ライフサイエンスコーパス: nephrin

1 ing were substituted with phenylalanine (3YF-Nephrin).

2 rstitial injury (fibronectin) and podocytes (nephrin).

3 it interacts with the slit diaphragm protein nephrin.

4 several phosphorylated tyrosine residues on nephrin.

5 n-dependent, raft-independent endocytosis of nephrin.

6 rier and required for the proper function of nephrin.

7 ical Notch signaling, prevented this loss of nephrin.

8 ophila myoblasts, has structural homology to nephrin.

9 n cytoskeleton via the transmembrane protein nephrin.

10 pression of SHP-1, which was associated with nephrin.

11 are required to allow SHP-1 interaction with nephrin.

12 se Shp2 to be associated with phosphorylated nephrin.

13 n RGDfv blocked suPAR-induced suppression of nephrin.

14 < 0.05), and reduced expression of podocyte nephrin (-29%, p < 0.01).

15 negative Dynamin mutant (K44A-Dynamin) in WT-Nephrin, 3YF-Nephrin, or Nephrin siRNA-transfected cells

16 Nephrin, a critical podocyte membrane component that is

17 Nephrin, a podocyte-specific protein, is the main compon

18 In kidneys of Ae1(-/-) mice, nephrin abundance was normal but its distribution was al

19 emia accelerated podocyte injury and reduced nephrin, acetylated nephrin, and miR-29a levels in prima

20 on of histone deacetylase (HDAC) actions and nephrin acetylation by miR-29 contributes to podocyte ho

21 glucose-induced apoptosis and inhibition of nephrin acetylation in podocyte cultures.

22 retion associated with diabetes and restored nephrin acetylation.

23 standing of nephrin function by showing that nephrin activation in cultured podocytes induced actin d

24 Nephrin activation induced cofilin dephosphorylation via

25 requires interactions between surface Neph1/nephrin adhesion receptors Roughest and Hibris, which bi

26 airs the polymerization of actin at sites of nephrin aggregates.

27 process effacement and F-actin collapse via nephrin, alphavbeta3 integrin, and MICAL1 interactions w

28 Hbs function appears conserved, as mammalian Nephrin also promotes N signaling in mammalian cells.

29 Nephrin, an immunoglobulin-like protein essential for th

30 upregulation of Snail and downregulation of nephrin and alpha-actinin-4.

31 sence of protein-protein interaction between Nephrin and Dynamin.

32 hat the podocyte protein kAE1 interacts with nephrin and ILK to maintain the structure and function o

33 on of activated Notch decreased cell surface nephrin and increased cytoplasmic nephrin in transfected

34 ized that cofilin-1 activity is regulated by Nephrin and is necessary in normal podocyte actin dynami

35 in clusters containing the adhesion receptor Nephrin and its cytoplasmic partners, Nck and N-WASP.

36 The cell adhesion proteins nephrin and neph1 localize to the slit diaphragm and tra

37 down sns and duf, the Drosophila homologs of nephrin and Neph1, respectively, in pericardial nephrocy

38 teins, orthologs of the human genes encoding nephrin and nephrin-like protein 1, colocalize within a

39 supported a functional relationship between nephrin and NF-kappaB and suggested the involvement of a

40 ured human podocytes increased expression of nephrin and other epithelial markers and reduced mesench

41 of CMP-sialic acid prevented sialylation of nephrin and podocalyxin in the maturing podocyte where i

42 The glomerular glycoproteins nephrin and podocalyxin were hyposialylated in this uniq

43 type mice, with improved sialylation of both nephrin and podocalyxin, as well as reduced albuminuria

44 altered endoderm development, as assessed by nephrin and podocin expression in double osr1/sox32-defi

45 We monitored podocyte loss by detecting nephrin and podocin mRNA in urine particulates with quan

46 duced expression and altered localization of nephrin and podocin proteins.

47 hanistically, claudin-1 interacted with both nephrin and podocin through cis- and trans-associations

48 so, KLF15 binding to the promoter regions of nephrin and podocin was increased in RA-treated podocyte

49 l surface expression of the podocyte markers nephrin and podocin, but there was no loss of cells.

50 express the foot process junctional markers nephrin and podocin.

51 rrelates with reduced urinary levels of both nephrin and podocin.

52 (e.g., ceruloplasmin), and podocytes (e.g., nephrin and prepronociceptin).

53 te that similarly to Neph1, Myo1c also binds nephrin and reduces its localization at the podocyte cel

54 though MAGI2 has been shown to interact with nephrin and regulate podocyte cytoskeleton and slit diap

55 TGF-beta1 down-regulated nephrin and synaptopodin expression in podocytes in cell

56 ) overexpression significantly downregulated nephrin and synaptopodin expression, promoted apoptosis

57 in 7 increased the interaction of VAMP2 with nephrin and syntaxin 4.

58 l strategy that posttranslationally modifies nephrin and the effects of this strategy in the pancreas

59 vation required a direct interaction between Nephrin and the p85 subunit of phosphatidylinositol 3-ki

60 s that control the expression of podocin and nephrin and thereby mediate podocyte differentiation.

61 in chicken, including the long-sought-after nephrin and tumor necrosis factor genes.

62 rk, we characterized the interaction between nephrin and VEGFR2 in cultured cells and in vitro.

63 GSIR and live images of Nephrin and vesicle trafficking were studied.

64 remains unknown whether SHP-1 interacts with nephrin and whether its elevated expression affects the

65 the infusion of suPAR inhibits expression of nephrin and WT-1 in podocytes and induces proteinuria.

66 ed cAMP, 2) activated PKA, 3) phosphorylated nephrin, and 4) attenuated albumin transcytosis.

67 rentiation marked by a loss of synaptopodin, nephrin, and foot process effacement, partly regulated b

68 ocyte injury and reduced nephrin, acetylated nephrin, and miR-29a levels in primary renal glomeruli f

69 slit diaphragm-associated proteins podocin, nephrin, and synaptopodin and to enhanced transient rece

70 Thus, Hbs/Nephrin appear to share a general requirement in Psn/gam

71 th increased urinary podocin:aquaporin 2 and nephrin:aquaporin 2 molar ratios.

72 obulin superfamily (IgSF) proteins Neph1 and Nephrin are co-expressed within podocytes in the kidney

73 the slit diaphragm in the absence of either nephrin (as in human congenital nephrotic syndrome of th

74 Nck enhances phase separation of Nck/N-WASP/nephrin assemblies.

75 We previously showed that in vivo nephrin associates with VEGF receptor-2 (VEGFR2), the si

76 e PCP protein Vangl2 leads to an increase of nephrin at the cell surface; loss of Vangl2 functions in

77 diates the dynamic organization of Neph1 and nephrin at the slit diaphragm and is critical for podocy

78 With Nephrin attached to the bilayer, multivalent interaction

79 In vitro changes of the Snail/nephrin axis were similar to those in renal biopsy speci

80 ates with CD2-associated protein (CD2AP) and nephrin, both essential for glomerular ultrafiltration.

81 ect expression of podocin, synaptopodin, and nephrin but reduced their expression as glomerular injur

82 expression of the podocyte-specific protein, nephrin, but not podocin, is reduced in preeclamptic com

83 Furthermore, reduction of nephrin by transforming growth factor-beta (TGF-beta) in

84 se exposure increases SHP-1 interaction with nephrin, causing decreased nephrin phosphorylation, whic

85 Coexpression of nephrin-CD16 and SHP-1 reduced nephrin tyrosine phosphor

86 We propose that a Neph1/nephrin-Cindr/ArfGAP complex accumulates to limit local

87 A nephrin clustering assay suggested that Cdc42 deficiency

88 sed podocalyxin and podocin proteins but not nephrin, compatible with detached podocytes' having an a

89 ms' tumor 1 and nephrin staining and urinary nephrin concentration, was found in diabetic WT but not

90 ne expression were increased and podocin and nephrin content were decreased by either the CB1R agonis

91 This interaction occurs through VEGFR2 and nephrin cytoplasmic domains.

92 n podocytes, and vitamin D analogs prevented nephrin decline in both type 1 and 2 diabetic mice.

93 MIN6-C3 Nephrin-deficient pancreatic beta cells and human islets

94 on at Tyr-1176/1193/1217 was associated with Nephrin degradation and impaired GSIR.

95 osphorylation following injury would prevent nephrin-dependent actin remodeling and foot process morp

96 glomeruli, podocyte survival is mediated via nephrin-dependent Akt signaling.

97 mediated through cAMP/protein kinase A (PKA)/nephrin-dependent pathways, we found that PKA inhibition

98 Vanadate, which prevented Nephrin dephosphorylation after glucose stimulation, imp

99 indings demonstrate the relationship between nephrin dephosphorylation and the mTORC1 pathway, mediat

100 We further demonstrate that, coincident with nephrin dephosphorylation in a transient model of podocy

101 T-Nephrin or to single tyrosine mutants, 3YF-Nephrin did not positively affect GSIR and led to impair

102 Here, we show that suPAR induces nephrin down-modulation in human podocytes.

103 Podocyte VEGF164 overexpression induced nephrin down-regulation without podocyte loss.

104 oteinuria, podocyte foot process effacement, nephrin down-regulation, and nephrinuria.

105 RNA-transfected cells were utilized to study Nephrin-Dynamin interaction.

106 d transgenic (Tg) mice using the promoter of nephrin-encoding Nphs1 to express the APOL1 reference se

107 ng of GFP-nephrin-transfected cells revealed nephrin endocytosis upon glucose stimulation.

108 s a binding partner of nephrin that mediates nephrin endocytosis via ubiquitination in podocytes.

109 -nephrin-transfected cells was used to study nephrin endocytosis.

110 ape, actin rearrangement, cell motility, and nephrin endocytosis.

111 d with an elevated urinary podocin(+) EVs-to-nephrin(+) EVs ratio and may be mediated by prolonged ex

112 hrin-positive urinary EVs (podocin(+) EVs-to-nephrin(+) EVs ratio) and increased nephrinuria, both of

113 with proteinuria, urinary podocin(+) EVs-to-nephrin(+) EVs ratio, and nephrinuria.

114 evealed a loss of the slit diaphragm protein nephrin exclusively in podocytes expressing activated No

115 gnaling, nephrin ubiquitination, and urinary nephrin excretion associated with diabetes and restored

116 governed by the degree of phosphorylation of nephrin, explaining how this property of the system can

117 ression, resulted in a sustained increase in nephrin expression and a decrease in albuminuria.

118 vivo, immunoblot analysis demonstrated that nephrin expression and phosphorylation were decreased in

119 Here we demonstrate that the loss of nephrin expression and the onset of proteinuria in diabe

120 In vivo biotinylation assays confirmed that nephrin expression decreased at the cell surface and cor

121 In several glomerular diseases, nephrin expression decreases and podocyte survival corre

122 RESEARCH DESIGN AND Nephrin expression in human pancreas and in MIN6 insulin

123 as to investigate whether diabetes modulates nephrin expression in human pancreatic islets and to exp

124 ated forms of the lhx1a gene product rescued nephrin expression in osr1-deficient podocytes.

125 demonstrate that 1,25(OH)(2)D(3) stimulates nephrin expression in podocytes by acting on a VDRE in t

126 wk postnatally, which coincided with loss of nephrin expression in the glomeruli.

127 tured human podocytes, Ang II down-regulated nephrin expression via Notch1 activation and nuclear tra

128 Nephrin expression was decreased in islets from diabetic

129 itazone enhanced glomerular synaptopodin and nephrin expression, and reduced COX-2 expression, after

130 podocytes also demonstrated altered AE1 and nephrin expression, further supporting the functional in

131 he transcription factor Snail and suppressed nephrin expression, leading to podocyte dysfunction.

132 , eventually resulting in down-regulation of nephrin expression, the integrity of which is crucial fo

133 inuria and adriamycin-induced suppression of nephrin expression, whereas blockade of Wnt signaling wi

134 r podocytes, as determined by wt1b, hey1 and nephrin expression, while embryos deficient in any two o

135 e phosphorylation of the cytoplasmic tail of nephrin facilitates recruitment of Nck SH2/SH3 adaptor p

136 proteinuria and podocyte mRNAs (podocin and nephrin) followed 8 d later by a second peak of proteinu

137 present studies extend our understanding of nephrin function by showing that nephrin activation in c

138 Whether altered sialylation impairs nephrin function in human disease requires further study

139 MIN-6 cells/human islets were used to study nephrin function in vitro and in vivo after transplantat

140 of the 6-kb 5' upstream region of the mouse nephrin gene identified several putative vitamin D respo

141 Nephrin gene silencing abolished stimulated insulin rele

142 Nephrin gene silencing abolished the positive effects of

143 Drosophila Hibris (Hbs), a member of the Nephrin Immunoglobulin Super Family, has been implicated

144 nt and attenuated the expression of podocyte nephrin in APA-KO mice but not in wild-type controls.

145 pancreatic islets and to explore the role of nephrin in beta-cell function.

146 cated increased colocalization of SHP-1 with nephrin in diabetic mice compared with control littermat

147 nd further, the interaction of septin 7 with nephrin in glomeruli suggests that septin 7 may particip

148 We have previously demonstrated a role for Nephrin in glucose stimulated insulin release (GSIR).

149 us, CIN85/RukL is involved in endocytosis of nephrin in podocytes under diabetic conditions, causing

150 previous study has established any role for nephrin in skeletal muscle.

151 adducts, maintained a normal distribution of nephrin in the glomeruli, and provided significant prote

152 ll surface nephrin and increased cytoplasmic nephrin in transfected HEK293T cells; pharmacologic inhi

153 transfected with WT-Nephrin or with a mutant Nephrin in which the tyrosine residues responsible for S

154 This Nephrin-induced cofilin activation required a direct int

155 phosphorylation of the intracellular tail of nephrin initiates signaling events, including recruitmen

156 eature in diabetic nephropathy, with loss of nephrin integrity contributing to diabetic podocytopathy

157 Here, we report that nephrin interacts with the bicarbonate/chloride transpor

158 ut heterologous re-introduction of wild-type nephrin into these podocytes rescued kAE1 expression.

159 llular and in vitro assays, we show that the Nephrin intracellular domain (NICD), a disordered protei

160 The transmembrane protein nephrin is a key component of the kidney slit diaphragm

161 Nephrin is a key structural component of the podocyte sl

162 Nephrin is a protein expressed in kidney that is part of

163 Our data suggest that nephrin is an active component of insulin vesicle machin

164 The transmembrane protein nephrin is an essential component of slit diaphragms, th

165 phosphorylation of the Nck binding sites on nephrin is decreased during podocyte injury.

166 Because nephrin is important to glomerular permselectivity, we n

167 The cell adhesion protein nephrin is necessary for establishing the morphology of

168 Loss of nephrin is observed in human and rodent models of diabet

169 ins including synaptopodin, alpha-actinin-4, nephrin, JAM4, and beta-catenin.

170 dent pathways, we found that PKA inhibition, nephrin knockdown, or targeted mutation of phosphorylate

171 Although nephrin-knockout (nephrin(KO)) myoblasts exhibit prolong

172 sive proteinuria, recapitulating features of nephrin-knockout mice and of patients with Finnish-type

173 ature myotubes; however, the contribution of nephrin(KO) myoblasts is minimal.

174 res of unaffected human fetal myoblasts with nephrin(KO) myoblasts or myotubes restore the formation

175 Although nephrin-knockout (nephrin(KO)) myoblasts exhibit prolonged activation of M

176 hosphotyrosine sites in the adhesion protein nephrin, leading to phase separation.

177 and accompanied by increased urinary soluble nephrin levels (nephrinuria) in preeclampsia.

178 Diabetic miR-29a transgenic mice had better nephrin levels, podocyte viability, and renal function a

179 logs of the human genes encoding nephrin and nephrin-like protein 1, colocalize within a fingerprint-

180 n the Sema3a signaling receptor plexinA1 and nephrin, linking extracellular Sema3a signals to the sli

181 ense oligonucleotides promoted HDAC4 action, nephrin loss, podocyte apoptosis, and proteinuria in non

182 tor 2 (VEGFR2) signaling and compensates for nephrin loss.

183 ally, excess Sema3a induces dysregulation of nephrin, matrix metalloproteinase 9, and alphavbeta3 int

184 In summary, nephrin may normally limit NF-kappaB activity in the pod

185 Development of drugs targeting nephrin may represent a novel approach to treat diabetes

186 in response to glucose and is necessary for Nephrin-mediated augmentation of GSIR.

187 odocytes 1,25(OH)(2)D(3) markedly stimulated nephrin mRNA and protein expression.

188 ment of mice with a vitamin D analog induced nephrin mRNA and protein in the kidney, accompanied by i

189 dingly, EP1 deletion in OVE26 mice prevented nephrin mRNA expression down-regulation and ameliorated

190 es were stressed (increased urine podocin-to-nephrin mRNA ratio).

191 n glomeruli homozygous for the NPHS1(FinMaj) nephrin mutation, whereas kAE1 expression remained uncha

192 ethod to the analysis of interactions in the nephrin-Nck-N-Wasp signaling system, demonstrating how m

193 and recovery, which correlated with loss of nephrin-Nck1/2 association during foot process effacemen

194 anism distinct from the previously described nephrin-Nck1/2 pathway necessary for assembly and polyme

195 odocyte mRNAs that were podocin positive but nephrin negative.

196 for months correlated with podocin-positive, nephrin-negative mRNAs in urine.

197 ted in NF-kappaB activation, suggesting that nephrin negatively regulates the NF-kappaB pathway.

198 docyte proteins, including those of podocin, nephrin, neph1, alpha-actinin-4, and vimentin.

199 Finnish type, that is caused by mutations in nephrin (NPHS1).

200 K44A-Dynamin prevented the effect of Nephrin on GSIR in the absence of protein-protein intera

201 yte slit diaphragm, and proper expression of nephrin on the cell surface is critical to ensure integr

202 ely lost in flies lacking the orthologues of nephrin or NEPH1-a phenotype resembling loss of the slit

203 In contrast to WT-Nephrin or to single tyrosine mutants, 3YF-Nephrin did n

204 ls and human islets were transfected with WT-Nephrin or with a mutant Nephrin in which the tyrosine r

205 min mutant (K44A-Dynamin) in WT-Nephrin, 3YF-Nephrin, or Nephrin siRNA-transfected cells were utilize

206 The podocyte proteins Neph1 and nephrin organize a signaling complex at the podocyte cel

207 p protein in mice with chronic disruption of nephrin phospho-signaling.

208 WT-Nephrin phosphorylation after glucose occurred at Tyr-11

209 knockout mice with selexipag augmented renal nephrin phosphorylation and attenuated albuminuria devel

210 d LPS-induced NF-kappaB and MAPK activation, nephrin phosphorylation and attenuated endoplasmic retic

211 equired for GSIR and that Dynamin influences Nephrin phosphorylation and function.

212 effects of protamine sulfate and vanadate on Nephrin phosphorylation and GSIR were studied in MIN6 ce

213 ditions, but the molecular mechanism linking nephrin phosphorylation and pathology is unclear so far.

214 We hypothesized that abrogation of nephrin phosphorylation following injury would prevent n

215 hether IP receptor agonism similarly affects nephrin phosphorylation in podocytes.

216 Nephrin phosphorylation is a proximal event that occurs

217 The ability of Nck to enhance nephrin phosphorylation is compromised in the presence o

218 We now hypothesize that Nephrin phosphorylation is required for GSIR and that Dy

219 Pharmacological modulation of Nephrin phosphorylation may thus facilitate pancreatic b

220 In conclusion, Dynamin-dependent Nephrin phosphorylation occurs in response to glucose an

221 whether its elevated expression affects the nephrin phosphorylation state in diabetes.

222 now demonstrate that Nck directly modulates nephrin phosphorylation through formation of a signaling

223 Diabetes-induced nephrin phosphorylation was also reduced in mice with an

224 interaction with nephrin, causing decreased nephrin phosphorylation, which may, in turn, contribute

225 Studies in cell culture suggest nephrin phosphorylation-dependent signaling events are p

226 prevented high glucose-induced reduction of nephrin phosphorylation.

227 sults suggest that increases in ShcA perturb nephrin phosphosignaling dynamics, leading to aberrant n

228 protein tyrosine phosphatase (PTPase) at the nephrin-PI3K binding site and renders PI3K for IRS-1, th

229 Nephrin plays a key role in maintaining the structure of

230 use podocyte intercellular junction receptor Nephrin plays a role in regulating actin dynamics, and g

231 These studies suggest that nephrin plays a role in secondary fusion of myoblasts in

232 hragm constituting molecules (SDCM), such as nephrin, podocin, and CD2-associated protein (CD2AP), we

233 contain both unique membrane proteins (e.g., nephrin, podocin, and Neph1) and typical adherens juncti

234 the podocyte markers Wilms tumor protein 1, nephrin, podocin, and synaptopodin.

235 ntrols, paricalcitol preserved expression of nephrin, podocin, and WT1; prevented proteinuria; and re

236 se proteins in the same protein complexes as nephrin, podocin, CD2AP, ZO-1, and Neph1 by cosedimentat

237 Expression of nephrin, podocin, desmin, and transient receptor potenti

238 ion prevented nephrin trafficking as well as nephrin-positive effect on insulin release.

239 ontained a high ratio of podocin-positive to nephrin-positive urinary EVs (podocin(+) EVs-to-nephrin(

240 t KLF4 expression reduced methylation at the nephrin promoter and the promoters of other epithelial m

241 Luciferase reporter assays of the proximal nephrin promoter fragment (-427 to +173) showed strong i

242 odocytes by acting on a VDRE in the proximal nephrin promoter.

243 phosphorylation of the transmembrane protein nephrin promotes recruitment of the Nck1/2 cytoskeletal

244 ,25(OH)(2)D(3) reversed high glucose-induced nephrin reduction in podocytes, and vitamin D analogs pr

245 Absence of the podocyte protein nephrin resulted in NF-kappaB activation, suggesting tha

246 its binding partner Lats1 to phosphorylated nephrin, resulting in decreased phospho-activation of La

247 els, zebrafish and mice, that the absence of nephrin results in poorly developed muscles and incomple

248 nephrin tyrosine phosphorylation and reduced nephrin signaling and cell surface expression in vitro I

249 xistence of a dynamic molecular link between nephrin signaling and the canonical Hippo pathway in pod

250 Nephrin signaling complex transduces extracellular cues

251 Nephrin signaling is important to reduce cell death indu

252 s demonstrate a crosstalk between Sema3a and nephrin signaling pathways that is functionally relevant

253 nce suggests a cross-talk between VEGF-A and nephrin signaling pathways.

254 K44A-Dynamin) in WT-Nephrin, 3YF-Nephrin, or Nephrin siRNA-transfected cells were utilized to study N

255 of podocytes, assessed by Wilms' tumor 1 and nephrin staining and urinary nephrin concentration, was

256 ion of cholesterol, blocked these effects on nephrin, suggesting that Notch promotes dynamin-dependen

257 CIN85/RukL deficiency preserved nephrin surface expression on the slit diaphragm and red

258 s were associated with altered expression of nephrin, synaptopodin, WT-1, and desmin, indicating that

259 ocyte injury and proteinuria, phosphorylated nephrin temporally colocalized with endocytic structures

260 d on podocytes results in down-modulation of nephrin that may affect kidney functionality in differen

261 form of CIN85 (RukL) is a binding partner of nephrin that mediates nephrin endocytosis via ubiquitina

262 d biological partners NCK and phosphorylated nephrin, the phase transition corresponds to a sharp inc

263 that Notch signaling induces endocytosis of nephrin, thereby triggering the onset of proteinuria.

264 Actin stabilization prevented nephrin trafficking as well as nephrin-positive effect o

265 g an association between Notch signaling and nephrin trafficking, electron microscopy revealed shorte

266 zation, slit diaphragm formation, and proper nephrin trafficking.

267 Confocal imaging of GFP-nephrin-transfected cells revealed nephrin endocytosis u

268 e imaging of green fluorescent protein (GFP)-nephrin-transfected cells was used to study nephrin endo

269 Nephrin transfection in MIN-6 cells/pseudoislets resulte

270 osphosignaling dynamics, leading to aberrant nephrin turnover and slit diaphragm disassembly.

271 ibutes to podocyte development by regulating nephrin turnover during junctional remodeling as the cel

272 osphotyrosine adaptor protein ShcA regulates nephrin turnover.

273 -to-phenylalanine mutation revealed that rat nephrin Tyr(1127) and Tyr(1152) are required to allow SH

274 zed knockin mice with mutations that disrupt nephrin tyrosine phosphorylation and Nck1/2 binding (nep

275 Overexpression of ShcA promoted nephrin tyrosine phosphorylation and reduced nephrin sig

276 Profiling of nephrin tyrosine phosphorylation dynamics in wild-type m

277 Moreover, reduced nephrin tyrosine phosphorylation has been observed in po

278 results define an essential requirement for nephrin tyrosine phosphorylation in stabilizing podocyte

279 We observed an increase in nephrin tyrosine phosphorylation in the presence of Shp2

280 expression of nephrin-CD16 and SHP-1 reduced nephrin tyrosine phosphorylation in transfected human em

281 Nephrin tyrosine phosphorylation is altered in human and

282 vivo is associated with a rapid reduction in nephrin tyrosine phosphorylation.

283 down, or targeted mutation of phosphorylated nephrin tyrosine residues 1176 and 1193 abrogated the ac

284 attenuated the promotion of HDAC4 signaling, nephrin ubiquitination, and urinary nephrin excretion as

285 Nephrin up-regulation likely accounts for part of the re

286 We propose that the nephrin-VEGFR2 complex acts as a key mediator to transdu

287 Furthermore, the nephrin-VEGFR2 complex involves Nck and actin.

288 We demonstrate that nephrin-VEGFR2 interaction is direct using mass spectrom

289 Nephrin-VEGFR2 interaction is modulated by tyrosine phos

290 ocytosis of the core slit diaphragm protein, nephrin, via a clathrin/beta-arrestin-dependent endocyti

291 Nephrin was found at the plasma membrane and on insulin

292 Expression of nephrin was reduced in CTGF +/+ animals; this reduction

293 This requires nephrin, which interacts with vesicle-associated membran

294 y promoting Fyn-dependent phosphorylation of nephrin, which may be important in the regulation of foo

295 We now reveal that Nck integrates nephrin with the Hippo kinase cascade through associatio

296 central role of the multifunctional protein nephrin within the macromolecular complex forming the gl

297 Maintenance of nephrin within this unique cell junction has been propos

298 Nephrin, WT1 and VEGFR2 were downregulated in Sema3a-ove

299 Homozygous nephrin(Y3F/Y3F) mice developed progressive proteinuria

300 Furthermore, compared with wild-type mice, nephrin(Y3F/Y3F) mice displayed delayed recovery in podo

301 tyrosine phosphorylation and Nck1/2 binding (nephrin(Y3F/Y3F) mice).