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PMID |
Sentence |
1 |
11106563
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We studied the developmental expression of nephrin, ZO-1 and P-cadherin in normal fetal kidneys and in NPHS1 kidneys.
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2 |
11106563
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Fetal NPHS1 kidneys with Fin-major/Fin-major genotype did not express nephrin, whereas the expression of ZO-1 and P-cadherin was comparable to that of control kidneys.
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3 |
11411021
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Phorbol-12-myristate-13-acetate significantly upregulated the nephrin expression in A293 cells, while no change was found after treatment with additional stimulants for other main signalling pathways, e.g. okadaic acid, lysophosphatidic acid, bradykinin, angiotensin II (ANG II) and arginine vasopressin (AVP).
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4 |
11508272
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We studied the expression of nephrin in a hypertensive model of diabetic nephropathy and investigated the potential influence of angiotensin II blockade on nephrin gene and protein expression.
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5 |
11508272
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These changes in nephrin levels were completely prevented by angiotensin II antagonist treatment, suggesting a potential novel mechanism to explain the antiproteinuric effect of agents which interrupt the renin-angiotensin system.
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6 |
11562357
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Mutations of NPHS1 or NPHS2, the genes encoding for the glomerular podocyte proteins nephrin and podocin, cause steroid-resistant proteinuria.
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7 |
11562357
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Nephrin-induced signaling is greatly enhanced by podocin, which binds to the cytoplasmic tail of nephrin.
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8 |
11793093
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We therefore analyzed kidney tissue from normal children (n=3), children with congenital nephrotic syndrome of the Finnish type (CNF, n=3), minimal change disease (MCD, n=3), focal segmental glomerulosclerosis (FSGS, n=3), and Galloway-Mowat syndrome (n=4) by immunohistochemistry for expression of synaptopodin, GLEPP1, intracellular domain of nephrin (nephrin-I), and extracellular domain of nephrin (nephrin-E).
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9 |
11793093
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Nephrin was absent, and synaptopodin and GLEPP1 expression were decreased in CNF.
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10 |
12424224
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Mutations of NPHS1 or NPHS2, the genes encoding for the glomerular podocyte proteins nephrin and podocin, cause steroid-resistant proteinuria.
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11 |
12424224
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NEPH1 triggers AP-1 activation similarly to nephrin but requires the presence of Tec family kinases for efficient transactivation.
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12 |
12424224
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We conclude that NEPH1 defines a new family of podocin-binding molecules that are potential candidates for hereditary nephrotic syndromes not linked to either NPHS1 or NPHS2.
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13 |
12663475
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In vitro studies on human cultured podocytes demonstrated that glycated albumin and angiotensin II reduced nephrin expression.
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14 |
12663475
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Glycated albumin inhibited nephrin synthesis through the engagement of receptor for advanced glycation end products, whereas angiotensin II acted on cytoskeleton redistribution, inducing the shedding of nephrin.
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15 |
12663475
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This study indicates that the alteration in nephrin expression is an early event in proteinuric patients with diabetes and suggests that glycated albumin and angiotensin II contribute to nephrin downregulation.
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16 |
12832477
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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.
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17 |
12832477
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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.
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18 |
14507316
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Podocytes in IGB expressed WT1, synaptopodin, podocalyxin, and nephrin, and their expression was stronger in MGB.
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19 |
15153558
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Use of the nephrin promoter to target the podocytes resulted in an expression of the hAT1 at a level roughly two times higher than the endogenous AT1 throughout life.
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20 |
15388893
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In relation to beta-actin, the protein level of nephrin decreased by about 78%.
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21 |
15388893
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Thus, the significant decreased expression of nephrin along with the redistribution were detected with the knockdown of podocin mRNA, whereas the expression and distribution of alpha-actinin-4 showed no change.
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22 |
15388893
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These results suggest that podocin may interact directly with nephrin, but not with alpha-actinin.
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23 |
15465010
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In summary, our data show that in the course of mesangioproliferative glomerulonephritis in rats, an upregulation of nephrin expression occurs with a concomitant transient downregulation of podocin and CD2AP which may account for a highly dysregulated filtration barrier and increased proteinuria.
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24 |
15339792
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We therefore investigated whether VEGF signals to reduce apoptosis and the role of nephrin in this survival mechanism.
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25 |
15339792
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Although VEGF reduced apoptosis in human conditionally immortalized podocytes [wild-type (WT)] by 18.1% of control (P < 0.001), it was unable to do so in nephrin-deficient human conditionally immortalized podocytes.
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26 |
15339792
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Moreover, Western blotting and immunodetection with an anti-nephrin antibody showed that the phosphorylation of nephrin, compared with serum-starved WTs, was significantly increased (ratio of 3.36 +/- 1.2 to control, P < 0.05) by VEGF treatment and significantly reduced by treatment with a neutralizing VEGF monoclonal antibody (mAb) (ratio of 0.2 +/- 0.09 to control, P < 0.05).
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27 |
15339792
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We suggest therefore that both exogenous and endogenous (podocyte derived) VEGF can stimulate the phosphorylation of nephrin and through this action may prevent podocyte apoptosis.
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28 |
15780077
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These studies demonstrate that mutation of NPHS1 is not a major cause of CNS in Japanese patients, and that mutation of NPHS2 can be responsible for CNS in this population.
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29 |
15942677
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Since these patients show reduced nephrin and podocin expression at renal biopsy, we evaluated the effect of serum and PF from patients with FSGS on nephrin and podocin expression in human podocytes.
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30 |
15942677
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We found that serum and PF from FSGS patients rapidly induced redistribution and loss of nephrin in podocytes.
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31 |
15843472
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Nephrin reduction was preceded by inhibition of nephrin tyrosine phosphorylation and of its association with p85 phosphatidylinositol 3-kinase (PI3K).
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32 |
15843472
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Moreover, three different statins, mevastatin, pravastatin, and simvastatin, inhibited in a dose-dependent manner apoptosis and loss of nephrin induced by oxLDL by stimulating Akt activity.
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33 |
15997642
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Mutations in NPHS1 lead to congenital nephrotic syndrome of the Finnish type (CNF), whereas NPHS2 mutations result in focal segmental glomerulosclerosis (FSGS).
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34 |
16155592
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Biochemical studies reveal that nephrin directly binds to the middle PDZ domains of MAGI-1 through its carboxyl terminus but does not bind to ZO-1.
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35 |
16155592
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MAGI-1 forms a tripartite complex with nephrin and JAM4 in vitro.
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36 |
16288986
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Neither IL-1beta nor TNFalpha alone has an effect on nephrin promoter activity suggesting that additional posttranscriptional regulatory events might be operative.
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37 |
16288986
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In the presence of PPARalpha agonists, IL-1beta or TNFalpha, the decay of nephrin mRNA was drastically reduced thus arguing for an additional posttranscriptional mode of action.
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38 |
16382022
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In cultured podocytes subjected to recombinant IP-10 treatment, the expression of slit-diaphragm (SD) components nephrin and podocin clearly was heightened.
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39 |
16518627
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His native and allograft kidneys were evaluated for nephrin expression by immunohistochemistry, DNA analysis for the NPHS1 mutation, serum for the presence of auto-antibodies to nephrin by both enzyme-linked immunosorbent assay (ELISA) and fetal glomeruli immunofluorescence assay, and serum for glomerular permeability to albumin (Palb) activity using a functional in vitro assay for Palb.
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40 |
16571784
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In contrast, in mature glomerular, nestin immunoreactivity was observed only outside laminin-positive glomerular basement membrane, and co-localized with nephrin, consistent with podocyte nestin expression.
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41 |
16631587
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PAX2 activation caused repression of the podocyte key regulator molecule Wt1 and consequently a dramatic reduction of nephrin expression.
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42 |
16631587
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Finally, treatment of mice with an angiotensin-converting enzyme (ACE) inhibitor normalized renal function and induced upregulation of the important structural molecule nephrin via a Wt1-independent pathway.
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43 |
16636307
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After lisinopril and prednisone intervention, podocin exhibited prominent earlier changes compared with those of nephrin and CD2AP, whereas CD2AP showed more prominent changes after ATRA intervention.
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44 |
16837631
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ILK deficiency caused an aberrant distribution of nephrin and alpha-actinin-4 in podocytes, whereas the localization of podocin and synaptopodin remained relatively intact.
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45 |
16837631
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Co-immunoprecipitation demonstrated that ILK physically interacted with nephrin to form a ternary complex, and alpha-actinin-4 participated in ILK/nephrin complex formation.
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46 |
16820792
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In contrast, inflammatory cytokines interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha as well as phorbol ester significantly downregulated the activity of the nephrin promoter as well as nephrin gene expression.
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47 |
16943307
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The mRNA expression of SV2B clearly is altered not only in PAN nephropathy but also in another proteinuric state that is caused by an antibody against nephrin, a functional molecule of the slit diaphragm.
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48 |
17429054
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Glomerular gene expression of nephrin, podocin, dystroglycan, B7-1, and IL-13 receptor subunits were examined using real-time PCR with hybridization probes and expressed as an index against beta-actin.
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49 |
17429054
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In conclusion, these results suggest that IL-13 overexpression in the rat could lead to podocyte injury with downregulation of nephrin, podocin, and dystroglycan and a concurrent upregulation of B7-1 in the glomeruli, inducing a minimal change-like nephropathy that is characterized by increased proteinuria, hypoalbuminemia, hypercholesterolemia, and fusion of podocyte foot processes.
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50 |
17596726
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Urinary nephrin expression was significantly correlated with proteinuria (r = 0.502, p = 0.020); urinary synaptopodin was significantly correlated with proteinuria (r = 0.585, p = 0.005), serum creatinine (r = 0.516, p = 0.017) and estimated GFR (r = -0.560, p = 0.008), and urinary WT-1 expression was significantly correlated with the degree of tubulointerstitial fibrosis (r = 0.558, p = 0.009).
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51 |
17596726
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Urinary nephrin and synaptopodin expressions are correlated with baseline clinical parameters such as proteinuria or renal function, while WT-1 expression is related to the degree of histological damage.
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52 |
18287402
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Indeed, ET-1 was synthesized and released from glomerular endothelial cells when incubated with PE sera, and recombinant ET-1 triggered nephrin shedding from podocytes.
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53 |
18287402
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Moreover, VEGF blockade induced ET-1 release from endothelial cells, and in turn the conditioned medium obtained triggered nephrin loss.
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54 |
18391505
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Rats administered albumin exhibited massive proteinuria and podocyte injury manifested by decreased nephrin immunostaining and foot process effacement.
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55 |
19129671
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Using tensin2-deficient mice (ICGN/Oa strain), we provide evidence that tensin2 is important for glomerular nephrin expression in vivo.
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56 |
19129671
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In heterozygous mice with a single mutated tensin2 allele, nephrin expression was maintained, while albuminuria was not observed.
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57 |
19129671
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In contrast, nephrin expression was impaired, especially in the central zones of glomeruli of homozygous mice (with double mutated tensin2 alleles), even at one week after birth.
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58 |
19129671
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Therefore, we suggested that tensin2 is involved in expression and extension of nephrin, while tensin2 deficiency may result in proteinuria, associated with the loss of slit integrity.
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59 |
19403392
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To evaluate the effect of bone morphogenic protein 7 (BMP-7) on nephrin expression and distribution in diabetic rat kidneys.
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60 |
19403392
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The rats in BMP-7 group showed less urinary protein excretion, lower TGF-beta1 expression and greater glomerular podocyte number than those in the DM group, and the expression and distribution of nephrin remained normal in the kidney.
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61 |
19403392
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Administration of BMP-7 can significantly suppress the down-regulation of nephrin expression and maintain its normal distribution in the podocytes in diabetic rats possibly in association with a direct suppression of TGF-betasignaling.
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62 |
19397686
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Our findings implicate that local renin angiotensin system activation in podocytes is partly involved in down-regulation of nephrin by mesangial medium in IgA nephropathy.
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63 |
19420107
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Glomerular podocytes in culture, verified to express the marker nephrin, were exposed to diabetic mediators such as high glucose or angiotensin II and assayed for MCP-1.
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64 |
19474283
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In this report, we investigated roles of the retinoic acid receptor (RAR), the retinoid X receptor (RXR) and the vitamin D receptor (VDR) in the regulation of the nephrin gene.
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65 |
19474283
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Reporter podocytes were treated with agonists and/or antagonists of RAR, RXR or VDR, and activities of the nephrin gene promoter, the retinoic acid response element (RARE) and the vitamin D response element (VDRE) were evaluated.
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66 |
19474283
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The nephrin gene promoter was also activated by these agents, which was mediated by RAR and VDR, but unexpectedly, not by RXR.
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67 |
19474283
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ATRA-triggered, RAR-mediated activation of the nephrin gene promoter was not suppressed by the VDR antagonist.
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68 |
19474283
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In contrast, the 1,25(OH)(2)D(3)-triggered, VDR-mediated activation of the nephrin gene promoter was significantly suppressed by the RAR antagonist, but not by RXR antagonists.
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69 |
19794150
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In podocytes, Neph1 siRNA also caused a decrease in nephrin, even though the Neph1 siRNA had no sequence homology with nephrin.
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70 |
19906946
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Indeed, podocyte stretching induced both angiotensin II secretion and AT(1) receptor overexpression, podocyte exposure to angiotensin II reduced nephrin protein expression, and both the AT-1 receptor antagonist candesartan and a specific anti-angiotensin II antibody completely abolished stretch-induced nephrin downregulation.
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71 |
20404345
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Here, CD2AP links the cell adhesion protein nephrin to the actin cytoskeleton.
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72 |
20576809
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Here, we report that nephrin interacts with the bicarbonate/chloride transporter kidney anion exchanger 1 (kAE1), detected by yeast two-hybrid assay and confirmed by immunoprecipitation and co-localization studies.
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73 |
20576809
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We could not detect endogenous kAE1 expression in NPHS1(FinMaj) podocytes in primary culture, but heterologous re-introduction of wild-type nephrin into these podocytes rescued kAE1 expression.
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74 |
20576809
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In kidneys of Ae1(-/-) mice, nephrin abundance was normal but its distribution was altered along with the reported kAE1-binding protein integrin-linked kinase (ILK).
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75 |
20576809
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Glomeruli with ILK-deficient podocytes also demonstrated altered AE1 and nephrin expression, further supporting the functional interdependence of these proteins.
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76 |
20576809
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These data suggest that the podocyte protein kAE1 interacts with nephrin and ILK to maintain the structure and function of the glomerular basement membrane.
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77 |
20668098
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Compared with podocytes transformed with a thermo-sensitive SV40 large T antigen mutant tsA58U19 (tsT podocytes), podocytes transformed with CDK4 (CDK4 podocytes) exhibited significantly higher expression of nephrin mRNA.
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78 |
20629321
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After second injected with adriamycin,the model group nephrin presented a weak signal in the end of the first week (P < 0.05), and the expression of VEGF started to increase at the end of the eighth week (P < 0.05).
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79 |
20629321
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The expression of nephrin and the number of podocyte were negatively correlated with the 24-hour urine protein, blood urea nitrogen and serum creatinine; while the expression of VEGF was positively correlated with the 24-hour urine protein, blood urea nitrogen and serum creatinine.
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80 |
20719975
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Defective nephrin expression of diabetes was increased by dual RAS blockade or statin and restored by the triple therapy.
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81 |
20889563
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To better understand the effects of SLK in vivo, a transgenic mouse model was developed where SLK was expressed in a podocyte-specific manner using the mouse nephrin promoter.
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82 |
20505657
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Ectopic expression of ILK in podocytes decreased levels of the epithelial markers nephrin and ZO-1, induced mesenchymal markers such as desmin, fibronectin, matrix metalloproteinase-9 (MMP-9), and alpha-smooth muscle actin (alpha-SMA), promoted cell migration, and increased the paracellular albumin flux across podocyte monolayers.
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83 |
20505657
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In vivo, this ILK inhibitor ameliorated albuminuria, repressed glomerular induction of MMP-9 and alpha-SMA, and preserved nephrin expression in murine adriamycin nephropathy.
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84 |
20840470
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Finally, our results showed that preservation of Bcl-2, Bax and nephrin expression accompanied the anti-apoptotic effects exerted by PPAR agonists in human podocytes.
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85 |
20588063
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Nephrin decreased further, while dendrin and plekhh2 also decreased but ?-actinin remained unchanged.
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86 |
18204248
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The present study evaluates the effects of Ang II infusion in rats on podocyte nephrin expression and apoptosis and the molecular mechanisms involved in Ang II-induced proteinuria and mesangial expansion.
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87 |
18204248
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On day 14, the Ang II-infused rats showed narrowing of the slit diaphragm, an increase in podocyte nephrin mRNA and protein expression, and alterations in its distribution along the foot processes.
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88 |
18204248
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These results suggest that changes in nephrin expression may play a role in the pathogenesis of Ang II-induced podocyte apoptosis.
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89 |
20962747
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Glomerulosclerosis in these mice was associated with the expression of desmin and the loss of nephrin, markers of podocyte damage and apoptosis.
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90 |
19470472
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Although nephrin-knockout (nephrin(KO)) myoblasts exhibit prolonged activation of MAPK/ERK pathway during myogenic differentiation, expression of myogenin does not seem to be altered.
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91 |
21186102
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It has been recently shown that nephrin once phosphorilated associates with PI3K and stimulates the Akt dependent signaling.
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92 |
10997929
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CD2-associated protein (CD2AP) is an adapter molecule that can bind to the cytoplasmic domain of nephrin, a component of the glomerular slit diaphragm.
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93 |
10997929
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Kidneys from Cd2ap -/- mice initially exhibited normal nephrin localization, but as the mice aged and foot processes became effaced, nephrin disappeared.
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94 |
17018845
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Decreasing the burden of glycated albumin in diabetic db/db mice significantly reduces glomerular overexpression of TGF-beta1 mRNA, restores glomerular nephrin immunofluorescence, and lessens proteinuria, mesangial expansion, renal extracellular matrix protein production, and increased glomerular vascular endothelial growth factor (VEGF) immunostaining.
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95 |
18480178
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We detected nephrin binding to the Slo1 VEDEC splice variant, which is typically retained in intracellular stores, and to the beta4-subunit.
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96 |
18480178
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Stimulation of Slo1 VEDEC surface expression in HEK-293T cells was also observed by coexpressing a small construct encoding only the distal COOH-terminal domains of nephrin that interact with Slo1.
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97 |
18480178
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Reduction of endogenous nephrin expression by application of small interfering RNA to differentiated cells of an immortalized podocyte cell line markedly reduced the steady-state surface expression of Slo1 as assessed by electrophysiology and cell-surface biotinylation assays.
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98 |
18667486
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Surprisingly, glomerular GLUT1 levels did not increase and nephrin levels did not decrease in the diabetic animals; neither changed with rosiglitazone.
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99 |
20071462
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The tyrosine phosphorylation of nephrin is reported to regulate podocyte morphology via the Nck adaptor proteins.
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100 |
20237236
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We previously reported that 1) expression of nephrin in cultured podocytes is reinforced by retinoic acid (RA) and 1,25-dihydroxyvitamin D(3), 2) these effects are mediated by retinoic acid receptor (RAR) and vitamin D receptor (VDR), and 3) basal and inducible expression of nephrin is downregulated by TNF-alpha.
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101 |
21318407
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It also led to increased VEGF receptor 2 and semaphorin3a levels, as well as nephrin and matrix metalloproteinase-2 downregulation, whereas circulating VEGF-A levels were similar to those in control diabetic mice.
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102 |
20375988
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When HGF was expressed ectopically in vivo, it ameliorated adriamycin-induced albuminuria, preserved WT1 and nephrin expression, and inhibited podocyte apoptosis.
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103 |
20375988
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In vitro, HGF was able to preserve WT1 and nephrin expression in cultured podocytes after adriamycin treatment.
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104 |
21321125
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Further, cellular knockdown of PKC? and/or PICK1 attenuated the nephrin-?-arrestin2 interaction and abrogated the amplifying effect of high blood glucose on nephrin endocytosis.
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105 |
20116427
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Hyperhomocysteinemia-induced decrease in nephrin expression and increase in desmin expression in gp91(+/+) mice were not observed in gp91(-/-) mice.
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106 |
21228103
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In addition, rhVASH-1 significantly recovered the mRNA levels of nephrin and the protein levels of ZO-1 and P-cadherin and suppressed the increase in protein levels of desmin, FSP-1, Snail, and Slug in podocytes under high-glucose condition.
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107 |
21402783
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We further demonstrate that similarly to Neph1, Myo1c also binds nephrin and reduces its localization at the podocyte cell membrane.
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108 |
21289599
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Further, both agonists restored WT-1 staining along with podocin and nephrin mRNA expression, suggesting podocyte protection.
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109 |
21336536
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In elegant biochemical studies, Garg et al. established that cofilin-1 activity is regulated by nephrin, which is part of the slit diaphragm complex.
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110 |
21258034
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Because IQGAP1 interacts with crucial podocyte proteins such as nephrin and PLC?1, the identification of mutations that may alter the putative INF2-IQGAP1 interaction provides additional insight into the pathophysiologic mechanisms linking formin proteins to podocyte dysfunction and FSGS.
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111 |
21402589
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Furthermore, co-immunoprecipitation studies demonstrated a direct interaction of nephrin with p75NTR.
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112 |
21402589
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Taken together, our data demonstrate that nephrin directly interacts with p75NTR and reveal an important role for nephrin in murine cardiac development by permitting survival of cardiovascular progenitor cells.
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113 |
21380797
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FSGS plasma also caused dispersion of slit diaphragm proteins (nephrin and podocin) and vinculin-positive focal adhesion complexes.
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114 |
19833886
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Actin stabilization prevented nephrin trafficking as well as nephrin-positive effect on insulin release.
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115 |
21451433
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Furthermore, PAN-induced up-regulation of desmin, down-regulation of synaptopodin and nephrin, and disruption of glomerular morphology were significantly attenuated in VEGF-induced transgenic mice.
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116 |
20419132
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We can demonstrate that PKCalpha mediates nephrin endocytosis in podocytes and that overexpression of PKCalpha leads to an augmented endocytosis response.
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117 |
16501493
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Contrarily, with podocin or CD2AP knockdown, nephrin decreased, while CD2AP or podocin increased.
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118 |
20472933
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Because podocyte intercellular junction receptor Nephrin plays a role in regulating actin dynamics, and given the described role of cofilin in actin filament polymerization and severing, we hypothesized that cofilin-1 activity is regulated by Nephrin and is necessary in normal podocyte actin dynamics.
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119 |
20472933
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This Nephrin-induced cofilin activation required a direct interaction between Nephrin and the p85 subunit of phosphatidylinositol 3-kinase.
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120 |
21471003
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Furthermore, nephrin, an adhesion protein between the foot processes of podocytes, binds to phosphorylated TRPC6 via its cytoplasmic domain, competitively inhibiting TRPC6-PLC-?1 complex formation, TRPC6 surface localization, and TRPC6 activation.
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121 |
21471003
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Importantly, FSGS-associated mutations render the mutated TRPC6s insensitive to nephrin suppression, thereby promoting their surface expression and channel activation.
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122 |
21303966
|
CRP did up-regulate the expression of the slit diaphragm proteins nephrin and CD2AP, as well as the structural proteins ezrin and podocalyxin-like protein-1, proteins known to be involved in signalling via the phosphotidylinositol-3 (PI-3) kinase pathway.
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123 |
20522599
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After use of pharmacological modulators or specific shRNA knockdown strategies, inhibition of Notch-1 signaling significantly abrogated VEGF activation and nephrin repression in HG-stressed cells and ameliorated proteinuria in the diabetic kidney.
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124 |
20522599
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Our findings suggest that upregulation of Notch-1 signaling in HG-treated renal podocytes induces VEGF expression and subsequent nephrin repression and apoptosis.
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125 |
20457601
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We can demonstrate that the loss of nephrin expression and onset of the proteinuria in CD2AP(-/-) mice correlates with an increased accumulation of ubiquitinated proteins and expression of CIN85/Ruk(L) in podocytes.
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126 |
20562105
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We also show that sdk-1 associates with the slit diaphragm linker protein MAGI-1, which is already known to interact with several critical podocyte proteins including synaptopodin, alpha-actinin-4, nephrin, JAM4, and beta-catenin.
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127 |
21630272
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In primary neuronal cells we find nephrin expression close to synaptic proteins and demonstrate that nephrin co-immunoprecipitates with Fyn kinase, glutamate receptors and the scaffolding molecule PSD95, an assembly that is reminiscent of those made by synaptic adhesion molecules.
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128 |
21803771
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ChIP scan of the 6-kb 5' upstream region of the mouse nephrin gene identified several putative vitamin D response elements (VDREs), and EMSA confirmed that the VDRE at -312 (a DR4-type VDRE) could be bound by vitamin D receptor (VDR)/retinoid X receptor.
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129 |
21695412
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Dex treatment for 24 h increased the phosphorylation of nephrin; this increased phosphorylation was inhibited by the glucocorticoid receptor antagonist but not by the mineral corticoid receptor antagonist.
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130 |
21695412
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The activation of Src-family kinases was correlated with nephrin phosphorylation, both of which were abolished by small interfering RNA (siRNA) treatment for serum/glucocorticoid-induced kinase 1 (SGK1).
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131 |
21695412
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These results clarify a novel action of glucocorticoid on nephrin phosphorylation through SGK1.
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132 |
22013520
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PTP1B directly binds to and dephosphorylates nephrin, while the action of PTP-PEST is indirect.
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133 |
18258597
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In pull-down assays using rat glomerular lysates, Neph1 but not nephrin specifically binds to adaptor protein Grb2 and tyrosine kinase Csk in a phosphorylation-dependent manner.
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134 |
21937443
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We previously showed that in vivo nephrin associates with VEGF receptor-2 (VEGFR2), the signaling receptor for VEGF-A.
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135 |
21832980
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Ectopic expression of Wnt1 or ?-catenin mimicked TGF-?1, induced Snail1, and suppressed nephrin expression.
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136 |
21832980
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The Wnt antagonist, Dickkopf-1, blocked TGF-?1-induced ?-catenin activation, Snail1 induction, and nephrin suppression.
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137 |
22099175
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Here we show that the expression of neph3 in pronephros starts before the onset of nephrin and podocin expression, peaks when the nephron primordium differentiates into glomerulus and tubulus, and is then downregulated upon glomerular maturation.
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138 |
21414970
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Regarding GKD subtypes, patients with focal segmental glomerulosclerosis (FSGS), but not patients with minimal change disease (MCD), had a significantly higher mRNA expression of B7-1 and NPHS1 than healthy subjects (P = 0.012 and P = 0.030, respectively).
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