ライフサイエンスコーパス: villin

1 nd facilitated binding of the FERM domain to villin.

2 ntry in animal cells mediated by host factor villin.

3 rization and enhances actin cross-linking by villin.

4 A inhibits all actin regulatory functions of villin.

5 tes that overlap with actin-binding sites in villin.

6 canine kidney cells that ectopically express villin.

7 el conformation as well as actin bundling by villin.

8 in-severing and actin-bundling properties of villin.

9 sms involving Jak3 and its interactions with villin.

10 actin and is crucial for F-actin bundling by villin.

11 lation sites in the amino-terminal domain of villin.

12 idues in villin and map them to functions of villin.

13 rotein derived from the C-terminal domain of villin.

14 ypoxia increases the nuclear accumulation of villin.

15 ece domain that was originally identified in villin.

16 differentiation markers SI, Dpp4, Glut2, and villin.

17 al differentiation, such as KRT20, MUC2, and VILLIN.

18 f bundling proteins like fimbrins, LIMs, and villins.

19 We studied the actin-binding proteins villin 1 (VIL1) and gelsolin (GSN) in intestinal epithel

20 We measured the presence of villin 1 by immunohistochemistry on kidney sections and

21 nlike the levels of other markers, plasmatic villin 1 decreased already after a short (3 hours) treat

22 Villin 1 is released in plasma during AKI and shows pote

23 During AKI, plasmatic villin 1 levels corresponded with the severity of kidney

24 Villin 1 levels were compared with other renal injury ma

25 The presence of plasmatic villin 1 was confirmed in patients who experienced AKI a

26 Villin 1, a protein typically found in the brush borders

27 roteins, we selected periplakin, envoplakin, villin-1, and complement C3 and C9 for confirmation beca

28 nced stages of ADPKD had increased levels of villin-1, periplakin, and envoplakin.

29 is study, we examine the folding dynamics of villin (a small fast folding protein) with explicit solv

30 Villin accumulates in the nucleus during wound repair, a

31 Altering the nuclear localization of villin affects the expression and activity of Slug, a ke

32 s in a pattern similar to that of the marked villin allele.

33 Phi values for Villin also are obtained and left as predictions to be t

34 ther with biochemical analysis revealed that villin, an actin-modifying protein, is differentially up

35 Previously, we have shown that villin, an epithelial cell-specific actin-binding protei

36 We have previously reported that villin, an epithelial cell-specific actin-modifying prot

37 ulted in loss of tyrosine phosphorylation of villin and a significant decrease in wound repair of the

38 f this study underscores the role of nuclear villin and its binding partner ZBRK1 in the regulation o

39 carrying a cell-specific deletion of Nod2 in villin and Lyz2-expressing cells.

40 in Caco-2 cells, which endogenously express villin and Madin-Darby canine kidney cells that ectopica

41 nt all phosphorylatable tyrosine residues in villin and map them to functions of villin.

42 pression patterns of Sox2, CK4, Cdx2, GATA4, villin and Muc2 with human MLE.

43 erentiation markers (Cdx2, GATA4, HNF1alpha, villin and Muc2) in all cases.

44 inal alkaline phosphatase (IAP) activity and villin and p27(kip1) expression; knockdown of either NFA

45 to Fascin, as other actin-binding proteins, Villin and Profilin, do not exhibit the same subcellular

46 orylated Jak3 prevented Jak3 from binding to villin and that tyrosine autophosphorylation of Jak3 at

47 ignificant correlation between expression of villin and the homeobox transcription factor Cdx-1.

48 to determine expression of cleaved Notch-1, villin, and claudin 5 in colon samples from mice and hum

49 -) mice induced expression of cleaved Notch, villin, and claudin 5 in colonocytes and significantly r

50 in, redefines the actin-bundling function of villin, and provides a molecular mechanism for actin bun

51 Villins belong to the villin/gelsolin/fragmin superfamil

52 uglutide reduced the mean (SD) expression of villin by 29% (6%), Cdx2 by 31% (10%), DPP-4 by 15% (6%)

53 y stimulates the tyrosine phosphorylation of villin by c-Src kinase.

54 study we demonstrate for the first time that villin can bundle actin filaments using a single F-actin

55 the microvilli of the absorptive epithelium, villin can bundle F-actin and, at higher calcium concent

56 is study, we describe for the first time how villin can switch between these disparate functions to c

57 , we predict that VLN3 is a Ca(2+)-regulated villin capable of severing actin filaments and contribut

58 KO mice showed reduced expression of colonic villin, carbonic anhydrase, secretory mucin muc2, and in

59 ex vivo and examined FVB wild-type (WT) and villin-CD98 transgenic mice overexpressing human CD98 in

60 Using specific transgenic mice (villin-CD98, T cell SMAD7, villin-TLR4) or specific knoc

61 Villin-Cdx2 transgenic mice had complex phenotypes that

62 We established 4 different lines of villin-Cdx2 transgenic mice.

63 ormation in the context of attachment to the villin core remains unexplored.

64 ance of the carboxyl-terminal domains of the villin core.

65 sites in the carboxyl-terminal region of the villin core.

66 one) or genetic intervention (SOX9 flox/flox Villin cre+/- mice) significantly attenuated intestinal,

67 in IEC-specific CD73 knockout mice (CD73(f/f)Villin(Cre) ) revealed a nearly 10-fold increase in colo

68 luminal colonization by Salmonella, CD73(f/f)Villin(Cre) mice were protected against Salmonella colit

69 (LtrLys(Cre)-p38alpha(Delta/Delta) mice and Villin(Cre)-p38alpha(Delta/Delta) mice), as well as p38b

70 We found that small intestinal crypts of Villin(Cre);Dclk1(f/f) mice were hypoplastic and more ap

71 ically deleted Fbxw7 in the murine gut using Villin-Cre (Fbxw7(DeltaG)).

72 erated by breeding TLR4(loxp/loxp) mice with villin-cre and Ella-cre, respectively.

73 and growth of colorectal tumors was found in Villin-Cre Foxm1-/- mice compared with Foxm1 fl/fl mice

74 eling were determined in Rosa26-Foxm1b mice, Villin-Cre Foxm1-/-, mice and wild-type mice after 12 we

75 intestine-specific deletion of Insig1 using Villin-Cre in combination with a germ line deletion of I

76 Atg16l1(f/f) x Villin-cre mice also had fewer Paneth cells and abnormal

77 e defective immune responses, Atg16l1(f/f) x Villin-cre mice had increased inflammation and systemic

78 floxed Slc3a2 alleles and crossed them with Villin-Cre mice such that CD98 was downregulated only in

79 malian target of rapamycin (Mtor) (mTOR(f/f):Villin-cre mice) or Atg7 (Atg7(flox/flox); Villin-Cre).

80 helia of the small intestine and colon using Villin-Cre mice.

81 um of control mice but not in Atg16l1(f/f) x Villin-cre mice.

82 breeding a PGC1alpha(loxP/loxP) mouse with a villin-cre mouse.

83 e intestinal epithelium of Dicer1(loxP/loxP);Villin-Cre mutant mice is disorganized, with a decrease

84 onic epithelial cells using the gut-specific Villin-Cre recombinase transgene (Villin-Cre).

85 d from the intestines of mice using the flox-Villin-Cre system (SIRT1 iKO mice).

86 8N) allele, Rb(tm2brn) floxed alleles, and a villin-cre transgene (RBVCA).

87 nsgene, and VCMsh2(LoxP/LoxP) mice carried a Villin-Cre transgene.

88 n the proximal convoluted epithelium using a Villin-Cre transgene.

89 that harbored a conditional Sox9 gene and a Villin-Cre transgene.

90 Floxed-MOR mice were crossed to Villin-cre transgenic mice to selectively delete the MOR

91 In this study, Villin-Cre transgenic mice were crossed with Rb (flox/fl

92 tional Rb(tm2Brn) allele with a constitutive Villin-Cre transgenic mouse.

93 e of Math1 in RBP-Jkappa(Fl/Fl);Math1(Fl/Fl);Villin-Cre((ER-T2)) mice.

94 Villin-Cre(+);Klf4(fl/fl) and control mice were given dr

95 Villin-Cre(+);Klf4(fl/fl) have greater susceptibility to

96 s developed significantly more frequently in Villin-Cre(+);Klf4(fl/fl) mice than in control mice, at

97 Klf4 in villin-positive antral mucosa cells (Villin-Cre(+);Klf4(fl/fl) mice).

98 stric tumors developed in 29% of 80-week-old Villin-Cre(+);Klf4(fl/fl) mice, which were located exclu

99 essively in the antrum in 35- to 80-week-old Villin-Cre(+);Klf4(fl/fl) mice.

100 Atg16l1 in epithelial cells (Atg16l1(f/f) x Villin-cre) or CD11c(+) cells (Atg16l1(f/f) x CD11c-cre)

101 t-specific Villin-Cre recombinase transgene (Villin-Cre).

102 ):Villin-cre mice) or Atg7 (Atg7(flox/flox); Villin-Cre).

103 intestinal epithelium of the Cdc42flox/flox-villin-Cre+ and Cdc42flox/flox-Rosa26-CreER+ mice appear

104 epithelial cells by creating Cdc42flox/flox-villin-Cre+ and Cdc42flox/flox-Rosa26-CreER+ mice.

105 lly in the intestinal epithelium (SIRT1 iKO, villin-Cre+, Sirt1(flox/flox) mice) and control mice (vi

106 We used Villin-Cre, which deletes specifically in the intestinal

107 e+, Sirt1(flox/flox) mice) and control mice (villin-Cre-, Sirt1(flox/flox)) on a C57BL/6 background.

108 We producedLpcat3-Flox/villin-Cre-ER(T2)mice, which were treated with tamoxifen

109 e intestinal and colonic epithelium, through Villin-Cre-mediated recombination.

110 ted intestinal epithelial cells (IECs) using Villin-Cre.

111 lacking EGFR in intestinal epithelial cells (Villin-Cre; Egfr(f/f) and Villin-CreER(T2); Egfr(f/f) mi

112 estinal adenocarcinomas in the Apc(1638N/wt);Villin-Cre;Tgfbr2(E2flx/E2flx) mice (called Apc(1638N/wt

113 ull for Tgfbr2 in the intestinal epithelium, Villin-Cre;Tgfbr2(E2flx/E2flx) mice.

114 LSL-KrasG12D mice were crossed with Villin-Cre;Tgfbr2E2flx/E2flx mice, which do not express

115 Villin-CreER(T2) was activated in developed tumors by ad

116 epithelial cells (Villin-Cre; Egfr(f/f) and Villin-CreER(T2); Egfr(f/f) mice) or myeloid cells (LysM

117 onsists of the sixth gelsolin-like domain of villin (D6) and the headpiece (HP).

118 we employ a 208-residue modular fragment of villin, D6-HP, which consists of the sixth gelsolin-like

119 e report that the anti-apoptotic response of villin depends on activation of the pro-survival protein

120 Villin dimers were also identified in Caco-2 cells, whic

121 ithelial cell-specific actin-binding protein villin directly associates with phosphatidylinositol 4,5

122 In addition, we find that villin directly interacts with a transcriptional corepre

123 with commercially available mice expressing villin-driven cre-recombinase.

124 ivity, the microvillar actin-binding protein villin drives both apical microvilli disassembly in vitr

125 redundancy among the actin-bundling proteins villin, espin, and plastin-1 has prevented definitive co

126 These findings demonstrate that loss of villin expression due to Cdx-1 loss is a feature of poor

127 Investigation of 577 CRCs linked loss of villin expression to poorly differentiated histology in

128 Loss of villin expression was not due to coding sequence mutatio

129 y, Cdx-1 knockdown down-regulated endogenous villin expression, and deletion of a key Cdx-binding sit

130 illin promoter activity reflected endogenous villin expression, suggesting transcriptional control.

131 ed brush border microvilli with decreases in villin expression.

132 escence measurements typically used to study villin folding.

133 experiments to further probe the kinetics of villin folding.

134 he notion that a norleucine double mutant of villin folds five times faster than the wild-type sequen

135 This cleaved villin fragment severs actin in an unregulated fashion t

136 Furthermore, mislocalization of villin from the membrane was prognostic for poorer outco

137 ng of F-actin, emphasizing the importance of villin function in intestinal homeostasis.

138 etween Jak3 and cytoskeletal proteins of the villin/gelsolin family.

139 inant full-length (wt) Jak3 using Jak3-wt or villin/gelsolin-wt as substrate showed that Jak3 autopho

140 Villins belong to the villin/gelsolin/fragmin superfamily and comprise at leas

141 As the fastest folding protein, the villin headpiece (HP35) serves as an important bridge be

142 ate the interaction of a MoS2 nanosheet with Villin Headpiece (HP35), a model protein widely used in

143 luding the helical subdomain and full-length villin headpiece (HP36 and HP67).

144 The helical subdomain of the villin headpiece (HP36) is one of the smallest naturally

145 Villin headpiece (HP67) harbors a highly helical, thermo

146 The villin headpiece (HP67) is a 67 residue, monomeric prote

147 Villin headpiece (HP67) is a commonly used model system

148 the fast dynamics of two variants of chicken villin headpiece 35 (HP35).

149 al-time kinetics of the ultrafast folding of villin headpiece 35 and a stable asparagine 68 alanine/l

150 cho experiments performed on nitrile-labeled villin headpiece [HP35-(CN)(2)] is described.

151 An analysis of the villin headpiece and FiP35 WW domain detects multiple na

152 Here we use existing MSMs for the villin headpiece and NTL9, which were constructed from a

153 ensive molecular dynamics simulations of the villin headpiece crystal unit cell to examine its stabil

154 he transition and intermediate states of the villin headpiece domain, HP67, are characterized in vary

155 The 36 residue villin headpiece helical subdomain (HP36) is one of the

156 tor unfolding in a model peptide system, the villin headpiece HP35 fragment.

157 c network of the 35-residue-fragment (HP-35) villin headpiece in implicit water at room temperature.

158 Villin headpiece is a small autonomously folding protein

159 The helical subdomain of the villin headpiece is the smallest naturally occurring coo

160 We find that the wild-type villin headpiece reliably folds to a native conformation

161 ing protein yet discovered, a variant of the villin headpiece subdomain (HP-35 NleNle).

162 lding transitions of two small proteins, the villin headpiece subdomain (HP35) and the lysin motif (L

163 te highly accurate folding of the 35 residue villin headpiece subdomain (HP35) by all-atom molecular

164 investigate the structure of the 35-residue villin headpiece subdomain (HP35) in folded, partially d

165 he urea-induced unfolding transitions of the villin headpiece subdomain (HP35), a designed betabetaal

166 The villin headpiece subdomain (HP36) is the smallest natura

167 ckbone of the 36 residue, three-helix bundle villin headpiece subdomain (HP36).

168 resolution structures of two variants of the villin headpiece subdomain (VHP) that contain a pentaflu

169 ), for hydrophobic mutants of four proteins: villin headpiece subdomain (VHP) with 36 residues, a sur

170 and stability of the small and well-studied villin headpiece subdomain (VHP).

171 ndary structure derived from the hyperstable villin headpiece subdomain consisting of helices 2 and 3

172 ve suggested that the denatured state of the villin headpiece subdomain contains a residual helical s

173 inated phenylalanines were incorporated into villin headpiece subdomain HP35, and their energetic con

174 To explore the folding landscape of villin headpiece subdomain HP35, we conducted two sets o

175 er a wide range of temperatures, the chicken villin headpiece subdomain protein (HP36) was labeled at

176 hydrophobic core leucine residue in chicken villin headpiece subdomain protein at 140-4 K using deut

177 tion of three solvent-exposed lysines in the villin headpiece subdomain significantly stabilizes the

178 ns in partially folded states of the helical villin headpiece subdomain, in which chemical denaturati

179 amics simulations totaling >50 micros on the villin headpiece subdomain, one of the most stable and f

180 simulations of a fast-folding variant of the villin headpiece using four different force fields.

181 main (HP36) derived from the F-actin binding villin headpiece was designed by targeting surface elect

182 gineered 35-residue subdomain of the chicken villin headpiece, an ultrafast-folding protein.

183 ng simulations of four variants of the human villin headpiece, how simulations of spontaneous folding

184 The 36-residue helical subdomain of the villin headpiece, HP36, is one of the smallest cooperati

185 proteins, the B domain of protein A and the Villin headpiece.

186 g protein, the 35-residue subdomain from the villin headpiece.

187 ake as examples the 35-residue alpha-helical Villin HP35 and 37 residue beta-sheet Pin WW domains, wh

188 elial cell-specific hPepT1 overexpression in villin-hPepT1 transgenic mice increased the severity of

189 DSS-induced colitis in beta-actin-hPepT1 and villin-hPepT1 transgenic mice, indicating that commensal

190 -, beta-actin-hPepT1 transgenic/Nod2-/-, and villin-hPepT1 transgenic/Nod2-/- littermates had similar

191 presses IL-15Ralpha exclusively by the IECs (Villin/IL-15Ralpha Tg) was generated.

192 cimens confirmed the nuclear distribution of villin in a subset of tumors.

193 pithelial cell-specific cytoskeletal protein villin in an IL-2-dependent manner.

194 mice, we validate the physiological role of villin in apoptosis and cell extrusion from the gastroin

195 gated the role of the actin-bundling protein villin in Arabidopsis (Arabidopsis thaliana).

196 Modulation of villin in host cells also resulted in a discernible effe

197 the intestinal-specific cytoskeletal protein villin in MSI colon cancer, with complete absence in 62%

198 optotic function of villin, we overexpressed villin in the Madin-Darby canine kidney Tet-Off epitheli

199 dy reveals that the moonlighting function of villin in the nucleus may play an important role in tiss

200 t on the previously unrecognized function of villin in the regulation of apoptosis in the gastrointes

201 cancer metastases and invasion by regulating villin-induced cell migration and cell invasion.

202 es not regulate phosphorylation of villin or villin-induced cell migration and is, in fact, not expre

203 e carboxyl-terminal phosphorylation sites in villin-induced cell migration.

204 molecular basis for tyrosine-phosphorylated villin-induced changes in cell motility.

205 t time the absolute requirement for c-Src in villin-induced regulation of cell migration.

206 We found that villin influences actin dynamics and that this influence

207 l of the STOP cassette by Cre recombinase in villin(+) intestinal epithelial cells activates permanen

208 Villin is a major actin-bundling protein in the brush bo

209 Villin is a tissue-specific, actin-binding protein invol

210 Nuclear villin is also associated with mouse models of tumorigen

211 Conversely, villin is also linked with the loss of epithelial polari

212 Villin is an actin regulatory protein that is expressed

213 study we demonstrate for the first time that villin is an epithelial cell-specific anti-apoptotic pro

214 Villin is an F-actin regulating, modular protein with a

215 In this study we report that villin is cleaved in the intestinal mucosa to generate a

216 The expression of villin is highest in the apoptosis-resistant villus cell

217 e had shown that tyrosine phosphorylation of villin is important for cytoskeletal remodeling and cell

218 Our results show that villin is involved in the generation of thick actin fila

219 Thus, the headpiece domain of villin is structurally and functionally independent of t

220 ve identified a putative calcium-insensitive villin isoform through comparison of sequence alignments

221 Different combinations of villin isovariants are coexpressed in various tissues an

222 ectively, these results demonstrate that two villin isovariants have overlapping and distinct activit

223 Using villin knockout mice, we validate the physiological role

224 inal tumors derived from mice transgenic for villin-KRAS(V12G) and human primary colorectal cancers w

225 er actin cross-linking proteins that share a villin-like headpiece domain.

226 A marked allele of the endogenous mouse villin locus was used to visualize single beta-galactosi

227 expressing Cre recombinase, regulated by the villin or CD11c promoters, to generate mice that lacked

228 ase 3), does not regulate phosphorylation of villin or villin-induced cell migration and is, in fact,

229 Expression of cleaved Notch-1, villin, or claudin 5 was not detected in RAG1(-/-) colon

230 We created mice with disruption of Klf4 in villin-positive antral mucosa cells (Villin-Cre(+);Klf4(

231 Inactivation of Klf4 in villin-positive gastric progenitor cells induces transfo

232 Rare, villin-positive progenitor cells in the gastric antrum h

233 Absence of villin predisposes mice to dextran sodium sulfate-induce

234 intestinal epithelium, under the control of villin promoter (iVP16LXRalpha).

235 Rb rearrangement due to ectopic Villin promoter activity in neural crest or neural crest

236 Conversely, in transient transfection assays villin promoter activity reflected endogenous villin exp

237 Villin promoter activity was measured by a luciferase-ba

238 Cdx-1 overexpression induced villin promoter activity, Cdx-1 knockdown down-regulated

239 transgenic mice expressing KRAS(V12G) under villin promoter and in human colorectal cancers with mut

240 eletion of a key Cdx-binding site within the villin promoter attenuated promoter activity.

241 The Villin promoter in these animals is highly expressed in

242 Because the Villin promoter is highly active throughout the GI and i

243 In this study, the mouse villin promoter was used to drive Neurogenin 3 expressio

244 A 12.4-kb villin promoter/enhancer fragment drives several transge

245 xpression was regulated by the beta-actin or villin promoters; colitis was induced using 2,4,6-trinit

246 cell line to demonstrate that expression of villin protects cells from apoptosis by maintaining mito

247 Hu li tai shao (Hts-RC) and Villin (Quail), an actin bundler, localize to all early

248 s for the first time microvillus assembly by villin, redefines the actin-bundling function of villin,

249 e expression in transgenic mice expressing a villin-regulated Math1 transgene.

250 Tyrosine-phosphorylated villin regulates actin dynamics, cell morphology, and ce

251 Our study demonstrates that nuclear villin regulates epithelial-mesenchymal transition (EMT)

252 study also highlights the potential role of villin's pro-apoptotic function in the pathogenesis of i

253 ce resonance energy transfer, we demonstrate villin self-association in living cells in microvilli an

254 erization site was identified that regulated villin self-association in parallel conformation as well

255 pair of colonic mechanical injuries requires villin severing of F-actin, emphasizing the importance o

256 Thus, villin severs F-actin to ensure microvillus depolarizati

257 Using truncation mutants of villin, site-directed mutagenesis, and fluorescence reso

258 Both SPAK-transfected Caco2-BBE cells and villin-SPAK transgenic (TG) FVB/6 mice exhibited loss of

259 bset of cells exhibited mucin-2 or polarized villin staining.

260 ructure, and small size make this engineered villin subdomain an ideal system for simulation by atomi

261 e double-norleucine mutant of the 35-residue villin subdomain is the focus of recent computer simulat

262 ty dependence of the folding kinetics of the villin subdomain under conditions where the viscogen has

263 he unfolded population for a sequence of the villin subdomain with one amino acid difference from tha

264 this native-centric model for the benchmark villin subdomain, with only two adjustable thermodynamic

265 alyzed for an ultrafast folding protein--the villin subdomain.

266 n of the enterocytic differentiation markers villin, sucrase-isomaltase, glucose transporter 2 (GLUT2

267 t Jak3 interacted with actin-binding protein villin, thereby facilitating cytoskeletal remodeling and

268 ucosa-associated microbiota differed between villin-TLR4 and wild-type (WT) littermates.

269 ed the genotoxic agent azoxymethane (AOM) to villin-TLR4 and WT mice.

270 Our results revealed that villin-TLR4 mice are characterized by increases in the d

271 In addition, villin-TLR4 mice developed spontaneous duodenal dysplasi

272 Interestingly, WT mice cohoused with villin-TLR4 mice displayed greater susceptibility to acu

273 We found that villin-TLR4 mice showed an increased number of colonic t

274 function and microbiota by using transgenic villin-TLR4 mice that overexpress TLR4 in the intestinal

275 expresses TLR4 in the intestinal epithelium (villin-TLR4 mice).

276 transgenic mice (villin-CD98, T cell SMAD7, villin-TLR4) or specific knockout mice, investigators ha

277 phosphorylation site mutant, as well as the villin truncation mutant S1-S3, inhibited cell migration

278 hosphorylation of the well folded C-terminal villin-type headpiece confers affinity for its intrinsic

279 structure and (15)N-relaxation analysis of a villin-type headpiece domain natively devoid of F-actin

280 lexible region (V-loop) present in all other villin-type headpiece domains and which is essential to

281 Villin-type headpiece domains are approximately 70 resid

282 Villin-type headpiece domains are compact F-actin-bindin

283 Villin-type headpiece domains are compact motifs that ha

284 rface potential map of SVHP to that of other villin-type headpiece domains with significant affinity

285 main which confers actin-binding activity to villin-type headpiece domains, even though the residues

286 lution structural information exists for the villin-type headpiece F-actin complex, our results demon

287 n ionization time-of-flight, the majority of villin was identified as a monomer or dimer.

288 wild type or phosphorylation site mutants of villin, we demonstrate for the first time the absolute r

289 mechanisms of the anti-apoptotic function of villin, we overexpressed villin in the Madin-Darby canin

290 p4); glucose transporter type 2 (Glut2); and villin were measured by quantitative reverse transcripta

291 a molecular mechanism for actin bundling by villin, which could have wider implications for other ac

292 gest that in cells, selective interaction of villin with either PIP(2) or LPA could have dramatically

293 found to be critical for the interaction of villin with its ligand phospholipase C-gamma1 and for it

294 restingly, unlike PIP(2), the association of villin with LPA inhibits all actin regulatory functions

295 As a result, association of villin with PIP(2) inhibits actin depolymerization and e

296 alignments between human gelsolin and plant villins with x-ray crystallography data for vertebrate g

297 However, the SH2 domain of Jak3 prevented P-villin-wt from binding to the FERM domain of nonphosphor

298 Pairwise binding between Jak3 mutants and P-villin-wt showed that the FERM domain of Jak3 was suffic

299 d that phosphorylated (P) Jak3-wt binds to P-villin-wt with a dissociation constant (K(d)) of 23 nM a

300 main of Jak3 was sufficient for binding to P-villin-wt with a K(d) of 40.0 nM.