ライフサイエンスコーパス: villin

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

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

3 nd facilitated binding of the FERM domain to villin.

4 rization and enhances actin cross-linking by villin.

5 A inhibits all actin regulatory functions of villin.

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

7 canine kidney cells that ectopically express villin.

8 el conformation as well as actin bundling by villin.

9 ntry in animal cells mediated by host factor villin.

10 ypoxia increases the nuclear accumulation of villin.

11 ece domain that was originally identified in villin.

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

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

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

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

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

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

18 Villin 1 levels were compared with other renal injury ma

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

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

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

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

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

24 development of cysts that were positive for Villin, a proximal tubular cell marker.

25 Villin accumulates in the nucleus during wound repair, a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

45 Villins belong to the villin/gelsolin/fragmin superfamil

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

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

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

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

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

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

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

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

54 Villin-Cdx2 transgenic mice had complex phenotypes that

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

56 Villin Cld-1 mice are used to carryout overexpressed stu

57 homeostasis accompanied the increased CAC in Villin-Cld-1-Tg mice.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 8N) allele, Rb(tm2brn) floxed alleles, and a villin-cre transgene (RBVCA).

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

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

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

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

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

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

85 rized a conditional knockout Prss8(fl/fl), p-Villin-Cre(+) mouse model.

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

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

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

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

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

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

92 Mice transgenic with only Cre alleles (Villin-Cre(ERT2), Lgr5-EGFP-IRES-Cre(ERT2), Hnf4alpha(+/

93 e conditional knockdown (KD) of Dsc2 in IEC (Villin-Cre(ERT2); Dsc2 (fl/fl)) exhibited impaired mucos

94 We performed studies with Villin-Cre(ERT2);Lgr5-EGFP-IRES-Cre(ERT2);Hnf4alpha(f/f)

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

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

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

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

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

100 Third, when Xist is deleted in gut using Villin-Cre, female mice remain healthy despite significa

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

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

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

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

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

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

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

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

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

110 estigate this possibility, here we generated Villin CreERT2:Igf2bp1flox/flox mice, which enabled indu

111 stine epithelial renewal was verified with a Villin-CreERT2 mouse model.

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

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

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

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

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

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

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

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

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

121 Lineage-tracing experiments identified villin-expressing gastric progenitor cells (VGPCs) as th

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

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

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

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

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

127 ed brush border microvilli with decreases in villin expression.

128 escence measurements typically used to study villin folding.

129 experiments to further probe the kinetics of villin folding.

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

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

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

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

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

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

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

137 ein, advillin which shares 75% homology with villin, has a tuft cell restricted expression in the gas

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

153 Villin headpiece is a small autonomously folding protein

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

155 We used this existing villin headpiece nuclear magnetic resonance data and per

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

173 at combines the available structural data on villin headpiece with functional assays to identify the

174 ns third IgG-binding domain of protein G and villin headpiece, diffuse not as isolated particles, but

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

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

177 three-dimensional structure of the isolated villin headpiece, including a description of the actin-b

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

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

180 The villin "headpiece" domain and the actin-binding residues

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

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

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

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

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

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

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

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

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

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

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

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

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

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

195 widespread agreement about the expression of villin in tuft cells there are several disagreements rel

196 A, 2020See also the commentary by Truong and Villines in this issue.

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

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

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

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

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

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

203 Villin is a major actin-bundling protein that assembles

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

205 Nuclear villin is also associated with mouse models of tumorigen

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

207 Villin is an actin regulatory protein that is expressed

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

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

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

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

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

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

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

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

216 Using villin knockout mice, we validate the physiological role

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

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

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

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

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

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

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

224 Villin-positive epithelial cells are a small population

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

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

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

228 e intestinal epithelium under control of the villin promoter (IDO1-TG).

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

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

231 Villin promoter activity was measured by a luciferase-ba

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

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

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

235 1) is used as a marker of tuft cells and the villin promoter is frequently used to drive expression o

236 We expressed PPARD from a villin promoter to investigate the role of these cells a

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

238 ss the Ppard (PPARD1 and PPARD2 mice) from a villin promoter, and mice that did not carry this transg

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

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

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

242 actin-bundling site in the full-length (FL) villin protein remains unidentified.

243 testinal tuft cells, in fact, do not express villin protein.

244 identify the actin-bundling site in FL human villin protein.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

262 to identify the actin-binding residues in FL villin that regulate its filament-bundling activity.

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

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

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

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

267 active form of TLR4, their littermates, and villin-TLR4 mice backcrossed to DUOXA-knockout mice.

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

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

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

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

272 ucosa-associated microbiota transferred from villin-TLR4 mice to wild-type germ-free mice caused incr

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

274 Colorectal cancer models were carried out in villin-TLR4 mice, carrying a constitutively active form

275 lial H(2)O(2) was significantly increased in villin-TLR4 mice; TLR4-dependent tumorigenesis required

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

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

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

279 cance in the over 30 proteins that contain a villin-type headpiece domain.

280 other actin-bundling proteins that contain a villin-type headpiece domain.

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

282 Villin-type headpiece domains are approximately 70 resid

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

284 Villin-type headpiece domains are compact motifs that ha

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

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

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

288 The actin-binding protein villin (Vil1) is used as a marker of tuft cells and the

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

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

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

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

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

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

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

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

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.