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Gene Information
Gene symbol: VIM
Gene name: vimentin
HGNC ID: 12692
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 34629746 | Expressions of podocytes injury-, apoptosis- and epithelial-to-mesenchymal transition (EMT)- and JNK-interacting protein 4/p38-Mitogen-Activated Protein Kinase (JIP4/p38-MAPK) pathway-related factors were measured using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot as needed. |
| 2 | 34629746 | Interaction between PP2A and JIP4/MAPK pathway was confirmed using co-immunoprecipitation (Co-Ip) assay. |
| 3 | 34629746 | In podocytes, ADR inhibited PP2A, Nephrin and Wilms' tumor (WT) 1 expressions yet upregulated apoptosis and Desmin expression, and suppressing PP2A expressionenhanced the effects. |
| 4 | 34629746 | Additionally, in ADR-treated podocytes, PP2A suppression enhanced the effects of ADR, yet silencing of JIP4 reversed the effects of PP2A suppression on regulating p38-MAPK pathway-, apoptosis- and EMT-related factors expressions and apoptosis, with upregulations of B-cell lymphoma-2 (Bcl-2) and E-cadherin and down-regulations of Bcl-2 associated protein X (Bax), cleaved (C)-casapse-3, N-cadherin, Vimentin and Snail. |
| 5 | 34629746 | PP2A protects ADR-treated podocytes against injury and EMT by suppressing JIP4/p38-MAPK pathway, showing their interaction in podocytes. |
| 6 | 33901627 | Meanwhile, C-peptide suppressed high glucose-induced epithelial-mesenchymal transition (EMT) and renal fibrosis via decreasing the expression of snail, vimentin, α-smooth muscle actin (α-SMA) and connective tissue growth factor (CTGF). |
| 7 | 33901627 | Moreover, the Notch and transforming growth factor-β (TGF-β) signaling pathways were activated by high glucose, and treatment with C-peptide down-regulated the expression of the Notch signaling molecules Notch 1 and Jagged 1 and the TGF-β signaling molecule TGF-β1. |
| 8 | 33613972 | Kidney tissues were subjected to histo-biochemical analysis along with mRNA gene expression quantification for cytoskeleton proteins encoding genes (vimentin, nestin, and connexin 43) by real-time reverse transcription polymerase chain reaction. |
| 9 | 33024228 | Western blot and immunocytochemistry confirmed the alteration in the protein expression of tubulin, vimentin, podocin, cofilin-1, vinculin, E-cadherin, nephrin, VCAM-1, tenascin-C, and β-catenin. |
| 10 | 32737144 | LIM-Nebulette Reinforces Podocyte Structural Integrity by Linking Actin and Vimentin Filaments. |
| 11 | 32597007 | Vimentin and α-SMA, markers of changes to the epithelial cell phenotype, were present in PECs in aged CD44+/+ mice, but absent in aged CD44-/- mice in both outer cortical (OC) and juxtamedullary (JM) glomeruli. |
| 12 | 32597007 | Because age-related glomerular hypertrophy was lower in CD44-/- mice, mTOR activation was assessed by phospho-S6 ribosomal protein (pS6RP) staining. |
| 13 | 32597007 | These results show that the increase in CD44 in PECs in aged kidneys contributes to several changes to the glomerulus during healthy aging in mice, and may involve ERK and mTOR activation. |
| 14 | 32451085 | TGF-β1 decreased the expression of epithelial markers such as nephrin, zonula occludens-1 (ZO-1), while it increased the mesenchymal markers, including fibronectin (FN), vimentin, and α-smooth muscle actin (α-SMA) in the podocytes. |
| 15 | 32028827 | Western blot analysis indicated that it could restore the expression of RhoA, ROCK and vimentin, nephrin, podocin and p65 and IκBα phosphorylation. |
| 16 | 31741405 | Furthermore, curcumin upregulated the expression of E-cadherin and LC3 proteins and downregulated the vimentin, TWIST1, p62, p-mTOR, p-Akt and P13K levels in DN rats and MPC5 cells. |
| 17 | 31741405 | Discussion and conclusions: The protection against development of DN by curcumin treatment involved changes in inducing autophagy and alleviating podocyte EMT, through the PI3k/Akt/mTOR pathway, providing the scientific basis for further research and clinical applications of curcumin. |
| 18 | 31432191 | KLF4 overexpression also inhibited podocyte apoptosis and downregulated vimentin and α‑smooth muscle actin, and upregulated E‑cadherin and nephrin, both in vivo and in vitro. |
| 19 | 31377057 | Inhibition of the ERK1/2-mTORC1 axis ameliorates proteinuria and the fibrogenic action of transforming growth factor-β in Adriamycin-induced glomerulosclerosis. |
| 20 | 31377057 | Here, we identified the regulation of mammalian target of rapamycin complex1 (mTORC1) by TGF-β via ERK1/2 in the Adriamycin-induced murine model of focal segmental glomerulosclerosis. |
| 21 | 31377057 | Phosphorylation of the TGF-β receptor-I (TGF-βRI), Smad3, ERK1/2 and ribosomal protein S6 were evident in the glomeruli of adriamycin-treated mice. |
| 22 | 31377057 | Targeting TGFβ-RI and mTORC1 with pharmacological inhibitors suppressed TGF-β signaling in glomeruli and significantly reduced albuminuria, glomerulosclerosis, protein levels of collagen 4α3, plasminogen activator inhibitor-1, and vimentin and restored mRNA levels of podocyte markers. |
| 23 | 31377057 | Low dose US Food and Drug Administration (FDA)-approved MEK/ERK inhibitor trametinib/GSK1120212 blunted TGF-β1-induced mTORC1 activation in podocytes, ameliorated up-regulation of TGF-β, plasminogen activator inhibitor-1, monocyte chemoattractant protein-1, fibronectin and α-smooth muscle actin and prevented albuminuria and glomerulosclerosis with improved serum albumin. |
| 24 | 31377057 | In cultured podocytes, this pathway was found to be associated with translation of fibrogenic collagen 4α3 and plasminogen activator inhibitor-1, without influencing their transcription. |
| 25 | 31191670 | Furthermore, these cells express the typical MSC markers CD73, CD90, and CD105. |
| 26 | 31191670 | Immunofluorescence-based stainings of sectioned 3D-NPCs revealed cells expressing the renal progenitor cell markers (SIX2 and PAX8), podocyte markers (Nephrin and Podocin), the endothelial marker (CD31), and mesenchymal markers (Vimentin and PDGFR-β). |
| 27 | 30258943 | The imPOD cells express most podocyte-related markers, including WT-1, Nephrin, Tubulin and Vinculin, but not differentiation marker Synaptopodin. |
| 28 | 30258943 | We further demonstrate that TGFβ1 induces a podocyte injury-like response in the FLP-reverted imPOD cells by suppressing the expression of slit diaphragm-associated proteins P-Cadherin and ZO-1 and upregulating the expression of mesenchymal markers, α-SMA, Vimentin and Nestin, as well as fibrogenic factors CTGF and Col1a1. |
| 29 | 29990736 | Differential susceptibility of kidneys and livers to proliferative processes and transcriptional level of the genes encoding desmin, vimentin, connexin 43, and nestin in rats exposed to furan. |
| 30 | 29990736 | Differential susceptibility of kidneys and livers to proliferative processes and transcriptional level of the genes encoding desmin, vimentin, connexin 43, and nestin in rats exposed to furan. |
| 31 | 29990736 | The transcriptional levels of intermediate filament proteins (desmin, vimentin, nestin, and connexin 43) were assessed by using quantitative real-time polymerase chain reaction (PCR), and the cell proliferation markers (proliferating cell nuclear antigen [PCNA] and proliferation-associated nuclear antigen [Ki-67]) were recognized by immunohistochemical analysis. |
| 32 | 29990736 | The transcriptional levels of intermediate filament proteins (desmin, vimentin, nestin, and connexin 43) were assessed by using quantitative real-time polymerase chain reaction (PCR), and the cell proliferation markers (proliferating cell nuclear antigen [PCNA] and proliferation-associated nuclear antigen [Ki-67]) were recognized by immunohistochemical analysis. |
| 33 | 29990736 | Moreover, furan enhances the expression of PCNA and Ki-67 in the liver tissues but not in the kidney tissues. |
| 34 | 29990736 | Moreover, furan enhances the expression of PCNA and Ki-67 in the liver tissues but not in the kidney tissues. |
| 35 | 29474904 | Moreover, kidney tissues were homogenized for inflammatory marker evaluation and real-time qPCR analysis to determine the changes in intermediate filament protein mRNA levels (desmin, vimentin, connexin 43 and nestin). |
| 36 | 29474904 | Moreover, QUR attenuated the inflammatory response as shown by decreased renal nitric oxide, tumor necrosis factor-α production and myeloperoxidase activity elicited by DOX injection. |
| 37 | 29436579 | In addition, knockdown of lncRNA ENSRNOG00000037522 repaired the damage to the podocytes via regulating vimentin, podocalyxin‑like 1 and nephrin expression. |
| 38 | 27751877 | This study aimed to assess whether histamine could exert a direct detrimental effect on podocyte permeability and the possible involvement of two key proteins for the glomerular slit diaphragm (SD) integrity, zonula occludens-1 (ZO-1) and P-cadherin. |
| 39 | 27751877 | This study aimed to assess whether histamine could exert a direct detrimental effect on podocyte permeability and the possible involvement of two key proteins for the glomerular slit diaphragm (SD) integrity, zonula occludens-1 (ZO-1) and P-cadherin. |
| 40 | 27751877 | ZO-1, P-cadherin and vimentin expression was assessed by qRT-PCR and quantitative immunoblotting. |
| 41 | 27751877 | ZO-1, P-cadherin and vimentin expression was assessed by qRT-PCR and quantitative immunoblotting. |
| 42 | 27751877 | Histamine exposure evoked a concentration-dependent reduction in both ZO-1 and P-cadherin and a parallel induction of vimentin mRNA expression with a maximum effect after 6h, and protein expression with a maximum effect after 8h. |
| 43 | 27751877 | Histamine exposure evoked a concentration-dependent reduction in both ZO-1 and P-cadherin and a parallel induction of vimentin mRNA expression with a maximum effect after 6h, and protein expression with a maximum effect after 8h. |
| 44 | 27751877 | In conclusion, our data demonstrate that histamine, via the H1R, modifies SD morphological and functional integrity, in part, by decreasing the expression of ZO-1 and P-cadherin. |
| 45 | 27751877 | In conclusion, our data demonstrate that histamine, via the H1R, modifies SD morphological and functional integrity, in part, by decreasing the expression of ZO-1 and P-cadherin. |
| 46 | 27704688 | FAK contributes to proteinuria in hypercholesterolaemic rats and modulates podocyte F-actin re-organization via activating p38 in response to ox-LDL. |
| 47 | 27704688 | FAK is also an adaptor protein initiating cascades of intracellular signals including c-Src, Rho GTPase and mitogen-activated protein kinase (MAPK). |
| 48 | 27704688 | Our cell culture data revealed oxidized low-density lipoprotein (ox-LDL) triggered hyper-phosphorylation of FAK and p38, ectopic expression of cellular markers (manifested as decreased WT1, podocin and NEPH1, and increased vimentin and mmp9), and re-arrangement of F-actin filaments with enhanced cell motility; these mutations were significantly rectified by FAK shRNA. |
| 49 | 27704688 | Notably, pre-treatment of p38 inhibitor did not alter FAK activation, albeit its deletion of p38 hyper-activity and attenuation of cellular abnormalities, demonstrating that p38 acted as a downstream effector of FAK signalling and ox-LDL damaged podocytes in a FAK/p38-dependent manner. |
| 50 | 27704688 | This was further identified by animal data that p38 activation was also abrogated by TAE226 treatment in hypercholesterolaemic rats, suggesting that FAK/p38 axis might also be involved in in vivo events. |
| 51 | 27695940 | Both MET and EMT processes involve changes in content and organization of cytoskeletal and actin filaments, accompanied by the increased glomerular vascularization. |
| 52 | 27695940 | Both MET and EMT processes involve changes in content and organization of cytoskeletal and actin filaments, accompanied by the increased glomerular vascularization. |
| 53 | 27695940 | Here, we analyze and compare normal human developing, postnatal and nephrotic podocytes and glomeruli, using immunohistochemical and double immunofluorescent methods for detection of markers of cytoskeletal filaments (nestin, cytokeratin 10-CK10, vimentin and α-SMA), vasculogenesis (CD31 and VEGF) and podocyte function (receptor for advanced glycation end products, RAGE). |
| 54 | 27695940 | Here, we analyze and compare normal human developing, postnatal and nephrotic podocytes and glomeruli, using immunohistochemical and double immunofluorescent methods for detection of markers of cytoskeletal filaments (nestin, cytokeratin 10-CK10, vimentin and α-SMA), vasculogenesis (CD31 and VEGF) and podocyte function (receptor for advanced glycation end products, RAGE). |
| 55 | 27695940 | In differentiating podocytes and cells of Bowman's capsule (parietal podocytes) nestin decreases, vimentin increases, while CK10 gradually disappears. |
| 56 | 27695940 | In differentiating podocytes and cells of Bowman's capsule (parietal podocytes) nestin decreases, vimentin increases, while CK10 gradually disappears. |
| 57 | 27145370 | CDK5 promotes renal tubulointerstitial fibrosis in diabetic nephropathy via ERK1/2/PPARγ pathway. |
| 58 | 27145370 | We report here that CDK5 is detrimental and promotes tubulointerstitial fibrosis (TIF) via the extracellular signal-regulated kinase 1/2 (ERK1/2)/peroxisome proliferator-activated receptor gamma (PPRAγ) pathway in DN. |
| 59 | 27145370 | In high glucose cultured NRK52E cells, blocking CDK5 activity inhibited epithelial-to-mesenchymal transition (EMT) and fibrosis via ERK1/2/PPARγ pathway. |
| 60 | 27145370 | In late staged DN patients, the upregulation of CDK5 and p35 activated phosphorylated ERK1/2 and PPARγ, leading to decreased levels of E-cadherin but increased Vimentin and Collagen IV. |
| 61 | 27145370 | These findings demonstrate a novel mechanism that CDK5 increases tubulointerstitial fibrosis by activating the ERK1/2/PPARγ pathway and EMT in DN. |
| 62 | 26936435 | As compared with the controls, DM rats exhibited reduced serum levels of high density lipoprotein, superoxide dismutase and glutathione peroxidase, and decreased renal mRNA expression levels of synaptopodin, connexin 43 and erythropoietin (EPO), which were further suppressed by NC and restored to normal levels by curcumin treatment. |
| 63 | 26936435 | Additionally, DM rats exhibited increases in their lipid profiles (cholesterol, triacylglycerol and phospholipids), oxidative markers (malondialdehyde, γ‑glutamyltranspeptidase and nitric oxide), kidney function markers (urea and creatinine) and the mRNA expression levels of vimentin, desmin, SREBP‑1, iNOS and TGF‑β1. |
| 64 | 26671788 | Semiautomated quantitative image analysis of glomerular immunohistochemistry markers desmin, vimentin, podocin, synaptopodin and WT-1 in acute and chronic rat kidney disease models. |
| 65 | 26671788 | Semiautomated quantitative image analysis of glomerular immunohistochemistry markers desmin, vimentin, podocin, synaptopodin and WT-1 in acute and chronic rat kidney disease models. |
| 66 | 26671788 | Semiautomated quantitative image analysis of glomerular immunohistochemistry markers desmin, vimentin, podocin, synaptopodin and WT-1 in acute and chronic rat kidney disease models. |
| 67 | 26671788 | Semiautomated quantitative image analysis of glomerular immunohistochemistry markers desmin, vimentin, podocin, synaptopodin and WT-1 in acute and chronic rat kidney disease models. |
| 68 | 26671788 | Immunohistochemistry was performed for desmin, vimentin, podocin, synaptopodin and Wilms tumor protein-1 (WT-1), and evaluation of glomerular immunohistochemistry markers was done by semiautomated quantitative image analysis. |
| 69 | 26671788 | Immunohistochemistry was performed for desmin, vimentin, podocin, synaptopodin and Wilms tumor protein-1 (WT-1), and evaluation of glomerular immunohistochemistry markers was done by semiautomated quantitative image analysis. |
| 70 | 26671788 | Immunohistochemistry was performed for desmin, vimentin, podocin, synaptopodin and Wilms tumor protein-1 (WT-1), and evaluation of glomerular immunohistochemistry markers was done by semiautomated quantitative image analysis. |
| 71 | 26671788 | Immunohistochemistry was performed for desmin, vimentin, podocin, synaptopodin and Wilms tumor protein-1 (WT-1), and evaluation of glomerular immunohistochemistry markers was done by semiautomated quantitative image analysis. |
| 72 | 26671788 | We found desmin and WT-1 as the most sensitive markers for podocyte damage in both acute and chronic glomerular damage followed by vimentin, podocin and synaptopodin. |
| 73 | 26671788 | We found desmin and WT-1 as the most sensitive markers for podocyte damage in both acute and chronic glomerular damage followed by vimentin, podocin and synaptopodin. |
| 74 | 26671788 | We found desmin and WT-1 as the most sensitive markers for podocyte damage in both acute and chronic glomerular damage followed by vimentin, podocin and synaptopodin. |
| 75 | 26671788 | We found desmin and WT-1 as the most sensitive markers for podocyte damage in both acute and chronic glomerular damage followed by vimentin, podocin and synaptopodin. |
| 76 | 26671788 | We were able to demonstrate that early podocyte damage as shown by increased desmin and vimentin staining together with either a phenotypic podocyte change or podocyte loss (reduced numbers of WT-1-stained podocytes) drives the progression of glomerular damage. |
| 77 | 26671788 | We were able to demonstrate that early podocyte damage as shown by increased desmin and vimentin staining together with either a phenotypic podocyte change or podocyte loss (reduced numbers of WT-1-stained podocytes) drives the progression of glomerular damage. |
| 78 | 26671788 | We were able to demonstrate that early podocyte damage as shown by increased desmin and vimentin staining together with either a phenotypic podocyte change or podocyte loss (reduced numbers of WT-1-stained podocytes) drives the progression of glomerular damage. |
| 79 | 26671788 | We were able to demonstrate that early podocyte damage as shown by increased desmin and vimentin staining together with either a phenotypic podocyte change or podocyte loss (reduced numbers of WT-1-stained podocytes) drives the progression of glomerular damage. |
| 80 | 26671788 | In addition to functional clinical chemistry markers, desmin and WT-1 immunohistochemistry offers reliable and valuable data on the morphologic state of podocytes. |
| 81 | 26671788 | In addition to functional clinical chemistry markers, desmin and WT-1 immunohistochemistry offers reliable and valuable data on the morphologic state of podocytes. |
| 82 | 26671788 | In addition to functional clinical chemistry markers, desmin and WT-1 immunohistochemistry offers reliable and valuable data on the morphologic state of podocytes. |
| 83 | 26671788 | In addition to functional clinical chemistry markers, desmin and WT-1 immunohistochemistry offers reliable and valuable data on the morphologic state of podocytes. |
| 84 | 26545114 | We found specific rearrangements of the actin cytoskeleton and slit diaphragm proteins (Nephrin, P-Cadherin, Vimentin) associated with this insulin resistance in palmitic-treated podocytes. |
| 85 | 26524507 | This was accompanied by upregulation of vimentin, a key mesenchymal marker, and active beta-catenin, associated with podocyte injury. |
| 86 | 25295576 | Immunostaining of the swollen and foamy podocytes using podocyte-associated antibodies (against podocalyxin, Wilms tumor-1, vimentin, and synaptopodin) revealed a unique distribution of synaptopodin surrounding globotriaosylceramide. |
| 87 | 25244654 | In mice exposed to indoxyl sulfate for 2 h, isolated glomeruli manifested increased Cyp1a1 expression, indicating AhR activation. |
| 88 | 25244654 | After 8 w of indoxyl sulfate, podocytes showed foot process effacement, cytoplasmic vacuoles, and a focal granular and wrinkled pattern of podocin and synaptopodin expression. |
| 89 | 25244654 | Furthermore, vimentin and AhR expression in the glomerulus was increased in the indoxyl sulfate-exposed glomeruli compared to controls. |
| 90 | 25244654 | Glomerular expression of characteristic podocyte mRNAs was decreased, including Actn4, Cd2ap, Myh9, Nphs1, Nphs2, Podxl, Synpo, and Wt1. |
| 91 | 25244654 | In vitro, immortalized-mouse podocytes exhibited AhR nuclear translocation beginning 30 min after 1 mM indoxyl sulfate exposure, and there was increased phospho-Rac1/Cdc42 at 2 h. |
| 92 | 24392227 | Constitutional Nephrin Deficiency in Conditionally Immortalized Human Podocytes Induced Epithelial-Mesenchymal Transition, Supported by β-Catenin/NF-kappa B Activation: A Consequence of Cell Junction Impairment? |
| 93 | 24392227 | In fact, a model of human podocyte with engineered nephrin deficiency constitutionally expressed high levels of α-SMA, vimentin, fibronectin, and other hallmarks of EMT. |
| 94 | 24392227 | The most intriguing was the activation of β-catenin pathway, which plays a critical role in podocyte ontogenesis as well as in the nephrin expression and EMT regulation. |
| 95 | 23676370 | We evaluated the effects of chronic treatment with tolvaptan on renal dysfunction, podocyte injury, inflammation, oxidative stress, Rho-kinase, epithelial-mesenchymal transition (EMT), and the extracellular signal-regulated protein kinase (ERK1/2) pathway in the renal cortex of Dahl salt-sensitive hypertensive (DS) rats with end-stage severe HF. |
| 96 | 23676370 | Decreased expression of nephrin and podocin and increased desmin-positive area in failing rats were restored by tolvaptan. |
| 97 | 23676370 | Upregulation of NAD(P)H oxidase p22(phox), p47(phox), and gp91(phox), EMT markers such as transforming growth factor-β1, vimentin, and fibronectin expression, and Rho-kinase and ERK1/2 phosphorylation in DS rats were significantly suppressed by tolvaptan. |
| 98 | 23676370 | Tolvaptan administration resulted in significant inhibition of tumor necrosis factor-α and monocyte chemoattractant protein-1 expression, and nuclear factor-κB phosphorylation. |
| 99 | 23676370 | We concluded that long-term tolvaptan therapy may improve renal dysfunction, glomerulosclerosis, podocyte injury, and inflammation associated with oxidative stress, as well as EMT, ERK, and the Rho-kinase pathway in the failing heart of DS rats. |
| 100 | 23447065 | Hyperplastic epithelium was negative for genetic podocyte tags, but positive for the parietal epithelial cell marker claudin-1, and expressed Notch1, Jagged1, and Hes1 mRNA and protein. |
| 101 | 23447065 | Enhanced Notch mRNA expression induced by transforming growth factor-β1 in cultured parietal epithelial cells was associated with mesenchymal markers (α-smooth muscle actin, vimentin, and Snail1). |
| 102 | 22484642 | These floating cells were immunohistologically identified as podocytes, by the expression of podocalyxin, vimentin, Wilms' tumor 1, synaptopodin and nephrin with positivities of 100%, 88.4%, 80.4%, 74.7% and 22.6%, respectively. |
| 103 | 22484642 | Immunostaining of both detached and capillary-attached podocytes for Bax, Bcl-2, desmin, fibroblast-specific protein-1, α-smooth muscle actin and Ki-67 was negative, as were TUNEL assays. |
| 104 | 20518888 | Sections were immunostained for nestin, alpha-smooth muscle actin (alpha-SMA), desmin, vimentin, CD34, and other stromal markers. |
| 105 | 20518888 | Interestingly, we observed a concomitant appearance of nestin- and CD34-positive myofibroblasts under fibrosing conditions. |
| 106 | 19241870 | [Intermediate filament proteins nestin and vimentin in the rat kidney cells]. |
| 107 | 19241870 | [Intermediate filament proteins nestin and vimentin in the rat kidney cells]. |
| 108 | 19241870 | [Intermediate filament proteins nestin and vimentin in the rat kidney cells]. |
| 109 | 19241870 | [Intermediate filament proteins nestin and vimentin in the rat kidney cells]. |
| 110 | 19241870 | The data on the presence of the kidney cells can contain neuroglial markers (nestin, vimentin, glial fibrillar acidic protein--GFAP) appeared unexpected and require a detailed investigation. |
| 111 | 19241870 | The data on the presence of the kidney cells can contain neuroglial markers (nestin, vimentin, glial fibrillar acidic protein--GFAP) appeared unexpected and require a detailed investigation. |
| 112 | 19241870 | The data on the presence of the kidney cells can contain neuroglial markers (nestin, vimentin, glial fibrillar acidic protein--GFAP) appeared unexpected and require a detailed investigation. |
| 113 | 19241870 | The data on the presence of the kidney cells can contain neuroglial markers (nestin, vimentin, glial fibrillar acidic protein--GFAP) appeared unexpected and require a detailed investigation. |
| 114 | 19241870 | It was demonstrated that the renal corpuscle contained both nestin- and vimentin-immunopositive cells (podocytes). |
| 115 | 19241870 | It was demonstrated that the renal corpuscle contained both nestin- and vimentin-immunopositive cells (podocytes). |
| 116 | 19241870 | It was demonstrated that the renal corpuscle contained both nestin- and vimentin-immunopositive cells (podocytes). |
| 117 | 19241870 | It was demonstrated that the renal corpuscle contained both nestin- and vimentin-immunopositive cells (podocytes). |
| 118 | 19241870 | Thus, the combination of nestin and vimentin was found to be typical for adult rat kidney podocytes. |
| 119 | 19241870 | Thus, the combination of nestin and vimentin was found to be typical for adult rat kidney podocytes. |
| 120 | 19241870 | Thus, the combination of nestin and vimentin was found to be typical for adult rat kidney podocytes. |
| 121 | 19241870 | Thus, the combination of nestin and vimentin was found to be typical for adult rat kidney podocytes. |
| 122 | 18776119 | Among 15 upregulated target genes of the mir-30 miRNA, four genes known to be expressed and/or functional in podocytes were identified, including receptor for advanced glycation end product, vimentin, heat-shock protein 20, and immediate early response 3. |
| 123 | 18776119 | Among 15 upregulated target genes of the mir-30 miRNA, four genes known to be expressed and/or functional in podocytes were identified, including receptor for advanced glycation end product, vimentin, heat-shock protein 20, and immediate early response 3. |
| 124 | 18776119 | Receptor for advanced glycation end product and immediate early response 3 are known to mediate podocyte apoptosis, whereas vimentin and heat-shock protein-20 are involved in cytoskeletal structure. |
| 125 | 18776119 | Receptor for advanced glycation end product and immediate early response 3 are known to mediate podocyte apoptosis, whereas vimentin and heat-shock protein-20 are involved in cytoskeletal structure. |
| 126 | 17929992 | Nestin co-localized with vimentin but not with actin or heavy chain myosin IIA, using a mouse podocyte cell line. |
| 127 | 17929992 | Nestin co-localized with vimentin but not with actin or heavy chain myosin IIA, using a mouse podocyte cell line. |
| 128 | 17929992 | Nestin co-localized with vimentin but not with actin or heavy chain myosin IIA, using a mouse podocyte cell line. |
| 129 | 17929992 | Knockdown of nestin in a murine podocyte cell line failed to produce any obvious phenotypic change or alteration in vimentin distribution but was associated with increased cell cycling. |
| 130 | 17929992 | Knockdown of nestin in a murine podocyte cell line failed to produce any obvious phenotypic change or alteration in vimentin distribution but was associated with increased cell cycling. |
| 131 | 17929992 | Knockdown of nestin in a murine podocyte cell line failed to produce any obvious phenotypic change or alteration in vimentin distribution but was associated with increased cell cycling. |
| 132 | 17929992 | Perhaps through an association with vimentin, nestin serves to bolster the mechanical strength of these cells that experience high tensile stress during glomerular filtration. |
| 133 | 17929992 | Perhaps through an association with vimentin, nestin serves to bolster the mechanical strength of these cells that experience high tensile stress during glomerular filtration. |
| 134 | 17929992 | Perhaps through an association with vimentin, nestin serves to bolster the mechanical strength of these cells that experience high tensile stress during glomerular filtration. |
| 135 | 17784648 | Co-expression of nestin and vimentin was observed in mature rat podocytes. |
| 136 | 17637254 | Time course of expression of intermediate filament protein vimentin, nestin and desmin in rat renal glomerular injury. |
| 137 | 17255215 | The present study characterizes the expression of nestin, an intermediate filament protein, in human kidneys. |
| 138 | 17255215 | Nestin also colocalized with vimentin in the periphery of capillary loops but not in the mesangium. |
| 139 | 17255215 | Semiquantitative analysis of immunostaining showed that glomerular nestin expression in IgA nephropathy without proteinuria was not different from normal kidney; however, nestin expression in kidneys of patients with IgA nephropathy and proteinuria, or MN and FSGS with proteinuria was significantly reduced compared with normal kidney (P < 0.01). |
| 140 | 17255215 | Reduced nestin mRNA expression in the patients with IgA nephropathy with proteinuria and FSGN was also observed by quantitative real-time PCR. |
| 141 | 17210924 | We investigated nestin expression in human adult and fetal kidney as well as CDK5 presence in adult human podocytes. |
| 142 | 17210924 | Confocal microscopy demonstrated that adult glomeruli display nestin immunoreactivity in vimentin-expressing cells with the podocyte morphology and not in cells bearing the endothelial marker CD31. |
| 143 | 17210924 | Glomerular nestin-positive cells were CDK5 immunoreactive as well. |
| 144 | 17210924 | Similar experiments carried out with antibodies raised against nestin and alpha-smooth muscle actin showed that the first mesangial cells that populate the developing glomeruli expressed nestin. |
| 145 | 16943305 | The expression of podocyte-specific proteins (podocalyxin, glomerular epithelial protein-1, podocin, nephrin, synaptopodin, and alpha-actinin-4), podocyte synthesized proteins (vascular endothelial growth factor and novH), transcription factors (WT1 and PAX2), cyclin-dependent kinase inhibitor p57, and intermediate filaments (cytokeratins and vimentin) was tested. |
| 146 | 16943305 | WT1 and p57 were expressed in some parietal cells, whereas PAX2 was present in all or most of them, so some parietal cells coexpressed WT1 and PAX2. |
| 147 | 16510766 | Eight weeks after disease induction, anti-PDGF-D therapy significantly ameliorated focal segmental glomerulosclerosis, podocyte damage (de novo desmin expression), tubulointerstitial damage, and fibrosis as well as the accumulation of renal interstitial matrix including type III collagen and fibronectin. |
| 148 | 16510766 | Treatment with anti-PDGF-D also reduced the cortical infiltration of monocytes/macrophages on day 56, possibly related to lower renal cortical complement activation (C5b-9 deposition) and/or reduced epithelial-to-mesenchymal transition (preserved cortical expression of E-cadherin and reduced expression of vimentin and alpha-smooth muscle actin). |
| 149 | 16418842 | Upregulation of nestin, vimentin, and desmin in rat podocytes in response to injury. |
| 150 | 16418842 | Upregulation of nestin, vimentin, and desmin in rat podocytes in response to injury. |
| 151 | 16418842 | Upregulation of nestin, vimentin, and desmin in rat podocytes in response to injury. |
| 152 | 16418842 | Upregulation of nestin, vimentin, and desmin in rat podocytes in response to injury. |
| 153 | 16418842 | Upregulation of nestin, vimentin, and desmin in rat podocytes in response to injury. |
| 154 | 16418842 | Upregulation of nestin, vimentin, and desmin in rat podocytes in response to injury. |
| 155 | 16418842 | Upregulation of nestin, vimentin, and desmin in rat podocytes in response to injury. |
| 156 | 16418842 | To gain insight into the role of IF proteins in podocytes, we investigated the expression of nestin, vimentin, and desmin in puromycin aminonucleoside (PAN) nephrosis. |
| 157 | 16418842 | To gain insight into the role of IF proteins in podocytes, we investigated the expression of nestin, vimentin, and desmin in puromycin aminonucleoside (PAN) nephrosis. |
| 158 | 16418842 | To gain insight into the role of IF proteins in podocytes, we investigated the expression of nestin, vimentin, and desmin in puromycin aminonucleoside (PAN) nephrosis. |
| 159 | 16418842 | To gain insight into the role of IF proteins in podocytes, we investigated the expression of nestin, vimentin, and desmin in puromycin aminonucleoside (PAN) nephrosis. |
| 160 | 16418842 | To gain insight into the role of IF proteins in podocytes, we investigated the expression of nestin, vimentin, and desmin in puromycin aminonucleoside (PAN) nephrosis. |
| 161 | 16418842 | To gain insight into the role of IF proteins in podocytes, we investigated the expression of nestin, vimentin, and desmin in puromycin aminonucleoside (PAN) nephrosis. |
| 162 | 16418842 | To gain insight into the role of IF proteins in podocytes, we investigated the expression of nestin, vimentin, and desmin in puromycin aminonucleoside (PAN) nephrosis. |
| 163 | 16418842 | A Western blot analysis for nestin, vimentin, and desmin demonstrated their exclusive expression in glomeruli and showed their increase in expression in nephrotic glomeruli. |
| 164 | 16418842 | A Western blot analysis for nestin, vimentin, and desmin demonstrated their exclusive expression in glomeruli and showed their increase in expression in nephrotic glomeruli. |
| 165 | 16418842 | A Western blot analysis for nestin, vimentin, and desmin demonstrated their exclusive expression in glomeruli and showed their increase in expression in nephrotic glomeruli. |
| 166 | 16418842 | A Western blot analysis for nestin, vimentin, and desmin demonstrated their exclusive expression in glomeruli and showed their increase in expression in nephrotic glomeruli. |
| 167 | 16418842 | A Western blot analysis for nestin, vimentin, and desmin demonstrated their exclusive expression in glomeruli and showed their increase in expression in nephrotic glomeruli. |
| 168 | 16418842 | A Western blot analysis for nestin, vimentin, and desmin demonstrated their exclusive expression in glomeruli and showed their increase in expression in nephrotic glomeruli. |
| 169 | 16418842 | A Western blot analysis for nestin, vimentin, and desmin demonstrated their exclusive expression in glomeruli and showed their increase in expression in nephrotic glomeruli. |
| 170 | 16418842 | Immunolocalization studies showed nestin and vimentin to be located predominantly in the podocytes in both normal and nephrotic glomeruli and that enhancement of desmin staining only occurred in podocytes. |
| 171 | 16418842 | Immunolocalization studies showed nestin and vimentin to be located predominantly in the podocytes in both normal and nephrotic glomeruli and that enhancement of desmin staining only occurred in podocytes. |
| 172 | 16418842 | Immunolocalization studies showed nestin and vimentin to be located predominantly in the podocytes in both normal and nephrotic glomeruli and that enhancement of desmin staining only occurred in podocytes. |
| 173 | 16418842 | Immunolocalization studies showed nestin and vimentin to be located predominantly in the podocytes in both normal and nephrotic glomeruli and that enhancement of desmin staining only occurred in podocytes. |
| 174 | 16418842 | Immunolocalization studies showed nestin and vimentin to be located predominantly in the podocytes in both normal and nephrotic glomeruli and that enhancement of desmin staining only occurred in podocytes. |
| 175 | 16418842 | Immunolocalization studies showed nestin and vimentin to be located predominantly in the podocytes in both normal and nephrotic glomeruli and that enhancement of desmin staining only occurred in podocytes. |
| 176 | 16418842 | Immunolocalization studies showed nestin and vimentin to be located predominantly in the podocytes in both normal and nephrotic glomeruli and that enhancement of desmin staining only occurred in podocytes. |
| 177 | 16418842 | A ribonuclease protection assay showed high levels of vimentin and nestin expression in normal glomeruli and an upregulation of all three IF transcripts in nephrotic glomeruli. |
| 178 | 16418842 | A ribonuclease protection assay showed high levels of vimentin and nestin expression in normal glomeruli and an upregulation of all three IF transcripts in nephrotic glomeruli. |
| 179 | 16418842 | A ribonuclease protection assay showed high levels of vimentin and nestin expression in normal glomeruli and an upregulation of all three IF transcripts in nephrotic glomeruli. |
| 180 | 16418842 | A ribonuclease protection assay showed high levels of vimentin and nestin expression in normal glomeruli and an upregulation of all three IF transcripts in nephrotic glomeruli. |
| 181 | 16418842 | A ribonuclease protection assay showed high levels of vimentin and nestin expression in normal glomeruli and an upregulation of all three IF transcripts in nephrotic glomeruli. |
| 182 | 16418842 | A ribonuclease protection assay showed high levels of vimentin and nestin expression in normal glomeruli and an upregulation of all three IF transcripts in nephrotic glomeruli. |
| 183 | 16418842 | A ribonuclease protection assay showed high levels of vimentin and nestin expression in normal glomeruli and an upregulation of all three IF transcripts in nephrotic glomeruli. |
| 184 | 16418842 | One day after the PAN injection, however, the vimentin transcripts were found to already have significantly increased, whereas those of nestin or desmin showed no such increase. |
| 185 | 16418842 | One day after the PAN injection, however, the vimentin transcripts were found to already have significantly increased, whereas those of nestin or desmin showed no such increase. |
| 186 | 16418842 | One day after the PAN injection, however, the vimentin transcripts were found to already have significantly increased, whereas those of nestin or desmin showed no such increase. |
| 187 | 16418842 | One day after the PAN injection, however, the vimentin transcripts were found to already have significantly increased, whereas those of nestin or desmin showed no such increase. |
| 188 | 16418842 | One day after the PAN injection, however, the vimentin transcripts were found to already have significantly increased, whereas those of nestin or desmin showed no such increase. |
| 189 | 16418842 | One day after the PAN injection, however, the vimentin transcripts were found to already have significantly increased, whereas those of nestin or desmin showed no such increase. |
| 190 | 16418842 | One day after the PAN injection, however, the vimentin transcripts were found to already have significantly increased, whereas those of nestin or desmin showed no such increase. |
| 191 | 16418842 | These findings indicate that podocytes express three IF proteins, namely, vimentin, desmin, and nestin, which are differentially regulated in response to injury. |
| 192 | 16418842 | These findings indicate that podocytes express three IF proteins, namely, vimentin, desmin, and nestin, which are differentially regulated in response to injury. |
| 193 | 16418842 | These findings indicate that podocytes express three IF proteins, namely, vimentin, desmin, and nestin, which are differentially regulated in response to injury. |
| 194 | 16418842 | These findings indicate that podocytes express three IF proteins, namely, vimentin, desmin, and nestin, which are differentially regulated in response to injury. |
| 195 | 16418842 | These findings indicate that podocytes express three IF proteins, namely, vimentin, desmin, and nestin, which are differentially regulated in response to injury. |
| 196 | 16418842 | These findings indicate that podocytes express three IF proteins, namely, vimentin, desmin, and nestin, which are differentially regulated in response to injury. |
| 197 | 16418842 | These findings indicate that podocytes express three IF proteins, namely, vimentin, desmin, and nestin, which are differentially regulated in response to injury. |
| 198 | 12915483 | The development of GS was preceded by widespread loss of ZO-1 signal in podocytes (even in kidneys where <5% of glomeruli contained Wt1 mutant podocytes), increased intra-renal renin expression, and de novo podocyte TGF-beta1 expression, but not podocyte Pax-2 expression or loss of WT1, synaptopodin, alpha-actinin-4 or nephrin expression. |
| 199 | 12915483 | However, podocytes in partially sclerotic glomeruli that still expressed WT1 at high levels showed reduced vimentin expression, cell cycle re-entry, and re-expressed desmin, cytokeratin and Pax-2. |
| 200 | 12915483 | The results suggest that: (i) GS is not due to loss of WT1 expression by podocytes; (ii) podocyte Pax-2 expression reflects re-expression rather than persistent expression, and is the consequence of GS; (iii) GS is mediated systemically and the mechanism involves activation of the renin-angiotensin system; and (iv) podocytes undergo typical maturational changes but subsequently de-differentiate and revert to an immature phenotype during disease progression. |
| 201 | 12488983 | Recently, abnormal expression of WT1 and PAX2 was shown in the podocytes in diffuse mesangial sclerosis (DMS) associated with DDS and isolated DMS. |
| 202 | 12488983 | Immunohistochemical analysis of WT1, PAX2, vimentin, cytokeratin, and epithelial membrane antigen was performed in the kidney specimens obtained at autopsy or surgery. |
| 203 | 12488983 | Abnormal expression of WT1 and PAX2 in the EHBCE was observed in both patients, supporting our hypothesis. |
| 204 | 11592103 | Female mouse recipients of male bone marrow grafts showed co-localization of Y-chromosomes and tubular epithelial markers Ricinus communis and Lens culinaris, and a specific cytochrome P450 enzyme (CYP1A2) indicating an appropriate functional capability of clustered newly formed marrow-derived tubular epithelial cells. |
| 205 | 11592103 | Within the murine kidney, these Y-chromosome-positive cells were negative for the mouse macrophage marker F4/80 antigen and leukocyte common antigen, but were vimentin-positive. |
| 206 | 11228169 | Immunohistochemical studies showed increased fibronectin and desmin expression in glomeruli and tubulointerstitium and increased vimentin and alpha-smooth muscle actin in the tubulointerstitial area from the renal cortex of RT18 rats (P: < 0.05). |
| 207 | 10707851 | Immunohistochemical demonstration of vimentin and S-100 protein in the kidneys. |
| 208 | 10707851 | Immunohistochemical demonstration of vimentin and S-100 protein in the kidneys. |
| 209 | 10707851 | Vimentin and S-100 protein expression was studied in the kidneys of adult sheep and goat using immunohistochemistry. |
| 210 | 10707851 | Vimentin and S-100 protein expression was studied in the kidneys of adult sheep and goat using immunohistochemistry. |
| 211 | 10668098 | Double-immunolabeling studies demonstrated that podocytes transiently acquire myofibroblastic features, characterized by the expression of smooth muscle alpha-actin (SMAA) and increased perinuclear reaction of GFAP in prolonged cultures. |
| 212 | 10668098 | The morphological differentiation of cobblestone-like podocytes into process-bearing cells was followed by loss of the myofibroblastic marker, SMAA, de novo expression of desmin, and distribution of GFAP, vimentin and desmin into the processes. |
| 213 | 10398535 | In vivo, expression of the epithelial-specific cell adhesion molecule E-cadherin is restricted to differentiated tubular epithelial cells, whereas the intermediate filament protein vimentin is present in mesonephrogenic mesenchyme and is undetectable in tubular epithelial cells. |
| 214 | 10090571 | Identification of renal podocytes in multiple species: higher vertebrates are vimentin positive/lower vertebrates are desmin positive. |
| 215 | 10090571 | Identification of renal podocytes in multiple species: higher vertebrates are vimentin positive/lower vertebrates are desmin positive. |
| 216 | 10090571 | These findings indicate that podocytes are characterized by intense vimentin staining in the higher vertebrates and by desmin staining in the lower vertebrates denoting potentially distinctive physiological functions of IF proteins in podocytes from each of these groups. |
| 217 | 10090571 | These findings indicate that podocytes are characterized by intense vimentin staining in the higher vertebrates and by desmin staining in the lower vertebrates denoting potentially distinctive physiological functions of IF proteins in podocytes from each of these groups. |
| 218 | 9691426 | In double immunolabelling analysis of adult rat kidney sections using antiserum against GFAP and monoclonal antibody (mAb) against vimentin or desmin, the presence of immunoreactivity for GFAP could be observed in the glomerulus of the kidney and vascular cells situated in the peritubular space which expressed vimentin and desmin. |
| 219 | 9551398 | Immunohistochemistry identified normal podocyte phenotypes by podocalyxin, vimentin and complement receptor 1 (CR1) labeling. |
| 220 | 9551398 | Immunohistochemistry identified normal podocyte phenotypes by podocalyxin, vimentin and complement receptor 1 (CR1) labeling. |
| 221 | 9551398 | In collapsed glomeruli, podocalyxin, vimentin and CR1 labeling tagged both normal and vacuolated podocytes still attached to the GBM, but labeling was not found in cobblestone-like podocytes or in podocytes detached from the GBM. |
| 222 | 9551398 | In collapsed glomeruli, podocalyxin, vimentin and CR1 labeling tagged both normal and vacuolated podocytes still attached to the GBM, but labeling was not found in cobblestone-like podocytes or in podocytes detached from the GBM. |
| 223 | 9377221 | Immunohistochemistry demonstrated that the tight junction protein, ZO-1, and specific podocytic markers, pp44, 5-1-6, podocalyxin and vimentin were expressed in a cell maturity-dependent manner, as observed in newborn rat kidneys. |
| 224 | 9176840 | Mouse glomerular epithelial cells in culture with features of podocytes in vivo express aminopeptidase A and angiotensinogen but not other components of the renin-angiotensin system. |
| 225 | 9176840 | By indirect immunofluorescence, the cells were positive for cytokeratin, vimentin, desmin, and the ZO-1 protein, a component of the tight junction complex. |
| 226 | 9176840 | The mRNA expression of several components of the renin-angiotensin system was also examined, and some factors indirectly coupled to the renin-angiotensin system component angiotensin II in this podocytic culture by RT-PCR analysis. mRNA Expression for the angiotensin II degrading hydrolase aminopeptidase A and angiotensinogen was found, but this was not found for any other component of this system, such as renin, angiotensin-converting enzyme, or the angiotensin II receptors AT1a, AT1b, and AT2. |
| 227 | 9176840 | In addition, expression of the growth factors transforming growth factor-beta and interleukin-7, and the extracellular matrix components fibronectin, laminin B2, perlecan, and collagen IV alpha 1, was observed. |
| 228 | 7586682 | Interferon-gamma (IFN-gamma) and IL-4 expressed during mercury-induced membranous nephropathy are toxic for cultured podocytes. |
| 229 | 7586682 | In diseased rats a five-fold increase in intraglomerular macrophages was found, but we could not detect intraglomerular IFN-alpha, IFN-beta, IL-1 beta or tumour necrosis factor-alpha (TNF-alpha) by using immunohistology. |
| 230 | 7586682 | IFN-gamma and IL-4 were the only cytokines that exerted toxic effects, resulting in a rapidly decreased transepithelial resistance of confluent monolayers, which was closely associated with altered immunoreactivity of the tight junction protein ZO-1. |
| 231 | 7586682 | IL-4 also affected vimentin and laminin immunoreactivity. |
| 232 | 7586682 | IFN-gamma and IL-4 only interfered with monolayer integrity when added to the basolateral side of the GVEC, indicating specific (receptor-mediated) effects. |
| 233 | 7586682 | From our experiments we concluded that IFN-gamma subtly affected monolayer integrity at the level of the tight junctions, and that IL-4 additionally induced cell death. |
| 234 | 7586682 | We hypothesize that the toxic effects of the cytokines IFN-gamma and IL-4 as seen with cultured podocytes are necessary together with the autoantibodies, for the ultimate induction of proteinuria in mercury nephropathy in the DZB rat. |
| 235 | 7952147 | Accompanied by the disappearance of proteinuria, the structural organization of the foot processes was completely restored, in which tubulin, vimentin, and myosin were scarcely observed. |
| 236 | 8396229 | Formalin-fixed, paraffin-embedded sections of 8 CCSK and 9 WT were stained, using the standard avidin-biotin peroxidase complex method, for vimentin (VIM), Factor-8 related antigen (F8A), epithelial membrane antigen (EMA), desmin (DES), S-100 protein and Mac 387. |
| 237 | 8396229 | Formalin-fixed, paraffin-embedded sections of 8 CCSK and 9 WT were stained, using the standard avidin-biotin peroxidase complex method, for vimentin (VIM), Factor-8 related antigen (F8A), epithelial membrane antigen (EMA), desmin (DES), S-100 protein and Mac 387. |
| 238 | 8396229 | CCSK cells consistently exhibited moderate to strong diffuse cytoplasmic positivity for VIM and were negative for F8A, EMA, DES, S-100 and Mac 387. |
| 239 | 8396229 | CCSK cells consistently exhibited moderate to strong diffuse cytoplasmic positivity for VIM and were negative for F8A, EMA, DES, S-100 and Mac 387. |
| 240 | 8396229 | Neither blastemal, stromal nor epithelial elements in WT were positive for F8A, S-100 or Mac 387. |
| 241 | 8396229 | Neither blastemal, stromal nor epithelial elements in WT were positive for F8A, S-100 or Mac 387. |
| 242 | 1477323 | Cultured GEC are positive for cytokeratin and negative for vimentin and desmin, identical to parietal cells in situ. |
| 243 | 1477323 | Cultured GEC are positive for cytokeratin and negative for vimentin and desmin, identical to parietal cells in situ. |
| 244 | 1477323 | In contrast, podocytes are positive for vimentin and desmin and negative for cytokeratin. |
| 245 | 1477323 | In contrast, podocytes are positive for vimentin and desmin and negative for cytokeratin. |
| 246 | 1354670 | Characterization of a simian virus 40-transformed human podocyte cell line producing type IV collagen and exhibiting polarized response to atrial natriuretic peptide. |
| 247 | 1354670 | Clone A4 has been exhibiting over 35 passages, a combination of markers unique to podocytes, including expression of vimentin, podocalyxin, ectoenzymes (CALLA antigen and mRNA), heparan-sulfate proteoglycans (molecular mass of core protein = 75 kDa), and production of type IV collagen (alpha 1 and alpha 5 chains) established by immunoprecipitation and Northern blot analysis. |
| 248 | 1963193 | Using an indirect immunoperoxidase technique, we tested frozen specimens from one Wilms' tumour composed of numerous glomeruloid bodies devoid of blood vessels, with monoclonal antibodies directed against vimentin, cytokeratin, CALLA/CD10, CD24, CR1/CD35, endothelium factor VIII, class I and II MHC molecules, laminin, fibronectin, and non-collagenic domain NC1 of type IV collagen. |
| 249 | 1963193 | Using an indirect immunoperoxidase technique, we tested frozen specimens from one Wilms' tumour composed of numerous glomeruloid bodies devoid of blood vessels, with monoclonal antibodies directed against vimentin, cytokeratin, CALLA/CD10, CD24, CR1/CD35, endothelium factor VIII, class I and II MHC molecules, laminin, fibronectin, and non-collagenic domain NC1 of type IV collagen. |
| 250 | 1963193 | Glomeruloid bodies comprised two cell types: a peripheral layer of parietal epithelial cells (cytokeratin and CD24-positive) and central cell clumps of podocytes (vimentin and CALLA-positive). |
| 251 | 1963193 | Glomeruloid bodies comprised two cell types: a peripheral layer of parietal epithelial cells (cytokeratin and CD24-positive) and central cell clumps of podocytes (vimentin and CALLA-positive). |
| 252 | 1707626 | Intermediate filaments vimentin and desmin share epitopes with M 1 protein of group A streptococci. |
| 253 | 1707626 | Intermediate filaments vimentin and desmin share epitopes with M 1 protein of group A streptococci. |
| 254 | 1707626 | The antibody PM II 40 not only react with vimentin but also with desmin suggesting that the recognized epitopes are distinct from that described by Kraus et al. for vimentin and type 1 M protein. |
| 255 | 1707626 | The antibody PM II 40 not only react with vimentin but also with desmin suggesting that the recognized epitopes are distinct from that described by Kraus et al. for vimentin and type 1 M protein. |
| 256 | 1692563 | Using an indirect immunoperoxidase technique, we tested frozen specimens from 12 Wilms' tumors with monoclonal antibodies (MoAbs) reacting against a large panel of molecules including laminin, fibronectin, cytokeratin, vimentin, villin, CD24, CALLA/CD10, CR1, CD26, class I and class II major histocompatibility complex (MHC) molecules, and endothelium factor VIII. |
| 257 | 1692563 | Using an indirect immunoperoxidase technique, we tested frozen specimens from 12 Wilms' tumors with monoclonal antibodies (MoAbs) reacting against a large panel of molecules including laminin, fibronectin, cytokeratin, vimentin, villin, CD24, CALLA/CD10, CR1, CD26, class I and class II major histocompatibility complex (MHC) molecules, and endothelium factor VIII. |
| 258 | 1692563 | Using an indirect immunoperoxidase technique, we tested frozen specimens from 12 Wilms' tumors with monoclonal antibodies (MoAbs) reacting against a large panel of molecules including laminin, fibronectin, cytokeratin, vimentin, villin, CD24, CALLA/CD10, CR1, CD26, class I and class II major histocompatibility complex (MHC) molecules, and endothelium factor VIII. |
| 259 | 1692563 | Using an indirect immunoperoxidase technique, we tested frozen specimens from 12 Wilms' tumors with monoclonal antibodies (MoAbs) reacting against a large panel of molecules including laminin, fibronectin, cytokeratin, vimentin, villin, CD24, CALLA/CD10, CR1, CD26, class I and class II major histocompatibility complex (MHC) molecules, and endothelium factor VIII. |
| 260 | 1692563 | Using an indirect immunoperoxidase technique, we tested frozen specimens from 12 Wilms' tumors with monoclonal antibodies (MoAbs) reacting against a large panel of molecules including laminin, fibronectin, cytokeratin, vimentin, villin, CD24, CALLA/CD10, CR1, CD26, class I and class II major histocompatibility complex (MHC) molecules, and endothelium factor VIII. |
| 261 | 1692563 | Some tubular formations showed signs of proximal maturation with the presence of CALLA, CD26, and even villin. |
| 262 | 1692563 | Some tubular formations showed signs of proximal maturation with the presence of CALLA, CD26, and even villin. |
| 263 | 1692563 | Some tubular formations showed signs of proximal maturation with the presence of CALLA, CD26, and even villin. |
| 264 | 1692563 | Some tubular formations showed signs of proximal maturation with the presence of CALLA, CD26, and even villin. |
| 265 | 1692563 | Some tubular formations showed signs of proximal maturation with the presence of CALLA, CD26, and even villin. |
| 266 | 1692563 | Large cystic cavities present in five cases were edged by cytokeratin, CD24-positive cells, or by vimentin, CALLA, CR1-positive cells. |
| 267 | 1692563 | Large cystic cavities present in five cases were edged by cytokeratin, CD24-positive cells, or by vimentin, CALLA, CR1-positive cells. |
| 268 | 1692563 | Large cystic cavities present in five cases were edged by cytokeratin, CD24-positive cells, or by vimentin, CALLA, CR1-positive cells. |
| 269 | 1692563 | Large cystic cavities present in five cases were edged by cytokeratin, CD24-positive cells, or by vimentin, CALLA, CR1-positive cells. |
| 270 | 1692563 | Large cystic cavities present in five cases were edged by cytokeratin, CD24-positive cells, or by vimentin, CALLA, CR1-positive cells. |
| 271 | 1692563 | Some glomeruloid bodies, present in two cases, were also composed of vimentin, CALLA, and CR1-positive cells which correspond to the mature podocyte phenotype. |
| 272 | 1692563 | Some glomeruloid bodies, present in two cases, were also composed of vimentin, CALLA, and CR1-positive cells which correspond to the mature podocyte phenotype. |
| 273 | 1692563 | Some glomeruloid bodies, present in two cases, were also composed of vimentin, CALLA, and CR1-positive cells which correspond to the mature podocyte phenotype. |
| 274 | 1692563 | Some glomeruloid bodies, present in two cases, were also composed of vimentin, CALLA, and CR1-positive cells which correspond to the mature podocyte phenotype. |
| 275 | 1692563 | Some glomeruloid bodies, present in two cases, were also composed of vimentin, CALLA, and CR1-positive cells which correspond to the mature podocyte phenotype. |
| 276 | 1692563 | The presence of large cells with muscular differentiation was noted; round vimentin and CD26-positive cells were also seen. |
| 277 | 1692563 | The presence of large cells with muscular differentiation was noted; round vimentin and CD26-positive cells were also seen. |
| 278 | 1692563 | The presence of large cells with muscular differentiation was noted; round vimentin and CD26-positive cells were also seen. |
| 279 | 1692563 | The presence of large cells with muscular differentiation was noted; round vimentin and CD26-positive cells were also seen. |
| 280 | 1692563 | The presence of large cells with muscular differentiation was noted; round vimentin and CD26-positive cells were also seen. |
| 281 | 1692563 | The endothelial cells of the vessels exhibited vimentin, factor VIII, and class I and class II MHC molecules as do mature cells, but in some cases the endothelial cells lacked class II molecule expression and were CALLA-positive. |
| 282 | 1692563 | The endothelial cells of the vessels exhibited vimentin, factor VIII, and class I and class II MHC molecules as do mature cells, but in some cases the endothelial cells lacked class II molecule expression and were CALLA-positive. |
| 283 | 1692563 | The endothelial cells of the vessels exhibited vimentin, factor VIII, and class I and class II MHC molecules as do mature cells, but in some cases the endothelial cells lacked class II molecule expression and were CALLA-positive. |
| 284 | 1692563 | The endothelial cells of the vessels exhibited vimentin, factor VIII, and class I and class II MHC molecules as do mature cells, but in some cases the endothelial cells lacked class II molecule expression and were CALLA-positive. |
| 285 | 1692563 | The endothelial cells of the vessels exhibited vimentin, factor VIII, and class I and class II MHC molecules as do mature cells, but in some cases the endothelial cells lacked class II molecule expression and were CALLA-positive. |
| 286 | 1692563 | Moreover, this study shows that tumoral cells in nephroblastoma share several antigens with cells from lymphoid lineage (CD24, CALLA, and CD26) as do developing and mature kidney cells. |
| 287 | 1692563 | Moreover, this study shows that tumoral cells in nephroblastoma share several antigens with cells from lymphoid lineage (CD24, CALLA, and CD26) as do developing and mature kidney cells. |
| 288 | 1692563 | Moreover, this study shows that tumoral cells in nephroblastoma share several antigens with cells from lymphoid lineage (CD24, CALLA, and CD26) as do developing and mature kidney cells. |
| 289 | 1692563 | Moreover, this study shows that tumoral cells in nephroblastoma share several antigens with cells from lymphoid lineage (CD24, CALLA, and CD26) as do developing and mature kidney cells. |
| 290 | 1692563 | Moreover, this study shows that tumoral cells in nephroblastoma share several antigens with cells from lymphoid lineage (CD24, CALLA, and CD26) as do developing and mature kidney cells. |
| 291 | 2515691 | An immunohistochemical study of canine tissues with vimentin, desmin, glial fibrillary acidic protein, and neurofilament antisera. |
| 292 | 2515691 | An immunohistochemical study of canine tissues with vimentin, desmin, glial fibrillary acidic protein, and neurofilament antisera. |
| 293 | 2515691 | An immunohistochemical study of canine tissues with vimentin, desmin, glial fibrillary acidic protein, and neurofilament antisera. |
| 294 | 2515691 | In a wide range of canine tissues the immunoreactivity with commercially available antisera against intermediate filament antigens viz. vimentin, desmin, glial fibrillary acidic protein (GFAP) and neurofilament proteins, was studied. |
| 295 | 2515691 | In a wide range of canine tissues the immunoreactivity with commercially available antisera against intermediate filament antigens viz. vimentin, desmin, glial fibrillary acidic protein (GFAP) and neurofilament proteins, was studied. |
| 296 | 2515691 | In a wide range of canine tissues the immunoreactivity with commercially available antisera against intermediate filament antigens viz. vimentin, desmin, glial fibrillary acidic protein (GFAP) and neurofilament proteins, was studied. |
| 297 | 2515691 | Epithelial cells did not react with any of the antisera, with exception of ovarian surface epithelium, which showed staining with the vimentin and desmin antisera. |
| 298 | 2515691 | Epithelial cells did not react with any of the antisera, with exception of ovarian surface epithelium, which showed staining with the vimentin and desmin antisera. |
| 299 | 2515691 | Epithelial cells did not react with any of the antisera, with exception of ovarian surface epithelium, which showed staining with the vimentin and desmin antisera. |
| 300 | 3314527 | MAC was co-deposited with C3, C5, C9, and properdin in the sclerotic area of the glomeruli, along with a decrease in the reactivity of podocytes with anti-vimentin antibody. |
| 301 | 3305702 | Immunocytochemical studies of desmin and vimentin in pericapillary cells of chicken. |
| 302 | 3305702 | Immunocytochemical studies of desmin and vimentin in pericapillary cells of chicken. |
| 303 | 3305702 | Our results also revealed that even in microvascular beds where pericytes are not found, cells having both desmin and vimentin exist next to endothelial cells and may assume similar functions to pericytes. |
| 304 | 3305702 | Our results also revealed that even in microvascular beds where pericytes are not found, cells having both desmin and vimentin exist next to endothelial cells and may assume similar functions to pericytes. |
| 305 | 2432791 | The distribution of intermediate filament proteins (vimentin, desmin, and cytokeratin) was studied by means of immunofluorescence in the normal human and rat glomerulus and in pathologic human glomeruli. |
| 306 | 2432791 | The distribution of intermediate filament proteins (vimentin, desmin, and cytokeratin) was studied by means of immunofluorescence in the normal human and rat glomerulus and in pathologic human glomeruli. |
| 307 | 2432791 | The distribution of intermediate filament proteins (vimentin, desmin, and cytokeratin) was studied by means of immunofluorescence in the normal human and rat glomerulus and in pathologic human glomeruli. |
| 308 | 2432791 | The distribution of intermediate filament proteins (vimentin, desmin, and cytokeratin) was studied by means of immunofluorescence in the normal human and rat glomerulus and in pathologic human glomeruli. |
| 309 | 2432791 | In normal human glomeruli, vimentin antibodies stained endothelial cells, podocytes, and mesangial cells; desmin antibodies, surprisingly, stained podocytes. |
| 310 | 2432791 | In normal human glomeruli, vimentin antibodies stained endothelial cells, podocytes, and mesangial cells; desmin antibodies, surprisingly, stained podocytes. |
| 311 | 2432791 | In normal human glomeruli, vimentin antibodies stained endothelial cells, podocytes, and mesangial cells; desmin antibodies, surprisingly, stained podocytes. |
| 312 | 2432791 | In normal human glomeruli, vimentin antibodies stained endothelial cells, podocytes, and mesangial cells; desmin antibodies, surprisingly, stained podocytes. |
| 313 | 2432791 | In normal rat glomeruli, the pattern of vimentin staining was the same as in humans, but desmin antibodies stained both mesangial cells and podocytes. |
| 314 | 2432791 | In normal rat glomeruli, the pattern of vimentin staining was the same as in humans, but desmin antibodies stained both mesangial cells and podocytes. |
| 315 | 2432791 | In normal rat glomeruli, the pattern of vimentin staining was the same as in humans, but desmin antibodies stained both mesangial cells and podocytes. |
| 316 | 2432791 | In normal rat glomeruli, the pattern of vimentin staining was the same as in humans, but desmin antibodies stained both mesangial cells and podocytes. |
| 317 | 2432791 | In human pathologic glomeruli, vimentin and desmin antibodies stained the structures that were positive in normal glomeruli, giving a characteristic pattern for each pathologic condition examined. |
| 318 | 2432791 | In human pathologic glomeruli, vimentin and desmin antibodies stained the structures that were positive in normal glomeruli, giving a characteristic pattern for each pathologic condition examined. |
| 319 | 2432791 | In human pathologic glomeruli, vimentin and desmin antibodies stained the structures that were positive in normal glomeruli, giving a characteristic pattern for each pathologic condition examined. |
| 320 | 2432791 | In human pathologic glomeruli, vimentin and desmin antibodies stained the structures that were positive in normal glomeruli, giving a characteristic pattern for each pathologic condition examined. |
| 321 | 3521974 | The C-binding structures had the same distribution as intermediate filaments (IMFs) of vimentin but not desmin or keratin types. |