ライフサイエンスコーパス: NHERF

1 NHERF contains two amino-terminal PDZ (postsynaptic dens

2 NHERF contains two modular PDZ domains that are modular

3 NHERF directs polarized expression of receptors and ion

4 NHERF is an estrogen-responsive gene that encodes an inh

5 NHERF tumorigenic mutations decreased or abolished its i

6 NHERF was shown previously to be capable of enhancing th

7 NHERF-1 (Na(+)-H(+) exchanger regulatory factor 1, also

8 NHERF-1 null animals challenged with a low phosphate die

9 NHERF-1 null mice demonstrate increased urinary excretio

10 NHERF-1 participates in the inflammatory response that i

11 NHERF-1 reduced the diffusion of the beta(2)AR and the P

12 NHERF-1 reduced the rate of ligand-induced internalizati

13 NHERF-1(-/-) cells also do not adapt to alterations in t

14 NHERF-1(-/-) proximal tubule cells demonstrate defective

15 NHERF-2 immunostaining was associated mainly with the pl

16 NHERF-2 promoted migration and invasion of colon cancer

17 NHERFs were shown to interact directly with platelet-der

18 in Na(+)/H(+) exchanger regulatory factor 1 (NHERF) to assemble protein complexes of cystic fibrosis

19 th the Na+/H+ exchanger regulatory factor 1 (NHERF-1) by binding the first of two PDZ (psd95, discs-l

20 to Na(+)/H(+) exchanger regulatory factor 1 (NHERF-1), a PDZ protein that cross-links membrane protei

21 odium-hydrogen exchange regulatory factor 1 (NHERF-1/EBP50) interacts with the C terminus of several

22 , Na(+) /H(+) exchanger regulatory factor 1 (NHERF-1/EBP50).

23 dium-hydrogen exchanger regulatory factor-1 (NHERF-1) plays a key role in the regulation of renal pho

24 by the Na+/H+ exchanger regulatory factor-1 (NHERF-1), an adaptor protein containing two tandem PSD-9

25 dium-hydrogen exchanger regulatory factor-1 (NHERF-1)-null mice were resistant to the inhibitory effe

26 dium-hydrogen exchanger regulatory factor-1 (NHERF-1).

27 ydrogen exchanger regulatory factory type 1 (NHERF-1).

28 three PDZ adaptor proteins, namely NHERF-1, NHERF-2 and PDZK1, are expressed in the apical membrane,

29 The Na+/H+ exchanger regulatory factor 2 (NHERF-2) is a scaffold protein that regulates cellular s

30 nd the Na+/H+ exchanger regulatory factor 2 (NHERF-2), but the biological effects of these interactio

31 he Na(+)/H(+) exchanger regulatory factor 2 (NHERF-2).

32 he Na(+)/H(+) exchanger regulatory factor-2 (NHERF-2) is an integral component of almost all endothel

33 , so as to form a specific 2:1:1 (C-CFTR)(2).NHERF.ezrin ternary complex.

34 were increases in NaPi-2c/PDZK1 and NaPi-2a/NHERF-1 interactions.

35 in-radixin-moesin-binding phosphoprotein-50 (NHERF-1/EBP50) co-immunoprecipitated with the human kapp

36 al nervous system, but little is known about NHERF-2 localization in the brain.

37 sphoprotein, but how phosphorylation affects NHERF to assemble macromolecular complexes is unknown.

38 All NHERF proteins are involved in anchoring membrane protei

39 erize as the strongest interaction among all NHERF dimerizations.

40 ecause mutation of either removed nearly all NHERF binding.

41 1)R and NHERF-2 associate in cells, allowing NHERF-2-mediated tethering of P2Y(1)R to key downstream

42 Although NHERF dimerizations have been reported, results have bee

43 en exchanger regulatory factors (NHERF-1 and NHERF-2) are a family of adaptor proteins characterized

44 Expression of MAGI-3 and NHERF-2 in human colon tumor tissues was analyzed using

45 We investigated the roles of MAGI-3 and NHERF-2 in LPA(2)-mediated signaling in human colon canc

46 The effects of MAGI-3 and NHERF-2 in LPA-induced cell migration, invasion, inosito

47 MAGI-3 and NHERF-2 were expressed differentially in colon adenocarc

48 OKH cells and NHERF siRNA OK-WT showed decreased expression of NHERF-1

49 ysiological significance in HEK293 cells and NHERF-1 knock-out mice.

50 nously expressing the CRLR-RAMP3 complex and NHERF-1, the CRLR-RAMP complex desensitizes but is unabl

51 f the concentrated distribution of ezrin and NHERF in the apical membrane regions of epithelial cells

52 Here we examine the interaction of Mrp2 and NHERF-1 and its physiological significance in HEK293 cel

53 Furthermore, we found that P2Y(1)R and NHERF-2 associate in cells, allowing NHERF-2-mediated te

54 mutational analysis indicated that RAMP3 and NHERF-1 interact via a PDZ type I domain on NHERF-1.

55 imal tubule cells derived from wild-type and NHERF-1 knockout animals examines the regulation of NHE3

56 ons occurred at the conserved PDZ domains at NHERF NH2-terminus that bound to SYK, or at its COOH-ter

57 d-type (WT) mice, both sham-operated and BDL NHERF-1(-/-) mice have lower levels of activated ERM and

58 ntrations in serum and liver of sham and BDL NHERF-1(-/-) mice were not significantly different from

59 regulator of endothelial homeostasis because NHERF-2-silenced ECs proliferate at a much higher rate e

60 o the beta2AR tail or to sequences that bind NHERF/EBP50.

61 In contrast, mGluR1a was found to bind NHERF-2 in vitro with a weaker affinity than mGluR5, and

62 lasin D disrupts apical localization of both NHERF-1 and the PTH1R and inhibits the PTH-mediated incr

63 of the CRLR-RAMP complex was not affected by NHERF-1 when CRLR was co-expressed with RAMP1 or RAMP2.

64 The diffusion of the CaSR was unaffected by NHERF-1 or the addition of calcium.

65 These data indicate that, in normal cells, NHERF proteins recruit PTEN to PDGFR to restrict the act

66 Na+,K+-ATPase in wild-type OK (OK-WT) cells, NHERF-deficient OKH cells, OK-WT transfected with siRNA

67 ino-terminal PDZ domain to form a 1:1 C-CFTR.NHERF complex.

68 gen exchanger regulatory factor-1-deficient (NHERF-1(-/-)) mice demonstrate increases in the urinary

69 aggressiveness, indicating that deregulated NHERF signaling may be associated with disease progressi

70 absent in OKH cells and depends on a direct NHERF-1-PTH1R interaction in OKH-N1 cells.

71 d other activators of PKC and PKA dissociate NHERF-1/Npt2a complexes, as assayed using quantitative c

72 signaling pathway, in which two PDZ domains (NHERF-2 PDZ2-N2P2 and MAGI-3 PDZ6-M3P6) compete for a re

73 Individually, each NHERF protein has been shown to be involved in the regul

74 Yet, it is clear that each NHERF protein exhibits distinct properties, translating

75 o Chinese hamster ovary cells and endogenous NHERF-1/EBP50 in opossum kidney proximal tubule epitheli

76 bitors calyculin A and okadaic acid enhanced NHERF-1 phosphorylation and inhibited its dimerization.

77 to disruption of the formation of ICAM-1/ERM/NHERF-1 complex and reduction of hepatic ERM proteins an

78 TH-mediated increases of [Ca2+]i and express NHERF-1 at markedly lower levels.

79 s were observed only in cells that expressed NHERF-1, whereas the PTH1R was localized to bundles that

80 eins Na(+)/H(+) exchanger regulatory factor (NHERF) 1 and 2.

81 the Na(+)/H(+) exchanger regulatory factor (NHERF) as an important molecular component that stabiliz

82 The Na exchanger regulatory factor (NHERF) family of epithelial-enriched PDZ domain scaffold

83 inds Na(+)/H(+) exchanger regulatory factor (NHERF) family scaffolding proteins that are required for

84 Na(+)/H(+) exchanger regulatory factor (NHERF) homologous adaptors 1 and 2 are membrane-associat

85 Na(+)/H(+) exchanger regulatory factor (NHERF) is an adapter protein that is responsible for org

86 Na(+)/H(+) exchanger regulatory factor (NHERF) proteins are a family of PSD-95/Discs-large/ZO-1

87 the Na(+)/H(+) exchanger regulatory factor (NHERF), a protein shown to potentiate dimerization of th

88 udy, Na(+)/H(+) exchanger regulatory factor (NHERF)-1 loss-of-function and gain-of-function experimen

89 entified Na+/H+ exchanger regulatory factor (NHERF)-2 as a novel binding partner for the cadherin-ass

90 sodium hydrogen exchanger regulatory factor (NHERF-1) lacking the ezrin-binding domain blocks parathy

91 odium-hydrogen exchanger regulatory factors (NHERF-1 and NHERF-2) are a family of adaptor proteins ch

92 of Na(+)/H(+) exchanger regulatory factors (NHERFs) in regulating SR-BI expression, SR-BI-mediated s

93 proteins, including NHE3 regulatory factors (NHERFs), inositol trisphosphate (IP(3)) receptor-binding

94 llular models, indicate a novel function for NHERF-1 and RAMP3 in the internalization of the AM recep

95 ulations of neurons, were immunopositive for NHERF-2 throughout the mouse brain.

96 le cells indicate a specific requirement for NHERF-1 for cAMP-mediated phosphorylation and inhibition

97 se studies indicate a unique requirement for NHERF-1 in cAMP regulation of NHE3 and in the traffickin

98 ERF-2 in brain is consistent with a role for NHERF-2 in forming complexes between cell surface and cy

99 OKH cells, OK-WT transfected with siRNA for NHERF (NHERF siRNA OK-WT), and OKH cells that were stabl

100 ial affinity of the Na/P(i) transporters for NHERF-1 and PDZK1 proteins could partially explain their

101 Infection of proximal tubule cells from NHERF-1 null mice with adenovirus-green fluorescent prot

102 that the endothelial neoplasms derived from NHERF-2-silenced cells were much larger in volume than t

103 mal tubule cells from wild-type but not from NHERF-1 null mice.

104 onsequent dissociation of the PDGFRbeta from NHERF.

105 Infection with adenovirus-GFP-NHERF-1 containing a S77A or T95D mutation also increase

106 al tubule cells infected with adenovirus-GFP-NHERF-1 containing an S77A mutation showed significantly

107 l tubule cells with wild-type adenovirus-GFP-NHERF-1 increased basal phosphate transport and restored

108 g in cultured cells expressing wild type GFP-NHERF-1 to define the physiological importance of NHERF-

109 ith adenovirus expressing full-length WT GFP-NHERF-1 increased basal phosphate transport and restored

110 the proteins PSD-95, Syntenin, Erbin, GRIP, NHERF, Inad, Dishevelled, and Shank).

111 GST-hKOR C-tail, but not GST, bound HA-NHERF-1/EBP50 transfected into Chinese hamster ovary cel

112 y elevation in cGMP, is used to describe how NHERF family proteins are involved in NHE3 complex forma

113 However, NHERF-2 and MAGI-3 reciprocally regulated LPA(2)-induced

114 However, NHERF-2 immunoreactivity was also observed in associatio

115 In NHERF-1 null kidney tissue; however, dopamine failed to

116 In NHERF-1(-/-) mice, ERM proteins are significantly reduce

117 In NHERF-1(-/-) mouse liver, Mrp2 mRNA was unchanged but Mr

118 In NHERF-1-null proximal tubule cells, neither PTH nor dopa

119 ated gene transfer, expression of NHERF-1 in NHERF-1(-/-) proximal tubule cells restored the inhibito

120 (-16.6 +/- 8.1%) inhibited NHE3 activity in NHERF-1(-/-) cells.

121 Bile flow in NHERF-1(-/-) mice was reduced to approximately 70% (p <

122 Cyp3a11 messenger RNA levels were higher in NHERF-1(-/-) BDL mice.

123 disrupts the autoinhibition interactions in NHERF.

124 uric acid uptake was significantly lower in NHERF-1(-/-) cells compared with wild-type cells over a

125 ted by the phosphate content of the media in NHERF-1 null cells although low phosphate media up-regul

126 order membrane (BBM) expression of mURAT1 in NHERF-1(-/-) compared with wild-type control kidneys (P

127 uced apical membrane expression of mURAT1 in NHERF-1(-/-) kidneys and demonstrated mislocalization of

128 +,K+-ATPase alpha1 in OK-WT cells but not in NHERF-deficient cells.

129 subunit phosphorylation in OK-WT but not in NHERF-deficient cells.

130 and C-terminal domains contact each other in NHERF, but such intramolecular domain-domain interaction

131 es of protein interaction modules present in NHERF/EBP50 (Na+/H+ exchanger 3 regulatory factor/ezrin-

132 liminated PDZ1 phosphorylation and increased NHERF-1 localization at the cell periphery.

133 in opossum kidney cells, dopamine increased NHERF-1 phosphorylation at serine 77 of the PDZ I domain

134 The internal NHERF-binding region contains both putative Class I (-(5

135 everal interacting proteins, one of which is NHERF-1.

136 xin/moesin-binding phosphoprotein of 50 kDa (NHERF/EBP50) family proteins and non-PDZ binding to the

137 Infection with full-length NHERF-1 containing a T95A mutation, however, increased b

138 hat were stably transfected with full-length NHERF-1 or constructs with mutated PDZ domains.

139 cells that were transfected with full-length NHERF-1 or NHERF-1 with mutated PDZ 2 but not in OKH cel

140 mGluR5 robustly associated with full-length NHERF-2 in cells, as assessed by co-immunoprecipitation

141 Here we show that membrane-localized NHERF scaffold proteins provide a nexus for tightly cont

142 or PDZ1 and ERM-binding domain in localizing NHERF-1 at the cell surface.

143 hosphorylation played key role in modulating NHERF-1 association with plasma membrane targets and ide

144 d signaling through the scaffolding molecule NHERF.

145 Murine NHERF-1-/- renal proximal tubule cells infected with ade

146 Cells expressing a mutant NHERF that is unable to associate with beta-catenin had

147 l tubule, three PDZ adaptor proteins, namely NHERF-1, NHERF-2 and PDZK1, are expressed in the apical

148 lls, OK-WT transfected with siRNA for NHERF (NHERF siRNA OK-WT), and OKH cells that were stably trans

149 The NH(2)-terminal PDZ domain (PDZ 1) of NHERF specifically binds to an internal peptide motif lo

150 he phosphorylation of Thr(95) and Ser(77) of NHERF-1 in the hormonal regulation of renal phosphate tr

151 The ability of NHERF to interact dynamically with the PTHR and cognate

152 vation of adenylyl cyclase in the absence of NHERF to principally stimulation of phospholipase C when

153 Association of NHERF-1/EBP50 with hKOR C-tail enhanced oligomerization

154 o NHERF regulates the cooperative binding of NHERF to bring two cytoplasmic tails of CFTR into spatia

155 Our results also demonstrate binding of NHERF to RACK1 at the WD5 repeat, which is distinct from

156 he cytoskeleton primarily via the binding of NHERF-1.

157 Deletion of NHERF-1 in mice leads to disruption of the formation of

158 his, in turn, results in the dissociation of NHERF-1 from Npt2a and a decrease in phosphate transport

159 NHERF-1 PDZ I domain and the dissociation of NHERF-1/Npt2a complexes.

160 analysis of the subcellular distribution of NHERF-2 immunostaining in four brain structures, cerebra

161 ts demonstrate that the C-terminal domain of NHERF functions as an intramolecular switch that regulat

162 The first PDZ domain of NHERF is known to bind platelet-derived growth factor-re

163 n binding activates the second PDZ domain of NHERF to interact with the cytoplasmic tails of CFTR (C-

164 -339 and Ser-340 in the C-terminal domain of NHERF, but a serine 162 of PDZ2 is specifically protecte

165 Expression of the first PDZ domain of NHERF-1 acts as a dominant-negative interactor by blocki

166 , we have identified the first PDZ domain of NHERF-1 as an interaction partner for the PDZ-binding mo

167 Ser(77) in the first PDZ domain of NHERF-1 is a downstream target of both hormones.

168 rylation at serine 77 of the PDZ I domain of NHERF-1, a site previously shown to attenuate binding of

169 cond of two PSD-95/Dlg/ZO-1 (PDZ) domains of NHERF interacts with a PDZ-binding motif at the very car

170 ein-coupled receptors, the overall effect of NHERF is to enhance the fraction of receptors present at

171 Expression of NHERF slows the rate of EGF-induced receptor degradation

172 F siRNA OK-WT showed decreased expression of NHERF-1 but equivalent expression of ezrin and Na+,K+-AT

173 ovirus-mediated gene transfer, expression of NHERF-1 in NHERF-1(-/-) proximal tubule cells restored t

174 Stable expression of NHERF-1 in the OKH parent (OKH-N1) restores the PTH-medi

175 proteins, and the preferential expression of NHERF-2 in astrocytes suggests that this scaffold protei

176 onsistent, and the physiological function of NHERF dimerizations is still unknown.

177 The PDZ domain I, but not II, of NHERF-1/EBP50 was involved in the interaction.

178 -1 to define the physiological importance of NHERF-1 phosphorylation.

179 that parallel stress fibers independently of NHERF-1.

180 Infection of NHERF-1(-/-) cells with adenovirus-green fluorescence pr

181 Infection of NHERF-1-null proximal tubule cells with wild-type adenov

182 ements showed a much stronger interaction of NHERF-1 with NaPi-2a than with NaPi-2c.

183 n functional experiments, the interaction of NHERF-2 with mGluR5 in cells was found to prolong mGluR5

184 lotting confirm the specific interactions of NHERF with the full-length CFTR and with ezrin in vivo.

185 of OK cells expressing a much lower level of NHERF-1/EBP50, U50,488H had no effect on Na(+)/H(+) exch

186 The subcellular localization of NHERF-2 in brain is consistent with a role for NHERF-2 i

187 alized at the apical/canalicular membrane of NHERF-1(-/-) mouse hepatocytes, although its immunofluor

188 terminal serines abolished the modulation of NHERF-1 dimerization by phosphatase inhibitors and ident

189 expression of a dominant negative mutant of NHERF enhances EGF-induced receptor down-regulation.

190 NHERF-1/EBP50 facilitates oligomerization of NHERF-1/EBP50, leading to stimulation of NHE3.

191 with hKOR C-tail enhanced oligomerization of NHERF-1/EBP50.

192 how that the hyperproliferation phenotype of NHERF-2-silenced EC is because of an accelerated cell cy

193 However, in the presence of NHERF-1, although the AM receptor (CRLR/RAMP3) undergoes

194 for the NHERF PDZ domains, the regulation of NHERF by ezrin may be employed as a general mechanism to

195 3 by PTH and indicate that reintroduction of NHERF-1 repairs this defect.

196 een made in our understanding of the role of NHERF proteins in regulation of intestinal Na+ absorptio

197 We examined the role of NHERF-1 and the cytoskeleton on the distribution, dynami

198 However the role of NHERF-1 in the expression and functional regulation of M

199 Further study of the role of NHERF-1 in the inflammatory response in cholestasis and

200 These studies examine the role of NHERF-1 in the tubular reabsorption of uric acid and reg

201 sphorylation-mimicking mutant S339D/S340D of NHERF has increased affinity and stoichiometry when bind

202 nant polypeptides representing PDZ I, S77 of NHERF-1 is phosphorylated by PKC but not PKA.

203 PDZ2, and thus controls the stoichiometry of NHERF to assemble protein complexes.

204 The carboxyl terminus of NHERF interacts with the FERM domain (a domain shared by

205 Stable transfection of NHERF-1/EBP50 into OKH cells restored the stimulatory ef

206 of the ezrin/radixin/moesin (ERM) domain on NHERF-1 indicated that NHERF-1 inhibits CRLR/RAMP3 compl

207 NHERF-1 interact via a PDZ type I domain on NHERF-1.

208 were transfected with full-length NHERF-1 or NHERF-1 with mutated PDZ 2 but not in OKH cells that wer

209 cells knocked down for either N-cadherin or NHERF had impaired ability to migrate into the wounded a

210 we knocked-down expression of N-cadherin or NHERF.

211 ceptor, which does not bind either to NSF or NHERF/EBP50 and interacts selectively with a distinct gr

212 Knock-down of either RAMP3 or NHERF-1 by RNA interference technology enabled agonist-i

213 cells, GRK2 overexpression reduced PDGFRbeta/NHERF association by 60%.

214 From a morphological perspective, NHERF-1 and the PTH1R co-localize to apical patches of O

215 est a novel role for the PDZ adapter protein NHERF-1 in coordinating dopamine signals that inhibit re

216 processes that involve the scaffold protein NHERF-1.

217 is coassociated with the scaffolding protein NHERF-1 and PLCbeta2 in microvilli.

218 actions with the cytoplasmic sorting protein NHERF-1 (Na(+)/H(+) exchange regulatory factor-1) and N-

219 s with adenovirus-green fluorescence protein-NHERF-1 resulted in significantly higher rates of uric a

220 ce with adenovirus-green fluorescent protein-NHERF-1 restored the ability of dopamine to stimulate cA

221 )/H(+) exchanger regulatory factor proteins (NHERFs) (NHERF1, NHERF2, PDZ domain-containing kidney pr

222 assembly of a ternary complex between PTEN, NHERFs and PDGFR.

223 e (GST)-hKOR C-tail interacted with purified NHERF-1/EBP50, whereas GST or GST-C-tails of micro or de

224 signaling, whereas disruption of the P2Y(1)R-NHERF-2 interaction by point mutations attenuates the du

225 of the assembly and disassembly of receptor/NHERF complexes.

226 nhances recycling of internalized receptors, NHERF stabilizes EGFR at the cell surface and slows the

227 gment within Naked2; residues 1-173 redirect NHERF-1 from the apical cytoplasm to the basolateral mem

228 In contrast, S77D reduced NHERF-1 colocalization with cortical actin cytoskeleton.

229 n with the second PDZ domain of the scaffold NHERF-2 (Na(+)/H(+) exchanger regulatory factor type 2).

230 These findings demonstrate that NHERF interactions regulate PTHR signaling at the level

231 These results demonstrate that NHERF-1 is necessary for PTH-mediated inhibition of Na+,

232 Together, these studies establish that NHERF-1 plays a key role in dopamine signaling and is al

233 noprecipitation experiments established that NHERF-1 associated with D1-like receptors.

234 Here, we found that NHERF-2, is a key regulator of endothelial homeostasis b

235 These findings indicate that NHERF-1 exerts a significant effect on the renal tubular

236 oesin (ERM) domain on NHERF-1 indicated that NHERF-1 inhibits CRLR/RAMP3 complex internalization by t

237 These observations reveal that NHERF-2 can selectively modulate mGluR5 signaling, which

238 These findings reveal that NHERF-2 is a key regulator of the cellular activity of P

239 mmunohistochemical experiments revealed that NHERF-2 and mGluR5 exhibit overlapping patterns of expre

240 We show that NHERF proteins are direct regulators of ion channel acti

241 Here we show that NHERF-1 assembles ERM proteins, ICAM-1 and F-actin into

242 striatum, and cerebellar cortex, showed that NHERF-2 was expressed mainly in astrocytic processes but

243 Previous studies have shown that NHERF is a phosphoprotein, but how phosphorylation affec

244 These findings strongly suggest that NHERF-1 binds to Mrp2, and plays a critical role in the

245 th SYK promoter methylation, suggesting that NHERF and SYK may transduce a common suppressive signal.

246 The NHERF proteins are highly expressed in the kidney, small

247 The NHERF proteins toggle PTHR signaling from predominantly

248 Primary breast tumors with LOH at the NHERF locus had clinical presentations of higher aggress

249 revealed important associations between the NHERF proteins and several G protein-coupled receptors s

250 nding to the multi-PDZ domain containing the NHERF family.

251 lls and the diverse binding partners for the NHERF PDZ domains, the regulation of NHERF by ezrin may

252 n, but one of the candidates involved is the NHERF family of scaffolding PDZ proteins.

253 er full-length PC or a PC mutant lacking the NHERF binding site was established.

254 a+-H+ exchanger NHE3 binds to members of the NHERF (Na+-H+ exchanger regulatory factor) family.

255 To further evaluate the specificity of the NHERF family in calcium regulation of NHE3 activity, the

256 Specificity for only one member of the NHERF family in one example of NHE3 regulation, inhibiti

257 ely the role of NHERF4 in the context of the NHERF family.

258 We found intragenic mutation of the NHERF gene accompanied by loss of heterzygosity (LOH) in

259 enetically related to the PDZ domains of the NHERF proteins.

260 sport involves phosphorylation of S77 of the NHERF-1 PDZ I domain and the dissociation of NHERF-1/Npt

261 Actin is also an integral component of the NHERF-1-assembled complex because cytochalasin D disrupt

262 ncluding calcineurin homologous protein, the NHERF family and SNX27 (related PDZ domains).

263 The hypothesis that the NHERF-1 PDZ domains contribute to PTH regulation of Na+,

264 NHERF1, NHERF2, and NHERF3 belong to the NHERF (Na(+)/H(+) exchanger regulatory factor) family of

265 ally stimulation of phospholipase C when the NHERF proteins are expressed.

266 The NHERFs bind both to an internal region (amino acids 586-

267 The NHERFs exhibit some overlap in tissue distribution and b

268 to study close association of NHE3 and these NHERFs and fluorescence recovery after photobleaching to

269 tions and heterodimerizations of these three NHERF proteins by pulldown and co-immunoprecipitation as

270 PC activates RhoA through NHERF and ezrin, leading to redistribution of actin fila

271 Thus, NHERF-1 assembles a signaling complex in the apical doma

272 Thus, NHERF-1/EBP50 binds directly to KOR, and this associatio

273 Thus, NHERF-2 is a negative regulator of endothelial prolifera

274 In conclusion, NHE3 binds to NHERF proteins via both an internal Class II PBM and C-t

275 that only the Class II motif contributes to NHERF binding.

276 that binding of the FERM domain of ezrin to NHERF regulates the cooperative binding of NHERF to brin

277 We hypothesize that binding of the KOR to NHERF-1/EBP50 facilitates oligomerization of NHERF-1/EBP

278 er-based kinase activity reporter for PKD to NHERF scaffolds reveals a unique signature of PKD activa

279 compared with cells infected with wild-type NHERF-1.

280 n CFTR-null mice, PLCbeta2 was undetectable, NHERF-1 mislocalized, and IP3 R3 more intensely stained,

281 Studies using NHERF-1 null mice have begun to provide insights into th

282 contrast to beta-adrenergic receptors where NHERF enhances recycling of internalized receptors, NHER

283 teraction of LPA(2) with Galpha(12), whereas NHERF-2 preferentially promoted interaction between LPA(

284 (PDZ)-scaffolding proteins, three of which (NHERFs 1-3) are localized to the brush border in kidney

285 re mGluR1a did not detectably associate with NHERF-2 in a cellular context.

286 in-coupled receptor through association with NHERF-1/EBP-50 stimulates NHE3.

287 Transfection of OKH cells with NHERF constructs that contained an intact PDZ1 domain re

288 in wild-type cells (41 +/- 2%) compared with NHERF-1(-/-) cells (8.2 +/- 3%).

289 MAGI-3 competed with NHERF-2 for binding to LPA(2) and phospholipase C-beta3.

290 catenin and N-cadherin are in a complex with NHERF and PDGF-Rbeta at membrane ruffles in the highly i

291 Several proteins known to interact with NHERF-2 are abundantly expressed in the central nervous

292 tin and PLCbeta1 and -beta3 co-localize with NHERF-1 and the PTH1R in OKH-N1 cell apical patches.

293 death, whereas coexpression of mGluR1a with NHERF-2 had no evident effects on mGluR1a functional act

294 transient association of PKD1 and PKD2 with NHERF-1 in live cells that is triggered by phorbol ester

295 Mrp2 co-precipitated with NHERF-1 in co-transfected HEK293 cells, an interaction t

296 , we found that coexpression of P2Y(1)R with NHERF-2 in glial cells prolongs P2Y(1)R-mediated Ca(2+)

297 eta), and the interaction of PDGF-Rbeta with NHERF leads to enhanced cell spreading and motility.

298 Transfection with NHERF expressing both mutated PDZ domains resulted in di

299 in interactions of Na/P(i) transporters with NHERF-1 and PDZK1 by FRET.

300 The screening yielded NHERF (Na+/H+ exchanger regulatory factor, also known as