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

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

5 se Shp2 to be associated with phosphorylated nephrin.

6 n RGDfv blocked suPAR-induced suppression of nephrin.

7 it interacts with the slit diaphragm protein nephrin.

8 red phosphorylation of transmembrane protein nephrin.

9 afficking of Sns, the Drosophila ortholog of nephrin.

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

11 rier and required for the proper function of nephrin.

12 ical Notch signaling, prevented this loss of nephrin.

13 several phosphorylated tyrosine residues on nephrin.

14 n cytoskeleton via the transmembrane protein nephrin.

15 < 0.05), and reduced expression of podocyte nephrin (-29%, p < 0.01).

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

17 Nephrin, a critical podocyte membrane component that is

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

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

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

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

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

23 retion associated with diabetes and restored nephrin acetylation.

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

25 Nephrin activation induced cofilin dephosphorylation via

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

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

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

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

30 erized by a podocytopathy with mistrafficked nephrin, an essential component of the slit diaphragm.

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

32 glomerular capillary knot, dysregulation of nephrin and collagen IV, and ultrastructural changes in

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

34 Nephrin and IgG levels were significantly higher in pati

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

51 express the foot process junctional markers 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 so interacts with the slit diaphragm protein nephrin, and colocalizes with it in immortalized cell li

68 n of adherens complex's constituents (CD2AP, nephrin, and dendrin).

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

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

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

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

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

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

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

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

77 With Nephrin attached to the bilayer, multivalent interaction

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

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

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

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

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

83 Our findings suggest that Nephrin can mediate a signaling pathway that results 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 had lower affinity for endogenous RAB11 and nephrin compared with wild-type Tbc1d8b protein.

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 proteinuria than with mild proteinuria, and nephrin correlated strongly with biomarkers of glomerula

92 This interaction occurs through VEGFR2 and nephrin cytoplasmic domains.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

114 nuria (e.g. immunoglobulin G [IgG]), urinary nephrin excretion (podocyte injury) and serum levels of

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 glomerulopathies also feature alterations in Nephrin expression and function.

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

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

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

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

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

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

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

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

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

128 IL-1beta/IL-1R1 signaling loop that reduces nephrin expression, causing actin cytoskeleton rearrange

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

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

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

132 n-regulation of miR193a, but upregulation of nephrin expression.

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

134 the gene encoding the slit diaphragm protein Nephrin fail to develop functional slit diaphragms and d

135 rts dynein-mediated postendocytic sorting of nephrin from recycling endosomes to lysosomes for degrad

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

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

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

139 Nephrin gene silencing abolished the positive effects of

140 suPAR correlated significantly with urinary nephrin, IgG and albumin levels, suggesting suPAR as a p

141 ients showed significantly increased urinary nephrin, IgG and serum suPAR concentrations compared to

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

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

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

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

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

147 trate altered dynein-mediated trafficking of nephrin in INF2 associated podocytopathy.

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

149 at dysregulated dynein-mediated transport of nephrin in R218Q knockin podocytes opens an avenue for d

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

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

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

153 Membrane association of nephrin increased the cluster size distribution in a den

154 ROBO2 is expressed in podocytes, inhibits nephrin-induced actin polymerization, down-regulates non

155 This Nephrin-induced cofilin activation required a direct int

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

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

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

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

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

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

162 Nephrin is a key structural component of the podocyte sl

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

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

165 Because nephrin is important to glomerular permselectivity, we n

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

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

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

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

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

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

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

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

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

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

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

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

178 luorescence analysis revealed that Neph1 and Nephrin, major slit diaphragm constituents, were misloca

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

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

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

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

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

184 RC1 activation), high urinary pellet podocin:nephrin mRNA ratio and accelerated podocyte detachment (

185 Podocyte stress (Urinary pellet podocin:nephrin mRNA ratio), podocyte detachment (Urinary pellet

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

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

188 hat this increase occurs because LLPS of the Nephrin-Nck-N-WASP signaling pathway on lipid bilayers i

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

190 We demonstrate that proteins in the nephrin/Nck/N-WASP actin-regulatory pathway cluster into

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

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

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

194 pression decreased in AMR, as did glomerular nephrin (NPHS1) and receptor-type tyrosine-phosphatase O

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

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

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

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

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

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

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

202 ragm-like filtration barrier and express the Nephrin ortholog Sticks and stones (Sns).

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

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

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

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

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

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

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

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

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

212 Nephrin phosphorylation induces larger clusters at the c

213 Nephrin phosphorylation is a proximal event that occurs

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

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

216 Pharmacological modulation of Nephrin phosphorylation may thus facilitate pancreatic b

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

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

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

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

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

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

223 prevented high glucose-induced reduction of nephrin phosphorylation.

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

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

226 Nephrin plays a key role in maintaining the structure of

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

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

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

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

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

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

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

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

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

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

237 We also found that activated Nephrin recruited phosphorylated C3G and resulted in act

238 ,25(OH)(2)D(3) reversed high glucose-induced nephrin reduction in podocytes, and vitamin D analogs pr

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

240 To investigate Nephrin's role in transmitting signals to the Integrin r

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

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

243 exocyst-based mechanisms regulate Neph1 and Nephrin signaling and trafficking, and thus podocyte dev

244 Nephrin signaling complex transduces extracellular cues

245 Nephrin signaling is important to reduce cell death indu

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

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

248 Nephrin signals from the podocyte slit diaphragm to the

249 t TG, cause a reduction in the expression of nephrin, significant podocyte actin cytoskeleton, and mo

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

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

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

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

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

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

256 e a fine-tuned affinity balance of CD2AP and nephrin that is influenced by receptor tyrosine kinase s

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

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

259 ternary system modeled after membrane-bound nephrin, the adaptor Nck1, and the actin nucleation prom

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

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

262 We found that the binding affinity of nephrin to CD2AP is significantly enhanced in the absenc

263 tions enhance dynein-mediated trafficking of nephrin to proteolytic pathways, diminishing its recycli

264 lex that connects the slit diaphragm protein nephrin to the cytoskeleton of the cell.

265 dings suggest that RAB11-dependent vesicular nephrin trafficking plays a role in the pathogenesis of

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

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

268 activates the Wnt pathway and stabilizes the nephrin transcriptional repressor SNAIL.

269 ion of focal adhesions, we hypothesized that Nephrin transmits signals to the Integrin receptor compl

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 nein-mediated trafficking and degradation of nephrin underlies puromycin aminoglycoside-induced podoc

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

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

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

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

290 Nephrin-VEGFR2 interaction is modulated by tyrosine phos

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

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 Homozygous nephrin(Y3F/Y3F) mice developed progressive proteinuria

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

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