levels of nephrin remains unclear. |
| 3 | 35126185 | In this study, we focused on whether SGK3 affects nephrin levels and the mechanisms involved in the same. |
| 4 | 35126185 | In the kidneys of adriamycin (ADR)-induced podocyte injury mouse model, the protein levels of SGK3 and nephrin were significantly decreased. |
| 5 | 35126185 | In ADR-treated conditionally immortalized mouse podocyte cells (MPCs), the protein levels of nephrin and SGK3 were inhibited, while the constitutive expression of SGK3 reversed the ADR-induced decline in nephrin protein levels. |
| 6 | 35126185 | Furthermore, ADR treatment or SGK3 inactivation enhanced the ubiquitin-proteasome degradation of nephrin in MPCs, and dramatically activated downstream effector proteins of SGK3, neural precursor cells expressing developmentally downregulated protein 4 subtype 2 (Nedd4-2) and glycogen synthase kinase-3 β (GSK3β). |
| 7 | 35126185 | Similarly, Nedd4-2 or GSK3β overexpression resulted in increased activity of Nedd4-2 or GSK3β, and significantly downregulated nephrin levels. |
| 8 | 35126185 | Interestingly, ubiquitin-mediated protein degradation of nephrin was regulated by Nedd4-2, rather than by GSK3β. |
| 9 | 35126185 | In summary, SGK3 inactivation downregulated the levels of nephrin by increasing Nedd4-2 and GSK3β activity in ADR-induced podocyte injury model; in particular, the SGK3/Nedd4-2 signaling pathway was found to be involved in ubiquitin-mediated proteasome degradation of nephrin. |
| 10 | 34780752 | In fructose-exposed conditionally immortalized human podocytes, we found that atractylodin inhibited podocyte hypermotility, and up-regulated slit diaphragm proteins podocin and nephrin, and cytoskeleton protein CD2-associated protein (CD2AP), α-Actinin-4 and synaptopodin expression, which were consistent with its anti-oxidative activity evidenced by up-regulation of catalase (CAT) and superoxide dismutase (SOD) 1 expression, and reduction of reactive oxygen species (ROS) production. |
| 11 | 34780752 | Atractylodin also significantly suppressed expression of transient receptor potential channels 6 (TRPC6) and phosphorylated Ca2+/calmodulin-dependent protein kinase IV (CaMK4) in cultured podocytes with fructose exposure. |
| 12 | 34780752 | Additionally, in fructose-exposed podocytes, CaMK4 siRNA up-regulated synaptopodin and reduced podocyte hypermotility, whereas, silencing of TRPC6 by siRNA decreased p-CaMK4 expression, inhibited podocyte hypermotility, showing TRPC6/p-CaMK4 signaling activation in podocyte hypermotility under fructose condition. |
| 13 | 34780752 | These results first demonstrated that the anti-oxidative property of atractylodin may contribute to the suppression of podocyte hypermotility via inhibiting TRPC6/p-CaMK4 signaling and restoring synaptopodin expression abnormality. |
| 14 | 34568396 | Podocyte Foot Process Effacement Precedes Albuminuria and Glomerular Hypertrophy in CD2-Associated Protein Deficient Mice. |
| 15 | 33936277 | Transforming growth factor-β1-induced podocyte injury is associated with increased microRNA-155 expression, enhanced inflammatory responses and MAPK pathway activation. |
| 16 | 33936277 | Synaptopodin, CD2-associated protein (CD2AP), p38, and extracellular signal-regulated kinase (Erk) 1/2 expressions were detected using western blotting. |
| 17 | 33936277 | Cell supernatants were collected for assaying tumor necrosis factor (TNF)-α and interleukin (IL)-6 concentrations using enzyme-linked immunosorbent assay. |
| 18 | 33936277 | The Pearson correlation analysis was used to analyze the correlation between miR-155 levels and TNF-α or IL-6. |
| 19 | 33936277 | Time- and dose-dependent TGF-β1 treatments downregulated synaptopodin and CD2AP expression levels, and activated the p38 and Erk 1/2 pathway. |
| 20 | 33936277 | Additionally, TNF-α and IL-6 secretions were elevated, and their concentrations were positively correlated with the expression of miR-155 during podocyte injury. |
| 21 | 33936277 | Thus, the present study indicated that miR-155 is a potential biomarker for the diagnosis of EGD, and its expression is associated with the release of pro-inflammatory cytokines and activation of mitogen-activated protein kinase (MAPK) pathway in TGF-β1-induced podocyte injury. |
| 22 | 33936277 | The present study suggests that the TGF-β1/miR-155/MAPK axis is a novel target in the mechanism of EGD. |
| 23 | 33155094 | Immunohistochemically stained with integrin α3β1, type IV collagen, laminin, nephrin, CD2-associated protein (CD2AP) and podocin to show the filtration barrier structure. |
| 24 | 33155094 | Immunohistochemical results showed an increase in nephrin, podocin, CD2AP, laminin and a decrease in integrin α3β1 and type IV collagen. |
| 25 | 32686524 | A number of key proteins are essential for podocyte function, including nephrin, podocin, CD2-associated protein (CD2AP), synaptopodin, and α-actinin-4 (ACTN4). |
| 26 | 32090080 | In the model group, the Psoriasis Area and Severity Index (PASI) scores of scaly and erythema obviously increased (p < 0.01), creatinine and blood urea nitrogen significantly increased (p < 0.01), the positive area of hematoxylin-eosin (HE) and periodic acid-Schiff (PAS) staining in kidney increased (p < 0.01), malondialdehyde significantly increased with superoxide dismutase (SOD) decreased (p < 0.01), 24-hour urine protein increased and the expressions of podocin and CD2 associate protein (CD2AP) decreased (p < 0.01), and kidney/serum inflammatory factors (IL-17, IL-1β, IL-6, TNF-α, and IL-22) and TLR/NF-κB-related expression (TLR2, TLR4, MyD88, and NF-κBp65) all increased (p < 0.01). |
| 27 | 30601089 | Ginseng Total Saponin Attenuates Podocyte Apoptosis Induced by Diabetic Conditions Through the Recovery of CD2-Associated Protein. |
| 28 | 30601089 | Ginseng Total Saponin Attenuates Podocyte Apoptosis Induced by Diabetic Conditions Through the Recovery of CD2-Associated Protein. |
| 29 | 30601089 | CD2-associated protein (CD2AP), an adaptor protein, plays several important roles in podocyte function, linking slit diaphragms to actin-based cytoskeleton and sending survival signals. |
| 30 | 30601089 | CD2-associated protein (CD2AP), an adaptor protein, plays several important roles in podocyte function, linking slit diaphragms to actin-based cytoskeleton and sending survival signals. |
| 31 | 30595084 | The changes in podocyte-specific proteins (nephrin, CD2-associated protein [CD2AP]), the cytoskeletal protein F-actin, the tight junction protein (ZO-1), and Mas receptor (MasR) were examined by immunofluorescence. |
| 32 | 30595084 | The expression of nephrin, F-actin, ZO-1, and MasR on podocytes interfered in serum of PE was significantly decreased compared to normal control and normal pregnant serum group in vitro, yet their expression was significantly increased after coculture by 10-6 mol/L Ang-(1-7) and the preeclamptic serum. |
| 33 | 29556761 | A third group of animal models involves genetic engineering techniques targeting podocyte expression molecules, such as podocin, CD2-associated protein, and TRPC6 channels. |
| 34 | 29138824 | However, FSGS does not result exclusively from podocyte‑associated genes, however also from other genes including collagen IV‑associated genes. |
| 35 | 29138824 | Patients who carry the collagen type IVA3 chain (COL4A3) or COL4A4 mutations usually exhibit Alport Syndrome (AS), thin basement membrane neuropathy or familial hematuria (FH). |
| 36 | 29138824 | Genomic DNA of the siblings affected by FH with biopsy‑proven FSGS was analyzed, and their father was screened for 18 gene mutations associated with FSGS [nephrin, podocin, CD2 associated protein, phospholipase C ε, actinin α 4, transient receptor potential cation channel subfamily C member 6, inverted formin, FH2 and WH2 domain containing, Wilms tumor 1, LIM homeobox transcription factor 1 β, laminin subunit β 2, laminin subunit β 3, galactosida α, integrin subunit β 4, scavenger receptor class B member 2, coenzyme Q2, decaprenyl diphosphate synthase subunit 2, mitochondrially encoded tRNA leucine 1 (UUA/G; TRNL1) and SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a like 1] using matrix‑assisted laser desorption/ionization time‑of‑flight mass spectrometry technology. |
| 37 | 29138824 | Using mass array technology, a TRNL1 missense homozygous mutation (m. 3290T>C) was identified in the probands diagnosed with FH and manifested as FSGS on biopsy. |
| 38 | 29138824 | In the present study, a mutation in TRNL1 (m. 3290T>C) was identified, which was the first reported variant associated with FSGS. |
| 39 | 29138824 | The COL4A4 (c. 4195A>T) may co‑segregate with FSGS. |
| 40 | 28878342 | Inhibition of SHIP2 in CD2AP-deficient podocytes ameliorates reactive oxygen species generation but aggravates apoptosis. |
| 41 | 28878342 | Lack of CD2-associated protein (CD2AP) in mice increases podocyte apoptosis and leads to glomerulosclerosis and renal failure. |
| 42 | 28878342 | We showed previously that SHIP2, a negative regulator of the PI3K/AKT signalling pathway, interacts with CD2AP. |
| 43 | 28878342 | PDK1 and CDK2, central regulators of AKT, were downregulated in CD2AP-/- or PA-treated podocytes. |
| 44 | 28878342 | Downregulation of PDK1 and CDK2, ROS generation and apoptosis were prevented by CD2AP overexpression in both models. |
| 45 | 28878342 | AKT- and ERK-mediated signalling was diminished and remained reduced after AS1949490 treatment in the absence of CD2AP. |
| 46 | 28814739 | Here we report the application of this powerful technology to examine the three-dimensional ultrastructural characteristics of proteinuric glomerulopathy in mice with CD2-associated protein (CD2AP) deficiency. |
| 47 | 28583549 | Glomerular mRNA expression profiling showed down-regulations of podocyte-related genes (Wilms tumor 1, synaptopodin, nephrin, CD2-associated protein, and podocin) and of transforming growth factor-beta (a marker of fibrosis) in sirolimus-treated mice. |
| 48 | 28583549 | In addition, expressions of the antiapoptotic genes Bcl-2 and Bcl-xL were also down-regulated. |
| 49 | 27590856 | CD2-associated protein/phosphoinositide 3-kinase signaling has a preventive role in angiotensin II-induced podocyte apoptosis. |
| 50 | 27590856 | CD2-associated protein/phosphoinositide 3-kinase signaling has a preventive role in angiotensin II-induced podocyte apoptosis. |
| 51 | 27590856 | The glomerular slit diaphragm (SD) serves as a size-selective barrier and is linked to the actin-based cytoskeleton by adaptor proteins, including CD2-associated protein (CD2AP). |
| 52 | 27590856 | The glomerular slit diaphragm (SD) serves as a size-selective barrier and is linked to the actin-based cytoskeleton by adaptor proteins, including CD2-associated protein (CD2AP). |
| 53 | 27590856 | In addition, CD2AP can facilitate the nephrin-induced phosphoinositide 3-kinase (PI3-K)/Akt signaling, which protects podocytes from apoptosis. |
| 54 | 27590856 | In addition, CD2AP can facilitate the nephrin-induced phosphoinositide 3-kinase (PI3-K)/Akt signaling, which protects podocytes from apoptosis. |
| 55 | 27590856 | Here we found that CD2AP staining was located diffusely but predominantly in the peripheral cytoplasm and CD2AP co-localized with nephrin in mouse podocytes; however, Ang II decreased CD2AP staining diffusely and induced a separation from concentrated nephrin. |
| 56 | 27590856 | Here we found that CD2AP staining was located diffusely but predominantly in the peripheral cytoplasm and CD2AP co-localized with nephrin in mouse podocytes; however, Ang II decreased CD2AP staining diffusely and induced a separation from concentrated nephrin. |
| 57 | 27590856 | Ang II notably reduced CD2AP expression in time- and concentration-dependent manners, and this was significantly recovered by losartan. |
| 58 | 27590856 | Ang II notably reduced CD2AP expression in time- and concentration-dependent manners, and this was significantly recovered by losartan. |
| 59 | 27590856 | LY294002, a PI3-K inhibitor, further reduced CD2AP expression and increased podocyte apoptosis, which was augmented by siRNA for CD2AP. |
| 60 | 27590856 | LY294002, a PI3-K inhibitor, further reduced CD2AP expression and increased podocyte apoptosis, which was augmented by siRNA for CD2AP. |
| 61 | 27590856 | Thus, Ang II induces the relocalization and reduction of CD2AP via AT1R, which would cause podocyte apoptosis by the suppression of CD2AP/PI3-K signaling. |
| 62 | 27590856 | Thus, Ang II induces the relocalization and reduction of CD2AP via AT1R, which would cause podocyte apoptosis by the suppression of CD2AP/PI3-K signaling. |
| 63 | 27575559 | Cathepsin L, a lysosomal cysteine protease, can be involved in the development of proteinuria by degradation of proteins that are important for normal podocyte architecture, such as the CD2-associated protein, synaptopodin, and dynamin. |
| 64 | 27575559 | Cathepsin L also activates heparanase, a heparan sulfate endoglycosidase previously shown to be crucial for the development of diabetic nephropathy. |
| 65 | 27575559 | In wild-type mice the early development of albuminuria correlated with the activation of heparanase and loss of heparan sulfate expression, whereas loss of synaptopodin expression and podocyte damage occurred at a later stage. |
| 66 | 27575559 | Most likely, cathepsin L-dependent heparanase activation is crucial for the development of albuminuria and renal damage. |
| 67 | 27441654 | Tankyrases, multifunctional poly(ADP-ribose) polymerase (PARP) superfamily members with features of both signaling and cytoskeletal proteins, antagonize Wnt/β-catenin signaling. |
| 68 | 27441654 | We found that tankyrases interact with CD2-associated protein (CD2AP), a protein essential for kidney ultrafiltration as CD2AP-knockout (CD2AP-/-) mice die of kidney failure at the age of 6-7 weeks. |
| 69 | 27441654 | The data revealed increased activity of β-catenin, and upregulation of lymphoid enhancer factor 1 (LEF1) (mediator of Wnt/β-catenin pathway) and fibronectin (downstream target of Wnt/β-catenin) in CD2AP-/- podocytes. |
| 70 | 27441654 | Total PARylation and active β-catenin were reduced in CD2AP-/- podocytes by tankyrase inhibitor XAV939 treatment. |
| 71 | 27441654 | However, instead of ameliorating podocyte injury, XAV939 further upregulated LEF1, failed to downregulate fibronectin and induced plasminogen activator inhibitor-1 (PAI-1) that associates with podocyte injury. |
| 72 | 27441654 | Collectively, the data reveal sustained activation of the Wnt/β-catenin pathway in CD2AP-/- podocytes, contributing to podocyte injury. |
| 73 | 27441654 | Furthermore, the data reveal that careful contemplation is required when targeting Wnt/β-catenin pathway to treat proteinuric kidney diseases associated with impaired CD2AP. |
| 74 | 26895305 | MicroRNA-939 down-regulates CD2-associated protein by targeting promoter in HEK-293T cells. |
| 75 | 26895305 | MicroRNA-939 down-regulates CD2-associated protein by targeting promoter in HEK-293T cells. |
| 76 | 26895305 | CD2-associated protein (CD2AP) serves as a slit diaphragm (SD) protein and plays essential roles in maintaining podocyte integrity and reducing proteinuria. |
| 77 | 26895305 | CD2-associated protein (CD2AP) serves as a slit diaphragm (SD) protein and plays essential roles in maintaining podocyte integrity and reducing proteinuria. |
| 78 | 26895305 | By scanning human CD2AP promoter in silico for sequences complementary to known miRNAs, we chose miR-939, miR-148b*, miR-191*, miR-638 as four candidates and transfected them into HEK-293T cells. |
| 79 | 26895305 | By scanning human CD2AP promoter in silico for sequences complementary to known miRNAs, we chose miR-939, miR-148b*, miR-191*, miR-638 as four candidates and transfected them into HEK-293T cells. |
| 80 | 26584949 | CD2-associated protein participates in podocyte apoptosis via PI3K/Akt signaling pathway. |
| 81 | 26584949 | CD2-associated protein participates in podocyte apoptosis via PI3K/Akt signaling pathway. |
| 82 | 26584949 | CD2-associated protein is one of the most important slit diaphragm proteins in maintaining podocyte integrity and reducing proteinuria. |
| 83 | 26584949 | CD2-associated protein is one of the most important slit diaphragm proteins in maintaining podocyte integrity and reducing proteinuria. |
| 84 | 26584949 | In this study, we demonstrate that CD2AP and p85 regulatory subunit of phosphoinositide 3-OH kinase (PI3K), recruit PI3K to the plasma membrane, and stimulate PI3K-dependent AKT signaling in podocytes the CD2AP-mediated AKT activity can regulate complex biological programs. |
| 85 | 26584949 | In this study, we demonstrate that CD2AP and p85 regulatory subunit of phosphoinositide 3-OH kinase (PI3K), recruit PI3K to the plasma membrane, and stimulate PI3K-dependent AKT signaling in podocytes the CD2AP-mediated AKT activity can regulate complex biological programs. |
| 86 | 26584949 | Our findings suggest that the activation of PI3K/AKT signaling represents an essential component to maintain the functional integrity of podocytes. |
| 87 | 26584949 | Our findings suggest that the activation of PI3K/AKT signaling represents an essential component to maintain the functional integrity of podocytes. |
| 88 | 26584949 | And PI3K/Akt signaling pathway play an important role in podocyte apoptosis. |
| 89 | 26584949 | And PI3K/Akt signaling pathway play an important role in podocyte apoptosis. |
| 90 | 26546360 | Lack of CD2AP disrupts Glut4 trafficking and attenuates glucose uptake in podocytes. |
| 91 | 26546360 | The adapter protein CD2-associated protein (CD2AP) functions in various signaling and vesicle trafficking pathways, including endosomal sorting and/or trafficking and degradation pathways. |
| 92 | 26546360 | Here, we investigated the role of CD2AP in insulin-dependent glucose transporter 4 (Glut4, also known as SLC2A4) trafficking and glucose uptake. |
| 93 | 26546360 | In subcellular membrane fractionations, CD2AP co-fractionated with Glut4, IRAP (also known as LNPEP) and sortilin, constituents of Glut4 storage vesicles (GSVs). |
| 94 | 26546360 | We further found that CD2AP forms a complex with GGA2, a clathrin adaptor, which sorts Glut4 to GSVs, suggesting a role for CD2AP in this process. |
| 95 | 26546360 | This leads to reduced insulin-stimulated trafficking of GSVs and attenuated glucose uptake into CD2AP(-/-) podocytes. |
| 96 | 26296892 | Differential Recognition Preferences of the Three Src Homology 3 (SH3) Domains from the Adaptor CD2-associated Protein (CD2AP) and Direct Association with Ras and Rab Interactor 3 (RIN3). |
| 97 | 26296892 | Thus, we studied the binding properties of each SH3 domain to the known interactor Casitas B-lineage lymphoma protein (c-CBL), conducted a peptide array screen based on the recognition motif PxPxPR and identified 40 known or novel candidate binding proteins, such as RIN3, a RAB5-activating guanine nucleotide exchange factor. |
| 98 | 26296892 | CD2AP SH3 domains 1 and 2 generally bound with similar characteristics and specificities, whereas the SH3-3 domain bound more weakly to most peptide ligands tested yet recognized an unusually extended sequence in ALG-2-interacting protein X (ALIX). |
| 99 | 26296892 | RIN3 peptide scanning arrays revealed two CD2AP binding sites, recognized by all three SH3 domains, but SH3-3 appeared non-functional in precipitation experiments. |
| 100 | 26296892 | RIN3 recruited CD2AP to RAB5a-positive early endosomes via these interaction sites. |
| 101 | 26296892 | Two high-resolution crystal structures (1.65 and 1.11 Å) of CD2AP SH3-1 and SH3-2 solved in complex with RIN3 epitopes 1 and 2, respectively, indicated that another extended motif is relevant in epitope 2. |
| 102 | 26296892 | In conclusion, we have discovered novel interaction candidates for CD2AP and characterized subtle yet significant differences in the recognition preferences of its three SH3 domains for c-CBL, ALIX, and RIN3. |
| 103 | 26234796 | Role of the heme oxygenase-adiponectin-atrial natriuretic peptide axis in renal function. |
| 104 | 26234796 | The mechanisms underlying the HO-mediated reno-protection include: (i) the restoration of renal morphology by enhancing proteins of regeneration, (ii) the potentiation of the HO-adiponectin-atrial natriuretic peptide axis, with corresponding suppression of oxidative/inflammatory insults and extracellular matrix/profibrotic factors, and (iii) the potentiation of podocyte cytoskeletal proteins such as nephrin, podocin, podocalyxin and CD2-associated-protein, which are fundamental for forming the glomerular filtration barrier that selectively allows small molecules to pass through but not large protein molecules. |
| 105 | 26234796 | Thus, this review highlights the HO-adiponectin-atrial natriuretic peptide axis in renoprotection. |
| 106 | 26082520 | The adaptor protein CD2BP2, originally identified as a binding partner of the adhesion molecule CD2, is a pre-spliceosomal assembly factor that utilizes its glycine-tyrosine-phenylalanine (GYF) domain to co-localize with spliceosomal proteins. |
| 107 | 26082520 | At the molecular level, we identified the phosphatase PP1 to be recruited to the spliceosome via the N-terminus of CD2BP2. |
| 108 | 26082520 | Given the strong expression of CD2BP2 in podocytes of the kidney, we use selective depletion of CD2BP2, in combination with next-generation sequencing, to monitor changes in exon usage of genes critical for podocyte functions, including VEGF and actin regulators. |
| 109 | 25460740 | Moreover, the effects of the HO-system on podocyte cytoskeletal proteins like podocin, podocalyxin, CD2-associated-protein (CD2AP) and proteins of regeneration/repair like beta-catenin, Oct3/4, WT1 and Pax2 in renal tissue from normoglycemic obese Zucker-fatty rats (ZFs) have not been reported. |
| 110 | 25460740 | These were associated with enhanced expression of beta-catenin, Oct3/4, WT1, Pax2 and nephrin, an essential transmembrane protein required for the formation of the scaffoldings of the podocyte slit-diaphragm, permitting the filtration of small ions, but not massive excretion of proteins, hence proteinuria. |
| 111 | 25460740 | Besides nephrin, hemin also enhanced other important podocyte-regulators including, podocalyxin, podocin and CD2AP. |
| 112 | 25460740 | Collectively, these data suggest that hemin ameliorates nephropathy by potentiating the expression of proteins of repair/regeneration, abating oxidative/inflammatory mediators, reducing renal histo-pathological lesions, while enhancing nephrin, podocin, podocalyxin, CD2AP and creatinine clearance, with corresponding reduction of albuminuria/proteinuria suggesting improved renal function in hemin-treated ZFs. |
| 113 | 25332898 | After then, CD2 associated protein, NEPH1 and transient receptor potential-6 were also found as crucial molecules of the slit diaphragm. |
| 114 | 25332898 | Then we have found that synaptic vesicle protein 2B, ephrin-B1 and neurexin were already downregulated at the early stage of puromycin aminonucleoside nephropathy, and that these molecules were localized close to nephrin. |
| 115 | 24986244 | Role of CD2-associated protein in podocyte apoptosis and proteinuria induced by angiotensin II. |
| 116 | 24986244 | Role of CD2-associated protein in podocyte apoptosis and proteinuria induced by angiotensin II. |
| 117 | 24986244 | In this study, we explored the role of CD2-associated protein in podocyte apoptosis and Proteinuria induced by Ang II. |
| 118 | 24986244 | In this study, we explored the role of CD2-associated protein in podocyte apoptosis and Proteinuria induced by Ang II. |
| 119 | 24511139 | Structure of the kidney slit diaphragm adapter protein CD2-associated protein as determined with electron microscopy. |
| 120 | 24511139 | Structure of the kidney slit diaphragm adapter protein CD2-associated protein as determined with electron microscopy. |
| 121 | 24511139 | CD2-associated protein (CD2AP) is a multidomain scaffolding protein that has a critical role in renal function. |
| 122 | 24511139 | CD2-associated protein (CD2AP) is a multidomain scaffolding protein that has a critical role in renal function. |
| 123 | 24425877 | CD2-associated protein (CD2AP) enhances casitas B lineage lymphoma-3/c (Cbl-3/c)-mediated Ret isoform-specific ubiquitination and degradation via its amino-terminal Src homology 3 domains. |
| 124 | 24425877 | In sympathetic neurons, Ret degradation is induced, at least in part, by a complex consisting of the adaptor protein CD2AP and the E3-ligase Cbl-3/c. |
| 125 | 24425877 | Knockdown of Cbl-3/c using siRNA reduced the GDNF-induced ubiquitination and degradation of Ret51 in neurons and podocytes, suggesting that Cbl-3/c was a predominant E3 ligase for Ret. |
| 126 | 24425877 | Coexpression of CD2AP with Cbl-3/c augmented the ubiquitination of Ret51 as compared with the expression of Cbl-3/c alone. |
| 127 | 24425877 | Ret51 ubiquitination by the CD2AP·Cbl-3/c complex required a functional ring finger and TKB domain in Cbl-3/c. |
| 128 | 24425877 | The SH3 domains of CD2AP were sufficient to drive the Cbl-3/c-dependent ubiquitination of Ret51, whereas the carboxyl-terminal coiled-coil domain of CD2AP was dispensable. |
| 129 | 24425877 | Interestingly, activated Ret induced the degradation of CD2AP, but not Cbl-3/c, suggesting a potential inhibitory feedback mechanism. |
| 130 | 24425877 | Taken together, these results suggest that only the SH3 domains of CD2AP were necessary to enhance the E3 ligase activity of Cbl-3/c toward Ret51. |
| 131 | 24175259 | These adaptor proteins, such as CD2-associated protein, zonula occludens 1, β-catenin, Nck and p130Cas, located at the intracellular SD insertion area near lipid rafts, have important structural and functional roles. |
| 132 | 23681557 | CD2-associated protein (CD2AP) is essential for podocyte function. |
| 133 | 23555556 | In both in vivo and in vitro studies, the expression of synaptopodin, a molecular marker for podocyte integrity, and the slit diaphragm constituting molecules (SDCM), such as nephrin, podocin, and CD2-associated protein (CD2AP), were decreased in morphine-treated podocytes. |
| 134 | 23555556 | In addition, AKT, p38, and JNK pathways were involved in morphine-induced down regulation of SDCM in human podocytes. |
| 135 | 23296190 | In addition to these receptors, Toll-like receptor 3 (TLR3) and retinoic acid-inducible gene 1 (RIG-I)-like helicases (RLHs), podocytes express the collateral proteins required to support intracellular signaling. |
| 136 | 23296190 | The transcription factor interferon regulatory factor 3 (IRF3) and nuclear factor kappa B (NF-ĸB) are phosphorylated and translocate to the nucleus, and dsRNA increases synthesis of proteins driven by IRF3 (P54, P56 and P60) or NF-ĸB (interleukin 8 and A20). |
| 137 | 23296190 | Furthermore, dsRNA suppresses podocyte cell migration, alters the expression of a panel of podocyte essential proteins (nephrin, podocin and CD2-associated protein or CD2AP) and changes transepithelial albumin flux. |
| 138 | 22693670 | The close relationships of slit diaphragm (SD) molecules such as nephrin, podocin, CD2-associated protein (CD2AP), a-actinin-4, transient receptor potential cation channel 6 (TRPC6), Densin and membrane-associated guanylate kinase inverted 1 (MAGI-1), α3β1 integrin, WT1, phospholipase C epsilon-1 (PLCE1), Lmx1b, and MYH9, and mitochondrial disorders and circulating factors in the pathogenesis of glomerular proteinuria were also gradually discovered. |
| 139 | 21911934 | Podocyte injury results in proteinuric kidney disease, and genetic deletion of SD-associated CD2-associated protein (CD2AP) leads to progressive renal failure in mice and humans. |
| 140 | 21911934 | Here, we have shown that CD2AP regulates the TGF-β1-dependent translocation of dendrin from the SD to the nucleus. |
| 141 | 21911934 | Nuclear dendrin acted as a transcription factor to promote expression of cytosolic cathepsin L (CatL). |
| 142 | 21911934 | CatL proteolyzed the regulatory GTPase dynamin and the actin-associated adapter synaptopodin, leading to a reorganization of the podocyte microfilament system and consequent proteinuria. |
| 143 | 21911934 | CD2AP itself was proteolyzed by CatL, promoting sustained expression of the protease during podocyte injury, and in turn increasing the apoptotic susceptibility of podocytes to TGF-β1. |
| 144 | 21911934 | Our study identifies CD2AP as the gatekeeper of the podocyte TGF-β response through its regulation of CatL expression and defines a molecular mechanism underlying proteinuric kidney disease. |
| 145 | 21799297 | Decreases in podocin, CD2-associated protein (CD2AP) and tensin2 may be involved in albuminuria during septic acute renal failure. |
| 146 | 21799297 | Decreases in podocin, CD2-associated protein (CD2AP) and tensin2 may be involved in albuminuria during septic acute renal failure. |
| 147 | 21799297 | There is now ample evidence that SD- and FP-associated molecules, such as podocin and CD2-associated protein (CD2AP), are down-regulated during albuminuria of chronic kidney disease. |
| 148 | 21799297 | There is now ample evidence that SD- and FP-associated molecules, such as podocin and CD2-associated protein (CD2AP), are down-regulated during albuminuria of chronic kidney disease. |
| 149 | 21799297 | Likewise, LPS treatment led to a significant decrease in CD2AP, an anchorage between podocin and F-actin. |
| 150 | 21799297 | Likewise, LPS treatment led to a significant decrease in CD2AP, an anchorage between podocin and F-actin. |
| 151 | 21799297 | Interestingly, glomerular tensin2 expression levels were also decreased during the albuminuric phase, associated with losses of glomerular F-actin and synaptopodin under septic states. |
| 152 | 21799297 | Interestingly, glomerular tensin2 expression levels were also decreased during the albuminuric phase, associated with losses of glomerular F-actin and synaptopodin under septic states. |
| 153 | 21799297 | Based on these data, we emphasize the importance of concomitant decreases in podocin, CD2AP and tensin2 during septic ARF-associated proteinuria. |
| 154 | 21799297 | Based on these data, we emphasize the importance of concomitant decreases in podocin, CD2AP and tensin2 during septic ARF-associated proteinuria. |
| 155 | 21679752 | Regulation of CD2-associated protein influences podocyte endoplasmic reticulum stress-mediated apoptosis induced by albumin overload. |
| 156 | 21679752 | Regulation of CD2-associated protein influences podocyte endoplasmic reticulum stress-mediated apoptosis induced by albumin overload. |
| 157 | 21679752 | In the present study, we investigated the role of CD2-associated protein (CD2AP) in protein overload-induced ER stress and subsequent podocyte apoptosis. |
| 158 | 21679752 | In the present study, we investigated the role of CD2-associated protein (CD2AP) in protein overload-induced ER stress and subsequent podocyte apoptosis. |
| 159 | 21679752 | The expressions of GRP78, caspase-12 and CD2AP were detected by RT-PCR or Western blot analysis. |
| 160 | 21679752 | The expressions of GRP78, caspase-12 and CD2AP were detected by RT-PCR or Western blot analysis. |
| 161 | 21679752 | Accumulation of albumin in podocytes induced ER stress and apoptosis in a concentration-dependent manner as indicated by upregulation of GRP78 and caspase-12. |
| 162 | 21679752 | Accumulation of albumin in podocytes induced ER stress and apoptosis in a concentration-dependent manner as indicated by upregulation of GRP78 and caspase-12. |
| 163 | 21679752 | Transfection of CD2AP eukaryotic expression vector into podocytes increased CD2AP expression, depressed GRP78 and caspase-12 expressions, and inhibited podocyte apoptosis. |
| 164 | 21679752 | Transfection of CD2AP eukaryotic expression vector into podocytes increased CD2AP expression, depressed GRP78 and caspase-12 expressions, and inhibited podocyte apoptosis. |
| 165 | 21679752 | It is concluded protein overload induces podocyte apoptosis via ER stress and CD2AP may play a crucial role in albumin overload-induced ER stress and apoptosis in podocytes. |
| 166 | 21679752 | It is concluded protein overload induces podocyte apoptosis via ER stress and CD2AP may play a crucial role in albumin overload-induced ER stress and apoptosis in podocytes. |
| 167 | 20654688 | Lipid phosphatase SHIP2 downregulates insulin signalling in podocytes. |
| 168 | 20654688 | To study the role of CD2-associated protein (CD2AP) in podocyte injury, we performed a yeast two-hybrid screening on a glomerular library, and found that CD2AP bound to SH2-domain-containing inositol polyphosphate 5-phosphatase 2 (SHIP2), a negative regulator of insulin signalling. |
| 169 | 20654688 | SHIP2 interacts with CD2AP in glomeruli and is expressed in podocytes, where it translocates to plasma membrane after insulin stimulation. |
| 170 | 20654688 | Overexpression of SHIP2 in cultured podocytes reduces Akt activation in response to insulin, and promotes apoptosis. |
| 171 | 20654688 | SHIP2 is upregulated in glomeruli of insulin resistant obese Zucker rats. |
| 172 | 20654688 | These results indicate that SHIP2 downregulates insulin signalling in podocytes. |
| 173 | 19679673 | TGF-beta promotes proapoptotic signaling mediated by Smad3 but also activates prosurvival pathways such as phosphoinositide-3 kinase (PI3K)/AKT; the latter requires the CD2-associated adaptor protein (CD2AP) in podocytes. |
| 174 | 19679673 | Here, we report that CD2AP-dependent early activation of the antiapoptotic PI3K/AKT pathway does not require TGF-beta receptor-regulated Smad2 and Smad3. |
| 175 | 19679673 | We found that the C-terminal region of CD2AP interacts directly with the cytoplasmic tail of the TGF-beta receptor type I (TbetaRI) in a kinase-dependent manner and that the interaction between the TbetaRI and the p85 subunit of PI3K requires CD2AP. |
| 176 | 19679673 | Consistent with the proapoptotic function of Smad signaling, Smad2/3-deficient podocytes were hyperproliferative and resistant to TGF-beta-induced growth inhibition and apoptosis. |
| 177 | 19679673 | In contrast, CD2AP-deficient cells were hypoproliferative and hypersensitive to TGF-beta-induced apoptosis. |
| 178 | 19679673 | In vivo, to determine the effects of reduced Smad3 or CD2AP gene dosage on podocyte apoptosis and proteinuria characteristic of TGF-beta1 transgenic mice, we generated TGF-beta1 transgenic mice deficient for Smad3 or heterozygous for CD2AP. |
| 179 | 19679673 | Smad3 deficiency ameliorated podocyte apoptosis, and CD2AP heterozygosity increased both podocyte apoptosis and proteinuria. |
| 180 | 19679673 | These data define distinct canonical (Smad) and noncanonical (CD2AP/PI3K/AKT) pathways that arise from direct, independent interactions with the TbetaRI and that mediate opposing signals for podocyte death or survival. |
| 181 | 19306938 | Downregulation of CD2-associated protein impaired the physiological functions of podocytes. |
| 182 | 19306938 | Downregulation of CD2-associated protein impaired the physiological functions of podocytes. |
| 183 | 19306938 | Emerging evidences show that CD2-associated protein (CD2AP) is involved in podocyte injury and the pathogenesis of proteinuria. |
| 184 | 19306938 | Emerging evidences show that CD2-associated protein (CD2AP) is involved in podocyte injury and the pathogenesis of proteinuria. |
| 185 | 19306938 | These data suggest that CD2AP may play a crucial role in maintaining the normal function of podocytes and lowered CD2AP causes podocyte injury by disrupting the cytoskeleton and disturbing the nephrin-CD2AP signaling pathway. |
| 186 | 19306938 | These data suggest that CD2AP may play a crucial role in maintaining the normal function of podocytes and lowered CD2AP causes podocyte injury by disrupting the cytoskeleton and disturbing the nephrin-CD2AP signaling pathway. |
| 187 | 19266252 | Some recent studies demonstrated that podocin, CD2-associated protein and NEPH1 are also functional molecules in the slit diaphragm, and their expressions are altered in membranous nephropathy and also in focal glomerulosclerosis. |
| 188 | 18753381 | CD2AP and Cbl-3/Cbl-c constitute a critical checkpoint in the regulation of ret signal transduction. |
| 189 | 18753381 | In an effort to elucidate mechanisms that control the half-life of Ret, we have identified two novel Ret interactors, CD2-associated protein (CD2AP) and Cbl-3. |
| 190 | 18753381 | After Ret activation by GDNF, CD2AP dissociates. |
| 191 | 18753381 | In contrast to their dissociation from autophosphorylated Ret, an interaction between CD2AP and Cbl-3 is induced by GDNF stimulation of sympathetic neurons, suggesting that CD2AP and Cbl-3 dissociate from Ret as a complex. |
| 192 | 18753381 | In neurons, the overexpression of CD2AP enhances the degradation of Ret and inhibits GDNF-dependent survival, and gene silencing of CD2AP blocks Ret degradation and promotes GDNF-mediated survival. |
| 193 | 18753381 | In combination with CD2AP, however, Cbl-3 promotes Ret degradation rapidly and almost completely blocks survival promotion by GDNF, suggesting that Cbl-3 acts as a switch that is triggered by CD2AP and oscillates between inhibition and promotion of Ret degradation. |
| 194 | 18753381 | Consistent with the hypothesis, Cbl-3 silencing in neurons only inhibited Ret degradation and enhanced neuronal survival in combination with CD2AP silencing. |
| 195 | 18753381 | CD2AP and Cbl-3, therefore, constitute a checkpoint that controls the extent of Ret downregulation and, thereby, the sensitivity of neurons to GFLs. |
| 196 | 18288369 | [Role of CD2-associated protein in podocyte differentiation.]. |
| 197 | 18288369 | [Role of CD2-associated protein in podocyte differentiation.]. |
| 198 | 18288369 | To study the cellular changes and the potential role of CD2-associated protein (CD2AP) in podocyte differentiation, conditionally immortalized murine podocyte cell line was cultured in RPMI 1640 medium under permissive condition at 33 °C. |
| 199 | 18288369 | To study the cellular changes and the potential role of CD2-associated protein (CD2AP) in podocyte differentiation, conditionally immortalized murine podocyte cell line was cultured in RPMI 1640 medium under permissive condition at 33 °C. |
| 200 | 18288369 | The expressions of CD2AP, WT1, synaptopodin and nephrin mRNAs were examined by RT-PCR. |
| 201 | 18288369 | The expressions of CD2AP, WT1, synaptopodin and nephrin mRNAs were examined by RT-PCR. |
| 202 | 18288369 | CD2AP, WT1 and nephrin protein expressions were examined by Western blot. |
| 203 | 18288369 | CD2AP, WT1 and nephrin protein expressions were examined by Western blot. |
| 204 | 18288369 | The distribution of CD2AP, nephrin, F-actin and tubulin in differentiated and undifferentiated podocytes was detected by laser scanning confocal microscopy. |
| 205 | 18288369 | The distribution of CD2AP, nephrin, F-actin and tubulin in differentiated and undifferentiated podocytes was detected by laser scanning confocal microscopy. |
| 206 | 18288369 | The results showed: (1) CD2AP, WT1 and nephrin were stably expressed in differentiated and undifferentiated podocytes while synaptopodin was only expressed in differentiated podocytes. (2) CD2AP and nephrin mRNA and protein expressions were up-regulated during podocyte differentiation (P<0.05). (3) CD2AP and tubulin were distributed in the cytoplasm and perinulcear region in undifferentiated podocytes, and F-actin was predominantly localized to a cortical belt and paralleled to the cell axis. |
| 207 | 18288369 | The results showed: (1) CD2AP, WT1 and nephrin were stably expressed in differentiated and undifferentiated podocytes while synaptopodin was only expressed in differentiated podocytes. (2) CD2AP and nephrin mRNA and protein expressions were up-regulated during podocyte differentiation (P<0.05). (3) CD2AP and tubulin were distributed in the cytoplasm and perinulcear region in undifferentiated podocytes, and F-actin was predominantly localized to a cortical belt and paralleled to the cell axis. |
| 208 | 18288369 | CD2AP colocalized with nephrin and F-actin in undifferentiated podocytes. (4) After transfection with CD2AP siRNA, the expression of CD2AP was partially inhibited and cell growth was arrested; Synaptopodin, the differentiation podocyte marker, was apparently down-regulated; The differentiation of podocytes was delayed. |
| 209 | 18288369 | CD2AP colocalized with nephrin and F-actin in undifferentiated podocytes. (4) After transfection with CD2AP siRNA, the expression of CD2AP was partially inhibited and cell growth was arrested; Synaptopodin, the differentiation podocyte marker, was apparently down-regulated; The differentiation of podocytes was delayed. |
| 210 | 18177421 | CD2-associated protein is widely expressed and differentially regulated during embryonic development. |
| 211 | 18177421 | CD2-associated protein is widely expressed and differentially regulated during embryonic development. |
| 212 | 18177421 | CD2-associated protein (CD2AP) is an adapter protein that is involved in various signaling and vesicular trafficking processes and also functions as a linker between plasma membrane proteins and the actin cytoskeleton. |
| 213 | 18177421 | CD2-associated protein (CD2AP) is an adapter protein that is involved in various signaling and vesicular trafficking processes and also functions as a linker between plasma membrane proteins and the actin cytoskeleton. |
| 214 | 18075495 | Here, we show that exogenous semaphorin3a caused acute nephrotic range proteinuria associated with podocyte foot process effacement and fusion, endothelial cell damage, decreased vascular endothelial growth factor-A receptor expression, and downregulation of the slit-diaphragm proteins podocin, nephrin, and CD2-associated protein. |
| 215 | 18075495 | When vascular endothelial growth factor 165 was administered at the same time as Semaphorin3a, no proteinuria or renal ultrastructural abnormalities occurred, suggesting that semaphorin3a effects may be mediated, in part, by downregulation of vascular endothelial growth factor receptor 2 signaling. |
| 216 | 17766183 | The intracellular domain of nephrin is associated with linker proteins, such as CD2-associated protein and Nck proteins that can connect nephrin to the actin cytoskeleton. |
| 217 | 17699558 | In addition, after knockdown of CD2-associated protein (CD2AP) and podocin, two well-characterized genetic contributors to podocyte differentiation in mammals, we observed glomerular loss of serum macromolecules similar to that seen in mammalian kidneys with inborn mutations in these genes. |
| 218 | 17667985 | Dual labeled IF showed ephrin-B1 colocalized with the slit diaphragm proteins nephrin and CD2-associated protein. |
| 219 | 17667985 | Dual labeled IF showed ephrin-B1 colocalized with the slit diaphragm proteins nephrin and CD2-associated protein. |
| 220 | 17667985 | Dual labeled IF showed ephrin-B1 colocalized with the slit diaphragm proteins nephrin and CD2-associated protein. |
| 221 | 17667985 | Ephrin-B1 colocalized with nephrin at the late capillary loop stage of kidney development. |
| 222 | 17667985 | Ephrin-B1 colocalized with nephrin at the late capillary loop stage of kidney development. |
| 223 | 17667985 | Ephrin-B1 colocalized with nephrin at the late capillary loop stage of kidney development. |
| 224 | 17667985 | Additionally, injection of rats with a nephritogenic anti-nephrin antibody (ANA) reduced ephrin-B1 expression. |
| 225 | 17667985 | Additionally, injection of rats with a nephritogenic anti-nephrin antibody (ANA) reduced ephrin-B1 expression. |
| 226 | 17667985 | Additionally, injection of rats with a nephritogenic anti-nephrin antibody (ANA) reduced ephrin-B1 expression. |
| 227 | 17667985 | When podocytes were cultured in vitro, they extruded processes that co-stained for ephrin-B1 and for CD2-associated protein. |
| 228 | 17667985 | When podocytes were cultured in vitro, they extruded processes that co-stained for ephrin-B1 and for CD2-associated protein. |
| 229 | 17667985 | When podocytes were cultured in vitro, they extruded processes that co-stained for ephrin-B1 and for CD2-associated protein. |
| 230 | 17667985 | When these podocytes were treated in culture with small interfering RNA for ephrin-B1, CD2-associated protein was reduced in the processes, with a remaining faint perinuclear staining. |
| 231 | 17667985 | When these podocytes were treated in culture with small interfering RNA for ephrin-B1, CD2-associated protein was reduced in the processes, with a remaining faint perinuclear staining. |
| 232 | 17667985 | When these podocytes were treated in culture with small interfering RNA for ephrin-B1, CD2-associated protein was reduced in the processes, with a remaining faint perinuclear staining. |
| 233 | 17537921 | Nuclear relocation of the nephrin and CD2AP-binding protein dendrin promotes apoptosis of podocytes. |
| 234 | 17537921 | Another SD protein, CD2-associated protein (CD2AP), is an adaptor molecule involved in podocyte homeostasis that can repress proapoptotic TGF-beta signaling in podocytes. |
| 235 | 17537921 | Here we show that dendrin, a protein originally identified in telencephalic dendrites, is a constituent of the SD complex, where it directly binds to nephrin and CD2AP. |
| 236 | 17459670 | TRPC6 and FSGS: the latest TRP channelopathy. |
| 237 | 17459670 | Resultant to these pursuits, several podocyte structural proteins such as nephrin, podocin, alpha-actinin 4 (ACTN4), and CD2-associated protein (CD2AP) have emerged to provide critical insight into the pathogenesis of hereditary nephrotic syndromes. |
| 238 | 17459670 | The latest advance in familial FSGS has been the discovery of a mutant form of canonical transient receptor potential cation channel 6 (TRPC6), which causes an increase in calcium transients and essentially a gain of function in this cation channel located on the podocyte cell membrane. |
| 239 | 17459670 | TRPC6 channels have been shown to be activated via phospholipase C stimulation. |
| 240 | 17459670 | Mutant TRPC6 may also amplify injurious signals mediated by Ang II, a common final pathway of podocyte apoptosis in various mammalian species. |
| 241 | 17459670 | Current evidence also suggests that blocking TRPC6 channels may be of therapeutic benefit in idiopathic FSGS, a disease with a generally poor prognosis. |
| 242 | 17459670 | This creates the exciting possibility that blocking TRPC6 channels within the podocyte may translate into long-lasting clinical benefits in patients with FSGS. |
| 243 | 17213204 | CD2AP/CIN85 balance determines receptor tyrosine kinase signaling response in podocytes. |
| 244 | 17213204 | CD2-associated protein (CD2AP) is highly expressed in podocytes and is considered to play an important role in the maintenance of the glomerular slit diaphragm. |
| 245 | 17213204 | In addition, we demonstrate that CIN85, a paralog of CD2AP, is involved in termination of RTK signaling in podocytes. |
| 246 | 17213204 | CIN85 protein expression is increased in CD2AP(-/-) podocytes in vitro. |
| 247 | 17213204 | Stimulation of CD2AP(-/-) podocytes with various growth factors, including insulin-like growth factor 1, vascular endothelial growth factor, and fibroblast growth factor, resulted in a significantly decreased phosphatidylinositol 3-kinase/AKT and ERK signaling response. |
| 248 | 17213204 | Moreover, increased CIN85 protein is detectable in podocytes in diseased CD2AP(-/-) mice, leading to decreased base-line activation of ERK and decreased phosphorylation after growth factor stimulation in vivo. |
| 249 | 17213204 | Because repression of CIN85 protein leads to a restored RTK signaling response, our results support an important role of CD2AP/CIN85 protein balance in the normal signaling response of podocytes. |
| 250 | 16889564 | Nephrin and podocin were identified as gene products mutated in Finnish-type congenital nephrotic syndrome and autosomal recessive steroid-resistant nephrotic syndrome, respectively. |
| 251 | 16889564 | The expression of nephrin and podocin was reduced in glomeruli of minimal change nephrotic syndrome, which suggested that the altered expression of these molecules contributes to the development of proteinuria also in acquired diseases. |
| 252 | 16889564 | Some recent studies demonstrated that CD2-associated protein (CD2AP) is also a functional molecule in the slit diaphragm, and its expression is altered in membranous nephropathy. |
| 253 | 16886065 | Increased ferritin permeability was not observed in nephrotic CD2-associated protein-null (Cd2ap-/-) mice, which have a primary podocyte defect. |
| 254 | 16841182 | Podocyte-associated proteins FAT, alpha-actinin-4 and filtrin are expressed in Langerhans islets of the pancreas. |
| 255 | 16841182 | Recently, genetic mapping of proteinuric kidney disease genes and animal models have revealed further important molecules for the kidney filtration function including alpha-actinin-4, podocin, FAT, and NEPH1. |
| 256 | 16841182 | This study was addressed to explore the pancreatic expression of the podocyte molecules podocin, FAT, alpha-actinin-4, NEPH1, NEPH2, filtrin/NEPH3, synaptopodin and CD2 associated protein (CD2AP). |
| 257 | 16841182 | Of the nephrin-associated podocyte proteins, filtrin/NEPH3, FAT, and alpha-actinin-4 were found to be expressed in the pancreas at the gene and protein level and localized to Langerhans islets. |
| 258 | 16752799 | Seven genes have been recognized till present, which mutations are responsible for severe forms of NS: NPHS1, NPHS2, ACTN4, CD2AP and WT1, TRPC6, LAMB2. |
| 259 | 16752799 | Proteins encoded by these genes (nephrin, podocin, alpha-actinin-4, an adapter protein anchoring CD2 and others) influence the function of the podocytes. |
| 260 | 16752799 | It was concluded that patients with steroid resistant nephrotic syndrome (SRNS) with homozygous or compound heterozygous mutations in NPHS2 have reduced risk for recurrence of focal segmental glomerulosclerosis (FSGS) in renal transplant (only 8% in comparison with 35% in patients without mutation in NPHS2). |
| 261 | 16752799 | This polymorphism appears to enhance susceptibility to FSGS in association with a second mutant NPHS2 allele. |
| 262 | 16752799 | There are also 3 genetic loci connected with autosomal dominant forms of FSGS: ACTN4, TRPC6 and CD2AP (found only in the mice models). |
| 263 | 16628251 | Defects in several podocyte proteins have been implicated in the etiology of FSGS, including podocin, alpha-actinin-4, CD2-associated protein (CD2AP), and TRPC6. |
| 264 | 16628251 | Combinations of Cd2ap heterozygosity and heterozygosity of either synaptopodin (Synpo) or Fyn proto-oncogene (Fyn) but not kin of IRRE like 1 (Neph1) resulted in spontaneous proteinuria and in FSGS-like glomerular damage. |
| 265 | 16628251 | These genetic interactions were also reflected at a functional level, as we found that CD2AP associates with Fyn and Synpo but not with Neph1. |
| 266 | 16541019 | Sema 3A decreased semaphorin 3B, plexin A1, A3, and D1 >/=50% and reduced plexin A2 mRNA to undetectable levels. |
| 267 | 16541019 | Sema 3A induced a dose-response podocin downregulation and decreased its interaction with CD2-associated protein and nephrin, as determined by Western analysis and co-immunoprecipitation. |
| 268 | 16541019 | Sema 3A induced a 10-fold increase in podocyte apoptosis and significantly decreased the activity of the Akt survival pathway. |
| 269 | 16388393 | Glomerular expression of transforming growth factor-beta (TGF-beta) isoforms in mice lacking CD2-associated protein. |
| 270 | 16388393 | Glomerular expression of transforming growth factor-beta (TGF-beta) isoforms in mice lacking CD2-associated protein. |
| 271 | 16388393 | Mice lacking CD2-associated protein (CD2AP-/-) develop glomerular lesions resembling human focal segmental glomerulosclerosis (FSGS) between 3-4 weeks of age and die approximately 2 weeks later from massive proteinuria and renal failure. |
| 272 | 16388393 | Mice lacking CD2-associated protein (CD2AP-/-) develop glomerular lesions resembling human focal segmental glomerulosclerosis (FSGS) between 3-4 weeks of age and die approximately 2 weeks later from massive proteinuria and renal failure. |
| 273 | 16280470 | In the case of the podocyte line, differentiation occurred on all three matrices as indicated by the expression of synaptopodin and CD2-associated protein (CD2AP) and organization of myosin heavy chain IIA into a linear pattern. |
| 274 | 16280470 | Evidence for podocytic differentiation occurred on all three collagen matrices as indicated by the redistribution of myosin IIA to a linear pattern and expression of synaptopodin, CD2AP, and alpha-actinin. |
| 275 | 16050398 | Other genes involved in the slit-diaphragm or the nephrotic syndrome are CD2-associated protein (CD2AP), FAT1, WT1, LMX1B, SMARCAL1. |
| 276 | 15997642 | The main components of the slit diaphragm are nephrin, the product of NPHS1 gene and podocin, the product of NPHS2 gene. |
| 277 | 15997642 | Mutations in NPHS1 lead to congenital nephrotic syndrome of the Finnish type (CNF), whereas NPHS2 mutations result in focal segmental glomerulosclerosis (FSGS). |
| 278 | 15997642 | Reduced expression and redistribution of nephrin and podocin are also seen in podocytes of patients with acquired glomerulopathies. |
| 279 | 15997642 | Together with podocin and CD2AP (CD2-associated protein), nephrin forms a complex determining the integrity of the slit diaphragm. |
| 280 | 15968559 | Also, the genes encoding the four major slit diaphragm proteins, nephrin, podocin, Neph1 and CD2-associated protein were sequenced in 38 patients with MCNS of varying severity. |
| 281 | 15968559 | The genetic analyses revealed heterozygous amino acid changes in nephrin and podocin in 10 of the 38 patients studied. |
| 282 | 15968559 | On the other hand, the genes coding for Neph1 and CD2AP were highly conserved and no amino acid substitutions were detected. |
| 283 | 15956777 | The docking protein CD2AP (CD2-associated protein) serves a nonredundant function in podocytes as CD2AP knockout mice die of renal failure at the age of 6-7 wk. |
| 284 | 15956777 | In conditionally immortalized mouse podocytes, we demonstrate that CD2AP colocalizes with cortactin and F-actin in spots of < or =0.5-microm diameter. |
| 285 | 15956777 | A significant portion of spot-associated vesicles belongs to a later endosomal-sorting compartment, characterized by delayed uptake of fluorescent dextran (10 kDa) and by colocalization with Rab4, but not Rab5 and AP-2. |
| 286 | 15951437 | CD2-associated protein (CD2AP) expression in podocytes rescues lethality of CD2AP deficiency. |
| 287 | 15951437 | CD2-associated protein (CD2AP) expression in podocytes rescues lethality of CD2AP deficiency. |
| 288 | 15951437 | Mice born without CD2-associated protein (CD2AP) develop renal failure and nephrotic syndrome about 4 weeks after birth and die around 6 weeks of age. |
| 289 | 15951437 | Mice born without CD2-associated protein (CD2AP) develop renal failure and nephrotic syndrome about 4 weeks after birth and die around 6 weeks of age. |
| 290 | 15659563 | Nephrotic plasma alters slit diaphragm-dependent signaling and translocates nephrin, Podocin, and CD2 associated protein in cultured human podocytes. |
| 291 | 15659563 | Nephrotic plasma alters slit diaphragm-dependent signaling and translocates nephrin, Podocin, and CD2 associated protein in cultured human podocytes. |
| 292 | 15659563 | Podocytes are critical in maintaining the filtration barrier of the glomerulus and are dependent on the slit diaphragm (SD) proteins nephrin, podocin, and CD2-associated protein (CD2AP) to function optimally. |
| 293 | 15659563 | Podocytes are critical in maintaining the filtration barrier of the glomerulus and are dependent on the slit diaphragm (SD) proteins nephrin, podocin, and CD2-associated protein (CD2AP) to function optimally. |
| 294 | 15659563 | With the use of a conditionally immortalized human podocyte cell line, it first was shown that exposure to normal and non-nephrotic human plasma leads to a concentration of nephrin, podocin, CD2AP, and actin at the cell surface. |
| 295 | 15659563 | With the use of a conditionally immortalized human podocyte cell line, it first was shown that exposure to normal and non-nephrotic human plasma leads to a concentration of nephrin, podocin, CD2AP, and actin at the cell surface. |
| 296 | 15659563 | When exposed to all nephrotic plasma samples (and a non-human serum control), nephrin podocin and CD2AP assumed a cytoplasmic distribution; nephrin and synaptopodin were selectively downregulated, and the relocation of nephrin induced by nephrotic plasma could be rescued back to the plasma membrane by co-incubation with non-nephrotic plasma. |
| 297 | 15659563 | When exposed to all nephrotic plasma samples (and a non-human serum control), nephrin podocin and CD2AP assumed a cytoplasmic distribution; nephrin and synaptopodin were selectively downregulated, and the relocation of nephrin induced by nephrotic plasma could be rescued back to the plasma membrane by co-incubation with non-nephrotic plasma. |
| 298 | 15213232 | A novel role for the adaptor molecule CD2-associated protein in transforming growth factor-beta-induced apoptosis. |
| 299 | 15213232 | A novel role for the adaptor molecule CD2-associated protein in transforming growth factor-beta-induced apoptosis. |
| 300 | 15213232 | CD2-associated protein (CD2AP) is an adaptor molecule involved in T cell receptor signaling and podocyte homeostasis. |
| 301 | 15213232 | CD2-associated protein (CD2AP) is an adaptor molecule involved in T cell receptor signaling and podocyte homeostasis. |
| 302 | 15213232 | Here we report that increased transforming growth factor-beta1 (TGF-beta1) expression and apoptosis were present in podocytes at the onset of albuminuria and were followed by depletion of podocytes associated with progressive focal-segmental glomerulosclerosis in CD2AP-/- mice. |
| 303 | 15213232 | Here we report that increased transforming growth factor-beta1 (TGF-beta1) expression and apoptosis were present in podocytes at the onset of albuminuria and were followed by depletion of podocytes associated with progressive focal-segmental glomerulosclerosis in CD2AP-/- mice. |
| 304 | 15213232 | Conditionally immortalized podocytes derived from CD2AP-/- mice were more susceptible to TGF-beta-induced apoptosis compared with CD2AP+/+ podocytes. |
| 305 | 15213232 | Conditionally immortalized podocytes derived from CD2AP-/- mice were more susceptible to TGF-beta-induced apoptosis compared with CD2AP+/+ podocytes. |
| 306 | 15213232 | Reconstitution of CD2AP rescued CD2AP-/- podocytes from TGF-beta-induced apoptosis. |
| 307 | 15213232 | Reconstitution of CD2AP rescued CD2AP-/- podocytes from TGF-beta-induced apoptosis. |
| 308 | 15213232 | CD2AP was required for early activation of anti-apoptotic phosphatidylinositol 3-kinase (PI3K)/AKT and extracellular signal-regulated kinase 1/2 by TGF-beta. |
| 309 | 15213232 | CD2AP was required for early activation of anti-apoptotic phosphatidylinositol 3-kinase (PI3K)/AKT and extracellular signal-regulated kinase 1/2 by TGF-beta. |
| 310 | 15213232 | In contrast, activation of pro-apoptotic p38 MAPK by TGF-beta was accelerated and enhanced in the absence of CD2AP. |
| 311 | 15213232 | In contrast, activation of pro-apoptotic p38 MAPK by TGF-beta was accelerated and enhanced in the absence of CD2AP. |
| 312 | 15213232 | CD2AP was not required for PI3K/AKT activation by insulin and epidermal growth factor, indicating that CD2AP is a selective mediator of anti-apoptotic TGF-beta signaling. |
| 313 | 15213232 | CD2AP was not required for PI3K/AKT activation by insulin and epidermal growth factor, indicating that CD2AP is a selective mediator of anti-apoptotic TGF-beta signaling. |
| 314 | 15213232 | In summary, we identified CD2AP as a novel mediator for selective activation of survival pathways and repression of apoptosis signaling by TGF-beta in podocytes. |
| 315 | 15213232 | In summary, we identified CD2AP as a novel mediator for selective activation of survival pathways and repression of apoptosis signaling by TGF-beta in podocytes. |
| 316 | 15213232 | Together, our in vitro and in vivo findings suggest that TGF-beta-induced podocyte apoptosis is an early pathomechanism in mice developing focal-segmental glomerulosclerosis associated with functional impairment of CD2AP. |
| 317 | 15213232 | Together, our in vitro and in vivo findings suggest that TGF-beta-induced podocyte apoptosis is an early pathomechanism in mice developing focal-segmental glomerulosclerosis associated with functional impairment of CD2AP. |
| 318 | 14643126 | CD2-associated protein and glomerular disease. |
| 319 | 12874460 | Protein levels of nephrin, podocin, CD2-associated protein, and podocalyxin were investigated using quantitative immunohistochemical assays. |
| 320 | 12874460 | Real-time PCR was used to determine the mRNA levels of nephrin, podocin, and podoplanin in microdissected glomeruli. |
| 321 | 12874460 | In most acquired renal diseases, except in IgA nephropathy, a marked reduction was observed at the protein levels of nephrin, podocin, and podocalyxin, whereas an increase of the glomerular mRNA levels of nephrin, podocin, and podoplanin was found, compared with controls. |
| 322 | 12874460 | The mean width of the podocyte foot processes was inversely correlated with the protein levels of nephrin (r = -0.443, P < 0.05), whereas it was positively correlated with podoplanin mRNA levels (r = 0.468, P < 0.05) and proteinuria (r = 0.585, P = 0.001). |
| 323 | 12832477 | Nephrin and CD2AP associate with phosphoinositide 3-OH kinase and stimulate AKT-dependent signaling. |
| 324 | 12832477 | Mutations of NPHS1 or NPHS2, the genes encoding nephrin and podocin, as well as the targeted disruption of CD2-associated protein (CD2AP), lead to heavy proteinuria, suggesting that all three proteins are essential for the integrity of glomerular podocytes, the visceral glomerular epithelial cells of the kidney. |
| 325 | 12832477 | We demonstrate that both nephrin and CD2AP interact with the p85 regulatory subunit of phosphoinositide 3-OH kinase (PI3K) in vivo, recruit PI3K to the plasma membrane, and, together with podocin, stimulate PI3K-dependent AKT signaling in podocytes. |
| 326 | 12832477 | Using two-dimensional gel analysis in combination with a phosphoserine-specific antiserum, we demonstrate that the nephrin-induced AKT mediates phosphorylation of several target proteins in podocytes. |
| 327 | 12832477 | One such target is Bad; its phosphorylation and inactivation by 14-3-3 protects podocytes against detachment-induced cell death, suggesting that the nephrin-CD2AP-mediated AKT activity can regulate complex biological programs. |
| 328 | 12832477 | Our findings reveal a novel role for the slit diaphragm proteins nephrin, CD2AP, and podocin and demonstrate that these three proteins, in addition to their structural functions, initiate PI3K/AKT-dependent signal transduction in glomerular podocytes. |
| 329 | 12764198 | CD2-associated protein haploinsufficiency is linked to glomerular disease susceptibility. |
| 330 | 12764198 | CD2-associated protein haploinsufficiency is linked to glomerular disease susceptibility. |
| 331 | 12764198 | Loss of CD2-associated protein (CD2AP), a component of the filtration complex in the kidney, causes death in mice at 6 weeks of age. |
| 332 | 12764198 | Loss of CD2-associated protein (CD2AP), a component of the filtration complex in the kidney, causes death in mice at 6 weeks of age. |
| 333 | 12704576 | This review will focus on the remnant kidney model, the podocyte injury models of puromycin aminonucleoside or adriamycin injection, and examples of newly developed genetic models, such as knockout of CD2 associated protein (CD2AP). |
| 334 | 12039988 | The immunohistochemical staining showed also that the interaction partner of nephrin, CD2-associated protein (CD2AP), and the slit-diaphragm-associated protein, ZO-1alpha (-), appeared unchanged, whereas the major anionic apical membrane protein of podocytes, podocalyxin, somewhat punctate as compared with the wild-type (wt) and nephrin(wt/trap) stainings. |
| 335 | 11912254 | In contrast, the intensity of staining for ZO-1 and CD2-associated protein (CD2AP), two other proteins that are located on the cytoplasmic face of the slit diaphragm, was undiminished. |
| 336 | 11912254 | Immunogold electron microscopy confirmed the progressive disappearance of nephrin from podocyte foot processes and retention of CD2AP. |
| 337 | 11880318 | CD2-associated protein (CD2AP) is also necessary for normal glomerular permeability and is a putative nephrin adapter molecule. |
| 338 | 11880318 | Here, we document that nephrin and CD2AP are linked to the actin cytoskeleton. |
| 339 | 11880318 | As detected by Western blot analysis, nephrin and CD2AP were both insoluble when cell membranes from normal rat glomeruli were extracted with 0.5% Triton X-100 (TX-100) at 4 degrees C in the presence of divalent cations, but they were solubilized when the extraction included potassium iodide (KI) to depolymerize F-actin. |
| 340 | 11880318 | In addition, a small fraction of the solubilized nephrin and CD2AP was recovered in the low-density fractions of OptiPrep flotation gradients, which indicates that a portion of nephrin, possibly associated with CD2AP, resides in a cholesterol- or sphingolipid-rich region of the plasma membrane. |
| 341 | 11880318 | Immunofluorescent staining of unfixed sections of normal rat kidney for nephrin, CD2AP, and F-actin was unaltered by treatment with TX-100 but was greatly diminished by addition of KI. |
| 342 | 11880318 | These results document that nephrin anchors the slit diaphragm to the actin cytoskeleton, possibly by linkage to CD2AP, and that nephrin traverses a relatively cholesterol-poor region of the podocyte plasma membrane. |
| 343 | 11880318 | In addition, a small pool of actin-associated nephrin and CD2AP resides in lipid rafts, possibly in the cholesterol-rich apical region of the podocyte-foot processes. |
| 344 | 11562357 | Interaction with podocin facilitates nephrin signaling. |
| 345 | 11562357 | Mutations of NPHS1 or NPHS2, the genes encoding for the glomerular podocyte proteins nephrin and podocin, cause steroid-resistant proteinuria. |
| 346 | 11562357 | In addition, mice lacking CD2-associated protein (CD2AP) develop a nephrotic syndrome that resembles NPHS mutations suggesting that all three proteins are essential for the integrity of glomerular podocytes. |
| 347 | 11562357 | Nephrin-induced signaling is greatly enhanced by podocin, which binds to the cytoplasmic tail of nephrin. |
| 348 | 11562357 | Mutational analysis suggests that abnormal or inefficient signaling through the nephrin-podocin complex contributes to the development of podocyte dysfunction and proteinuria. |
| 349 | 11553524 | CD2AP and p130Cas localize to different F-actin structures in podocytes. |
| 350 | 11553524 | CD2AP and p130Cas localize to different F-actin structures in podocytes. |
| 351 | 11553524 | Mice lacking the 80-kDa CD2-associated protein (CD2AP) develop progressive renal failure that starts soon after birth with proteinuria and foot process effacement by unknown mechanisms. |
| 352 | 11553524 | Mice lacking the 80-kDa CD2-associated protein (CD2AP) develop progressive renal failure that starts soon after birth with proteinuria and foot process effacement by unknown mechanisms. |
| 353 | 11553524 | CD2AP has been identified and cloned independently by virtue of its interaction with the T cell protein CD2 and with the docking protein p130Cas. |
| 354 | 11553524 | CD2AP has been identified and cloned independently by virtue of its interaction with the T cell protein CD2 and with the docking protein p130Cas. |
| 355 | 11553524 | In the present study we examined the localization of CD2AP and p130Cas in the mouse glomerulus and in cultured podocytes. |
| 356 | 11553524 | In the present study we examined the localization of CD2AP and p130Cas in the mouse glomerulus and in cultured podocytes. |
| 357 | 11553524 | In glomeruli, CD2AP and p130Cas immunofluorescence were observed in podocytes, where they colocalized with F-actin in foot processes. |
| 358 | 11553524 | In glomeruli, CD2AP and p130Cas immunofluorescence were observed in podocytes, where they colocalized with F-actin in foot processes. |
| 359 | 11553524 | In cultured podocytes, p130Cas was enriched at sites of focal adhesions, where it colocalized like vinculin with F-actin at stress fiber ends. |
| 360 | 11553524 | In cultured podocytes, p130Cas was enriched at sites of focal adhesions, where it colocalized like vinculin with F-actin at stress fiber ends. |
| 361 | 11553524 | The spot-shaped F-actin structures were also stained by antibodies against the actin nucleation Arp2/3 complex and cortactin, both contributing to dynamic actin assembly. |
| 362 | 11553524 | The spot-shaped F-actin structures were also stained by antibodies against the actin nucleation Arp2/3 complex and cortactin, both contributing to dynamic actin assembly. |
| 363 | 11553524 | Moreover, CD2AP spots in cultured podocytes were in close spatial association with actinin-4, but not actinin-1. |
| 364 | 11553524 | Moreover, CD2AP spots in cultured podocytes were in close spatial association with actinin-4, but not actinin-1. |
| 365 | 11553524 | Our results suggest that CD2AP and p130Cas, which both colocalize with F-actin in podocytes in situ, possess different functions. |
| 366 | 11553524 | Our results suggest that CD2AP and p130Cas, which both colocalize with F-actin in podocytes in situ, possess different functions. |
| 367 | 11553524 | Whereas p130Cas is found in focal adhesions, CD2AP seems to be involved in the regulation of highly dynamic F-actin structures in podocyte foot processes. |
| 368 | 11553524 | Whereas p130Cas is found in focal adhesions, CD2AP seems to be involved in the regulation of highly dynamic F-actin structures in podocyte foot processes. |
| 369 | 11458036 | However, more recent studies on nephrin, a key component of the slit diaphragm, as well as the podocyte and slit diaphragm-associated intracellular proteins, CD2-associated protein, podocin and alpha-actinin-4, have emphasized the role of the slit diaphragm as a central size-selective filtration barrier. |
| 370 | 11195047 | CD2-associated protein and the kidney. |
| 371 | 11195047 | CD2-associated protein and the kidney. |
| 372 | 11195047 | In particular, two proteins, CD2-associated protein and nephrin, have been identified as critical podocyte proteins that are both required for normal glomerular filtration. |
| 373 | 11195047 | In particular, two proteins, CD2-associated protein and nephrin, have been identified as critical podocyte proteins that are both required for normal glomerular filtration. |
| 374 | 10997929 | CD2AP is expressed with nephrin in developing podocytes and is found widely in mature kidney and elsewhere. |
| 375 | 10997929 | CD2-associated protein (CD2AP) is an adapter molecule that can bind to the cytoplasmic domain of nephrin, a component of the glomerular slit diaphragm. |
| 376 | 10997929 | Mice lacking CD2AP exhibit a congenital nephrotic syndrome characterized by extensive foot process effacement, suggesting that CD2AP-nephrin interactions are critical to maintaining slit diaphragm function. |
| 377 | 10997929 | We have examined the patterns of expression of both CD2AP and nephrin in developing mouse and human kidney. |
| 378 | 10997929 | Kidneys from Cd2ap -/- mice initially exhibited normal nephrin localization, but as the mice aged and foot processes became effaced, nephrin disappeared. |
| 379 | 10997929 | In laminin-beta(2) mutant mice exhibiting nephrotic syndrome, CD2AP in glomeruli was aberrantly localized in a primarily punctate pattern. |
| 380 | 10913159 | In vivo interaction of the adapter protein CD2-associated protein with the type 2 polycystic kidney disease protein, polycystin-2. |
| 381 | 10913159 | In vivo interaction of the adapter protein CD2-associated protein with the type 2 polycystic kidney disease protein, polycystin-2. |
| 382 | 10913159 | The deduced 70.5-kDa protein, originally named METS-1 (mesenchyme-to-epithelium transition protein with SH3 domains), has since been cloned as a CD2-associated protein (CD2AP). |
| 383 | 10913159 | The deduced 70.5-kDa protein, originally named METS-1 (mesenchyme-to-epithelium transition protein with SH3 domains), has since been cloned as a CD2-associated protein (CD2AP). |
| 384 | 10913159 | Independent yeast two-hybrid screens using the COOH-terminal region of either CD2AP or polycystin-2 as bait identified the COOH termini of polycystin-2 and CD2AP, respectively, as strong interacting partners. |
| 385 | 10913159 | Independent yeast two-hybrid screens using the COOH-terminal region of either CD2AP or polycystin-2 as bait identified the COOH termini of polycystin-2 and CD2AP, respectively, as strong interacting partners. |
| 386 | 10913159 | This interaction was confirmed in cultured cells by co-immunoprecipitation of endogenous polycystin-2 with endogenous CD2AP and vice versa. |
| 387 | 10913159 | This interaction was confirmed in cultured cells by co-immunoprecipitation of endogenous polycystin-2 with endogenous CD2AP and vice versa. |
| 388 | 10913159 | CD2AP shows a diffuse reticular cytoplasmic and perinuclear pattern of distribution, similar to polycystin-2, in cultured cells, and the two proteins co-localize by indirect double immunofluorescence microscopy. |
| 389 | 10913159 | CD2AP shows a diffuse reticular cytoplasmic and perinuclear pattern of distribution, similar to polycystin-2, in cultured cells, and the two proteins co-localize by indirect double immunofluorescence microscopy. |
| 390 | 10913159 | Such a function fits well with that hypothesized for the polycystin proteins in renal tubular epithelial cells, and the present findings suggest that CD2AP has a role in polycystin-2 function. |
| 391 | 10913159 | Such a function fits well with that hypothesized for the polycystin proteins in renal tubular epithelial cells, and the present findings suggest that CD2AP has a role in polycystin-2 function. |