ライフサイエンスコーパス: Aldrich

1 Analysis with the Horrigan, Cui, and Aldrich model indicated a decreased coupling between vol

2 nee River natural organic matter (SRNOM) and Aldrich humic acid (ALHA), in the dark ambient condition

3 t organic carbon and water (KOC) and between Aldrich humic acid dissolved organic carbon and water (K

4 (o)Cl) is a bench-stable, commercial entity (Aldrich, catalogue number L510092) that is facile to ins

5 ate), soon to be commercially available from Aldrich, can be prepared in two steps using an abundant

6 The Horrigan-Aldrich model suggests that GoSlo-SR-5-6 works by stabil

7 at soil, an OM-poor clay soil, a hydrophilic Aldrich humic acid salt, and water-insoluble leonardite.

8 yzed four conformational ensembles of neural Aldrich syndrome protein verprolin homology domain, two

9 ered verprolin homology domain of the neural Aldrich syndrome protein involved in the regulation of a

10 C-18, 30x4.6mm, particle size 2.7mum (Sigma Aldrich), the separation and determination of beta-carot

11 Cl was replaced by LiBr.H(2)O (99.95%; Sigma-Aldrich) and LiCl (99.95%; Sigma-Aldrich)" should read "

12 Cl was replaced by LiBr.H(2)O (99.95%; Sigma-Aldrich) and LiCl.H(2)O (99.95%; Sigma-Aldrich)".

13 .95%; Sigma-Aldrich) and LiCl (99.95%; Sigma-Aldrich)" should read "anhydrous LiBr/LiCl was replaced

14 Sigma-Aldrich) and LiCl.H(2)O (99.95%; Sigma-Aldrich)".

15 B lots relative to those for Oxoid and Sigma-Aldrich broth.

16 standards of NIST SRM3150, SCP Si, and Sigma-Aldrich Si.

17 cturers (Becton, Dickinson; Oxoid; and Sigma-Aldrich) were utilized.

18 e Cell Whole Genome Amplification Kit, Sigma-Aldrich, UK) and detailed analysis of genomic copy numbe

19 ing this assay, we screened the LOPAC (Sigma-Aldrich) Library of Pharmacologically Active Compounds a

20 n reaction with reduced and nonreduced Sigma-Aldrich humic acid (HA), at pH 6 under anoxic conditions

21 n BCF studies and differing from sorption to Aldrich-humic acid (AHA) utilized as reference sorbent.

22 Wiscott Aldrich Syndrome protein (WASP) deficiency results in de

23 change in the TCR that recruits Nck/Wiscott Aldrich Syndrome (WASp)/SLP76/F-actin/CD4 to TCR.

24 IS reformation is driven by the Wiscott Aldrich Syndrome protein (WASp).

25 on is mediated by phosphatidic acid, Wiscott-Aldrich Syndrome protein, growth receptor-bound protein

26 correlated to the phosphorylation of Wiscott-Aldrich syndrome protein (WASP) by studies in multiple c

27 Wiskott Aldrich syndrome (WAS) is caused by mutations in the WAS

28 Wiskott Aldrich syndrome (WAS), an X-linked immunodeficiency, re

29 we investigated the role of neuronal Wiskott Aldrich syndrome protein (N-WASP) in modulating P aerugi

30 levels of F-actin and phosphorylated Wiskott Aldrich syndrome protein, an actin nucleation promoting

31 The actin cytoskeletal regulator Wiskott Aldrich syndrome protein (WASp) has been implicated in m

32 ucleating machine activated by WASp (Wiskott Aldrich syndrome protein).

33 Wiskott-Aldrich Syndrome (WAS) family proteins are Arp2/3 activa

34 Wiskott-Aldrich syndrome (WAS) is a primary immunodeficiency ass

35 Wiskott-Aldrich syndrome (WAS) is a primary immunodeficiency tha

36 Wiskott-Aldrich syndrome (WAS) is a rare X-linked primary immuno

37 Wiskott-Aldrich syndrome (WAS) is a severe X-linked immunodefici

38 Wiskott-Aldrich syndrome (WAS) is an inherited immunodeficiency

39 Wiskott-Aldrich syndrome (WAS) is an X-linked disease caused by

40 Wiskott-Aldrich syndrome (WAS) is an X-linked immunodeficiency c

41 Wiskott-Aldrich syndrome (WAS) is an X-linked immunodeficiency d

42 Wiskott-Aldrich syndrome (WAS) is an X-linked primary immune def

43 Wiskott-Aldrich syndrome (WAS) is an X-linked primary immunodefi

44 Wiskott-Aldrich syndrome (WAS) is associated with mutations in t

45 Wiskott-Aldrich syndrome (WAS) is caused by loss-of-function mut

46 Wiskott-Aldrich syndrome (WAS) is caused by mutations in the WAS

47 Wiskott-Aldrich syndrome (WAS) patients have loss-of-function mu

48 Wiskott-Aldrich syndrome (WAS), an immunodeficiency disorder, an

49 Wiskott-Aldrich syndrome (WAS), X-linked thrombocytopenia (XLT),

50 Wiskott-Aldrich syndrome family proteins act downstream of these

51 Wiskott-Aldrich syndrome is a rare primary immunodeficiency asso

52 Wiskott-Aldrich syndrome is a rare, life-threatening, X-linked p

53 Wiskott-Aldrich syndrome is caused by mutations of the Wiskott-A

54 Wiskott-Aldrich syndrome protein (WASP) deficiency in mice resul

55 Wiskott-Aldrich syndrome protein (WASP) family verprolin homolog

56 Wiskott-Aldrich Syndrome protein (WASp) is a hematopoietic cell-

57 Wiskott-Aldrich syndrome protein (WASp) is essential for optimal

58 Wiskott-Aldrich syndrome protein (WASP) is in a complex with WAS

59 Wiskott-Aldrich syndrome protein (WASPs) control actin dynamics

60 Wiskott-Aldrich syndrome protein and SCAR homologue (WASH) is an

61 Wiskott-Aldrich syndrome protein family verprolin homologous (WA

62 Wiskott-Aldrich syndrome protein gene mutations result in four c

63 Wiskott-Aldrich syndrome protein is a signaling molecule and ins

64 Wiskott-Aldrich syndrome protein-deficient neutrophils are unabl

65 Wiskott-Aldrich syndrome proteins (WASP) are a family of protein

66 Wiskott-Aldrich syndrome proteins (WASPs), the prototypical Arp2

67 The scaffolding protein WAVE-1 (Wiskott-Aldrich syndrome protein family member 1) directs signal

68 pecific T-cell clones derived from a Wiskott-Aldrich syndrome (WAS) patient identified by flow cytome

69 with its downstream effector Wash, a Wiskott-Aldrich syndrome family protein.

70 own analyses show Robo4 binding to a Wiskott-Aldrich syndrome protein (WASP), neural Wiskott-Aldrich

71 latory domain (DAD) that resembles a Wiskott-Aldrich syndrome protein homology 2 (WH2) sequence C-ter

72 y either WAS gene mutation or absent Wiskott-Aldrich syndrome protein (WASP) expression or a Zhu clin

73 the ability of Nwk-SH3a to activate Wiskott-Aldrich syndrome protein (WASp)/actin related protein (A

74 amics and Ag transport by activating Wiskott-Aldrich syndrome protein via Vav and phosphatidylinositi

75 x and the endosomal Arp2/3 activator Wiskott-Aldrich syndrome protein and Scar homolog (WASH) on MT1-

76 The Arp2/3-activator Wiskott-Aldrich syndrome protein and Scar homologue (WASH) is su

77 re caused by WAS mutations affecting Wiskott-Aldrich syndrome protein (WASp) expression or activity,

78 erization, F-actin accumulation, and Wiskott-Aldrich symptom protein phosphorylation are enhanced in

79 n by activating Rho-like GTPases and Wiskott-Aldrich syndrome (WASp) family proteins.

80 severe combined immunodeficiency and Wiskott-Aldrich syndrome and metabolic conditions such as leukod

81 lets, which lack alpha-granules, and Wiskott-Aldrich syndrome platelets, which have cytoskeletal defe

82 he phagocyte-specific kinase Hck and Wiskott-Aldrich syndrome protein (WASP), 2 major regulators of p

83 ith the Wiskott-Aldrich syndrome and Wiskott-Aldrich syndrome protein (WASP)-deficient mice, T cell d

84 CK), p21-activated kinase (PAK), and Wiskott-Aldrich syndrome protein (WASP).

85 t increases actin polymerization and Wiskott-Aldrich syndrome protein activation in a Btk-dependent m

86 common variable immunodeficiency and Wiskott-Aldrich syndrome, to explain the occurrence of autoimmun

87 ng chronic granulomatous disease and Wiskott-Aldrich syndrome.

88 lly used to treat conditions such as Wiskott-Aldrich syndrome and chronic granulomatous disease, offe

89 Because Wiskott-Aldrich syndrome (WAS) and X-linked thrombocytopenia (XL

90 ematopoietic stem cells, and because Wiskott-Aldrich syndrome protein exerts a strong selective press

91 ine-rich domain and an actin-binding Wiskott-Aldrich syndrome protein homology 2 (WH2) domain that is

92 having only a single G-actin-binding Wiskott-Aldrich syndrome protein Homology 2 (WH2) domain, massiv

93 on a cluster of three actin-binding Wiskott-Aldrich syndrome protein homology 2 (WH2) domains that n

94 Actin polymerization mediated by Wiskott-Aldrich syndrome protein (WASp) and the actin-related pr

95 JIPs are recruited by Wiskott-Aldrich syndrome protein and scar homologue (WASH) on MT

96 in four clinical phenotypes: classic Wiskott-Aldrich syndrome and X-linked thrombocytopenia, intermit

97 ssue for all patients with classical Wiskott-Aldrich syndrome (WAS) and X-linked thrombocytopenia (XL

98 disorder associated with compromised Wiskott-Aldrich Syndrome Interacting Protein (WIP) function.

99 E proteins, members of the conserved Wiskott-Aldrich syndrome (WAS) family, promote actin polymerizat

100 but inhibits ingestion by decreasing Wiskott-Aldrich syndrome protein activation, and hence actin pol

101 f severe combined immune deficiency, Wiskott-Aldrich syndrome, and chronic granulomatous disease.

102 Macrophages from WASP-deficient Wiskott-Aldrich syndrome patients lack podosomes, resulting in d

103 c PIDs: hyper-IgE (STAT3-deficient), Wiskott-Aldrich, and dedicator of cytokinesis 8 syndromes.

104 The immunodeficiency disorder Wiskott-Aldrich syndrome (WAS) leads to life-threatening hematop

105 a genetic immunodeficiency disorder, Wiskott-Aldrich syndrome (WAS).

106 e gene defective in an Xid disorder, Wiskott-Aldrich syndrome.

107 cellular domain (AICD) downregulates Wiskott-Aldrich syndrome protein (WASP)-family verprolin homolog

108 The gene defective in WAS encodes Wiskott-Aldrich syndrome protein (WASP).

109 (N-WASP), the ubiquitously expressed Wiskott-Aldrich syndrome-like (WASL) protein, in mouse skin.

110 he actin nucleation-promoting factor Wiskott-Aldrich syndrome protein (WASP) contributes to maintenan

111 he actin nucleation-promoting factor Wiskott-Aldrich Syndrome protein (WASp).

112 tients treated with gene therapy for Wiskott-Aldrich syndrome (WAS) and beta-hemoglobinopathies.

113 drome gene (WAS) are responsible for Wiskott-Aldrich syndrome (WAS), a disease characterized by throm

114 ion was the only curative option for Wiskott-Aldrich syndrome (WAS).

115 ving undergone HSPC gene therapy for Wiskott-Aldrich syndrome or beta hemoglobinopathies.

116 A role for Wiskott-Aldrich syndrome protein (WASP) in chemotaxis to various

117 ce of platelets in a mouse model for Wiskott-Aldrich syndrome.

118 to 4 years after transplant in four Wiskott-Aldrich syndrome patients treated with HSPC gene therapy

119 e deficiency disorder resulting from Wiskott-Aldrich syndrome protein (WASp) deficiency.

120 in binding (profilin or the WH2 from Wiskott-Aldrich syndrome protein) decrease full-length INF2 acti

121 bind ATP, protein activators [e.g., Wiskott-Aldrich syndrome protein (WASp)], and the side of an act

122 The Src family kinase Hck, Wiskott-Aldrich-syndrome protein, and phospholipase Cgamma2 were

123 tein Las17 (a yeast homolog of human Wiskott-Aldrich syndrome protein) and participate in the endocyt

124 hort (SALS) is a recently identified Wiskott-Aldrich syndrome protein homology 2 (WH2) domain protein

125 Patients with the immunodeficiency Wiskott-Aldrich syndrome (WAS) frequently develop systemic autoi

126 s with the X-linked immunodeficiency Wiskott-Aldrich syndrome (WAS) have opposite alterations at cent

127 homology 3 (SH3) domain and impairs Wiskott-Aldrich syndrome protein (WASP) binding, but it does not

128 Mutations in Wiskott-Aldrich syndrome (WAS) protein (WASp), a regulator of ac

129 y, hematolymphoid cancers develop in Wiskott-Aldrich syndrome (WAS), an X-linked primary immunodefici

130 In Wiskott-Aldrich syndrome (WAS), immunodeficiency and autoimmunit

131 ely identify the B-cell phenotype in Wiskott-Aldrich syndrome (WAS), we used 3 distinct murine in viv

132 Defects in Wiskott-Aldrich Syndrome protein (WASp) underlie development of

133 op in patients and mice deficient in Wiskott-Aldrich syndrome protein (WASP), a hematopoietic cell-sp

134 Fusion of macrophages deficient in Wiskott-Aldrich syndrome protein and Cdc42, key molecules involv

135 This includes Wiskott-Aldrich syndrome protein, Wiskott-Aldrich syndrome prote

136 involved in actin dynamics including Wiskott-Aldrich syndrome protein (WASp) were regulated by NPM-AL

137 t cancer development and metastasis, Wiskott-Aldrich syndrome protein family member 3 (Wasf3) is up-r

138 ns with a wide network of molecules: Wiskott-Aldrich syndrome protein (WASp), Grb2, ribosomal S6 kina

139 ne-mediated activation of neural (N) Wiskott-Aldrich syndrome proteins (WASP) induces defects in cell

140 ads to recruitment of Nck and neural Wiskott-Aldrich syndrome protein (N-WASP) and strong actin polym

141 e nucleation-promoting factor neural Wiskott-Aldrich syndrome protein (N-WASP) and the actin nucleato

142 he actin nucleation promoters neural Wiskott-Aldrich syndrome protein (N-WASP) and WAVE2 in cell prot

143 family tyrosine kinases, and neural Wiskott-Aldrich syndrome protein (N-WASP) but not the Arp2/Arp3

144 es that the nuclear localized neural Wiskott-Aldrich syndrome protein (N-WASP) can induce de novo act

145 ed that S. flexneri relies on neural Wiskott-Aldrich Syndrome protein (N-WASP) in HT-29 cells.

146 tin-regulatory protein called neural Wiskott-Aldrich syndrome protein (N-WASP) interacting with its e

147 Co et al. now show that the neural Wiskott-Aldrich syndrome protein (N-WASP) mediates dynamic attac

148 In this study, we show neural Wiskott-Aldrich syndrome protein (N-WASP) regulates the formatio

149 d EGFR signaling up-regulated neural Wiskott-Aldrich syndrome protein (N-WASP), an actin nucleator wh

150 ng and -polymerizing proteins neural Wiskott-Aldrich syndrome protein (N-WASP), cortactin, and ARP2/3

151 pproach to assess the role of neural Wiskott-Aldrich syndrome protein (N-WASP), the ubiquitously expr

152 We altered the function of neural Wiskott-Aldrich syndrome protein (N-WASP), which induces actin p

153 IcsA, YapV recruits mammalian neural Wiskott-Aldrich syndrome protein (N-WASP).

154 the actin nucleation promoter neural Wiskott-Aldrich syndrome protein (N-WASP).

155 t replaces toca-1 to mobilize neural Wiskott-Aldrich syndrome protein and the Arp2/3 complex.

156 Neural Wiskott-Aldrich syndrome protein(N-Wasp) is an actin nucleation

157 ion-promoting protein N-WASP (Neural Wiskott-Aldrich syndrome protein) is up-regulated in breast canc

158 amics through the Nck/N-WASp (neural Wiskott-Aldrich syndrome protein)/Arp2/3 pathway is essential fo

159 rich syndrome protein (WASP), neural Wiskott-Aldrich syndrome protein, and WASP-interacting protein a

160 kinase, Rho GTPase Rac1, and neural Wiskott-Aldrich syndrome protein.

161 signals that locally activate neural Wiskott-Aldrich-syndrome protein (N-WASP) and the Arp2/3 complex

162 bl interactor 1 (Abi1) with neuronal Wiskott-Aldrich syndrome protein (N-WASP) (an actin-regulatory p

163 was necessary for cdc42 and neuronal Wiskott-Aldrich syndrome protein (N-WASP) activation, actin poly

164 he actin regulatory protein neuronal Wiskott-Aldrich syndrome protein (N-WASP) and an SH2 domain that

165 compound containing CrkII, neuronal Wiskott-Aldrich Syndrome Protein (N-WASP) and the Arp2/3 (Actin

166 Neuronal Wiskott-Aldrich syndrome protein (N-WASP) has an essential role

167 ucleating endocytic protein neuronal Wiskott-Aldrich syndrome protein (N-WASP) to facilitate PDGF rec

168 ve analysed the dynamics of neuronal Wiskott-Aldrich syndrome protein (N-WASP), WASP-interacting prot

169 oscopy, we demonstrate that neuronal Wiskott-Aldrich syndrome protein (N-WASP), which is coexpressed

170 Here, we demonstrate that neuronal Wiskott-Aldrich syndrome protein (N-WASP), which promotes actin

171 m led to the recruitment of neuronal Wiskott-Aldrich syndrome protein (N-WASp), which was not observe

172 Neuronal Wiskott-Aldrich syndrome protein (N-WASP)-activated actin polyme

173 sorting nexin 9 (SNX9) and neuronal Wiskott-Aldrich syndrome protein (N-WASP).

174 in polymerization catalyst, neuronal Wiskott-Aldrich syndrome protein (N-WASP).

175 Neuronal Wiskott-Aldrich syndrome protein regulates TGF-beta1-mediated lu

176 yrosine kinase) and N-WASP (neuronal Wiskott-Aldrich Syndrome Protein) at the cell edge without affec

177 integrin beta1, cortactin, neuronal Wiskott-Aldrich syndrome protein, membrane type 1 metalloproteas

178 uired actin polymerization, neuronal Wiskott-Aldrich syndrome protein, myosin II and Rho GTPase.

179 ore tightly associated with neuronal Wiskott-Aldrich syndrome protein, promoting actin-related protei

180 association to the actin-nucleating Wiskott-Aldrich syndrome and SCAR homolog (WASH) complex.

181 erization through Arp2/3 nucleation, Wiskott-Aldrich syndrome protein (WASP) and WASP family verproli

182 guineous parents, showed features of Wiskott-Aldrich syndrome (WAS), including recurrent infections,

183 ereof contribute to the pathology of Wiskott-Aldrich syndrome (WAS).

184 immunologic symptoms reminiscent of Wiskott-Aldrich syndrome (WAS).

185 understanding the molecular basis of Wiskott-Aldrich syndrome and its ramifications for the cure of t

186 The cytoplasmic functions of Wiskott-Aldrich syndrome family (WAS) proteins are well establis

187 mmunodeficiency caused by absence of Wiskott-Aldrich syndrome protein (WASP) expression, resulting in

188 sly that tyrosine phosphorylation of Wiskott-Aldrich syndrome protein (WASP) is important for diverse

189 Here we show that deficiency of Wiskott-Aldrich syndrome protein (WASp), which signals to the ac

190 actin cytoskeleton and activator of Wiskott-Aldrich syndrome protein (WASP).

191 to podosomes in the localization of Wiskott-Aldrich syndrome protein (WASP)/matrix metalloproteinase

192 very of unique functional domains of Wiskott-Aldrich syndrome protein has been instrumental in defini

193 Studies of Wiskott-Aldrich syndrome protein-deficient cell lines and wasp-k

194 ector copy numbers and expression of Wiskott-Aldrich syndrome protein.

195 echanisms that control activation of Wiskott-Aldrich syndrome protein.

196 s led to success in the treatment of Wiskott-Aldrich syndrome, while further applications are pending

197 ributes to the bleeding diathesis of Wiskott-Aldrich syndrome.

198 Nodule formation is dependent on Wiskott-Aldrich syndrome protein (WASp) and the ARP2/3 complex.

199 ility, independent of its effects on Wiskott-Aldrich syndrome protein and p21-activated kinase.

200 NK cell function relies on Wiskott-Aldrich syndrome protein for filamentous actin (F-actin)

201 ion in patients with food allergy or Wiskott-Aldrich syndrome (WAS) and defined whether spontaneous d

202 The actin-modulating protein Wiskott-Aldrich syndrome protein verprolin homologous-1 (WAVE1)

203 es Wiskott-Aldrich syndrome protein, Wiskott-Aldrich syndrome protein-interacting protein, cofilin, M

204 etic-specific cytoskeletal regulator Wiskott-Aldrich syndrome protein (WASP).

205 e combined immune deficiency (SCID), Wiskott-Aldrich syndrome (WAS), and chronic granulomatous diseas

206 re combined immunodeficiency (SCID), Wiskott-Aldrich syndrome, and chronic granulomatous disease thro

207 n 7 consecutive patients with severe Wiskott-Aldrich syndrome lacking HLA antigen-matched related or

208 rim analysis of patients with severe Wiskott-Aldrich syndrome who received lentiviral vector-derived

209 y in paediatric patients with severe Wiskott-Aldrich syndrome, defined by either WAS gene mutation or

210 ment option for patients with severe Wiskott-Aldrich syndrome, particularly for those who do not have

211 Since Wiskott-Aldrich syndrome protein is expressed exclusively in hem

212 Here, we show that Wiskott-Aldrich syndrome protein (WASP)-family verprolin homolog

213 Here, we demonstrate that Wiskott-Aldrich syndrome protein (WASp)-interacting protein (WIP

214 model disease and establish that the Wiskott-Aldrich gene product (WASP) serves an essential role in

215 The Wiskott-Aldrich syndrome (WAS) interacting protein (WIP) stabili

216 The Wiskott-Aldrich syndrome (WAS) is characterized by defective cyt

217 The Wiskott-Aldrich syndrome (WAS), caused by mutations in the WAS g

218 of immunodeficient patients with the Wiskott-Aldrich syndrome and Wiskott-Aldrich syndrome protein (W

219 Mutations of the Wiskott-Aldrich syndrome gene (WAS) are responsible for Wiskott-

220 ts that result from mutations in the Wiskott-Aldrich syndrome gene (WAS), which have a broad impact o

221 constitutively active mutant of the Wiskott-Aldrich Syndrome protein (CA-WASp) is the cause of X-lin

222 The Wiskott-Aldrich syndrome protein (WASP) and neural WASP (N-WASP)

223 In T lymphocytes, the Wiskott-Aldrich Syndrome protein (WASP) and WASP-interacting-pro

224 The proteins of the Wiskott-Aldrich syndrome protein (WASP) family are activators of

225 Members of the Wiskott-Aldrich syndrome protein (WASP) family control actin dyn

226 Members of the Wiskott-Aldrich syndrome protein (WASP) family control cytoskele

227 We recently showed that the Wiskott-Aldrich syndrome protein (WASP) family member, WASH, loc

228 ycolactone operates by hijacking the Wiskott-Aldrich syndrome protein (WASP) family of actin-nucleati

229 idic (VCA) region of proteins in the Wiskott-Aldrich syndrome protein (WASp) family, Arp2/3 complex p

230 in machinery, such as members of the Wiskott-Aldrich syndrome protein (WASp) family.

231 onse to signals from proteins in the Wiskott-Aldrich syndrome protein (WASP) family.

232 s actin by activating members of the Wiskott-Aldrich syndrome protein (WASP) family.

233 s, known filament nucleators use the Wiskott-Aldrich syndrome protein (WASP) homology 2 (WH2 or W) do

234 The role of the Wiskott-Aldrich syndrome protein (WASp) in platelet function is

235 The Wiskott-Aldrich syndrome protein (WASP) is a key cytoskeletal re

236 The Wiskott-Aldrich syndrome protein (WASP) is a product of the gene

237 The Wiskott-Aldrich syndrome protein (WASp) is important for actin p

238 The Wiskott-Aldrich syndrome protein (WASp) regulates actin polymeri

239 (Leu270Pro) in the gene encoding the Wiskott-Aldrich syndrome protein (WASp) resulting in an X-linked

240 The Wiskott-Aldrich Syndrome protein (WASp) serves as a crucial link

241 tions in the human gene encoding the Wiskott-Aldrich syndrome protein (WASp) that compromise normal a

242 aused by activating mutations in the Wiskott-Aldrich syndrome protein (WASP) that result in aberrant

243 function caused by deficiency of the Wiskott-Aldrich syndrome protein (WASp) to explore the contribut

244 or-bound protein 2 (Grb2) and to the Wiskott-Aldrich syndrome protein (WASp) to form a heterotrimer c

245 earing inactivating mutations in the Wiskott-Aldrich syndrome protein (WASP), a key regulator of acti

246 B) and fused the Cdc42 effector, the Wiskott-Aldrich Syndrome Protein (WASP), to the light-dependent

247 Podosome formation requires the Wiskott-Aldrich syndrome protein (WASP), which is a product of t

248 WAVE1--the Wiskott-Aldrich syndrome protein (WASP)--family verprolin homolo

249 ze other motility proteins, like the Wiskott-Aldrich syndrome protein (WASP).

250 tion-promoting factors (NPFs) of the Wiskott-Aldrich syndrome protein (WASP)/Scar family are the curr

251 umpellin, is a core component of the Wiskott-Aldrich syndrome protein and SCAR homolog (WASH) complex

252 hich also binds retromer, within the Wiskott-Aldrich syndrome protein and SCAR homologue (WASH) compl

253 he COMMD/CCDC22/CCDC93 (CCC) and the Wiskott-Aldrich syndrome protein and SCAR homologue (WASH) compl

254 regions of TOCA1 and a member of the Wiskott-Aldrich syndrome protein family, N-WASP.

255 ndrome is caused by mutations of the Wiskott-Aldrich syndrome protein gene, which codes for a cytopla

256 in-RVS-domain protein Rvs167 and the Wiskott-Aldrich syndrome protein Las17 at the point of penetrati

257 WASH is an Arp2/3 activator of the Wiskott-Aldrich syndrome protein superfamily that functions duri

258 n endosomal protein belonging to the Wiskott-Aldrich syndrome protein superfamily that participates i

259 direct interaction of Skap2 with the Wiskott-Aldrich syndrome protein via its SH3 domain is critical

260 in a macromolecular complex with the Wiskott-Aldrich syndrome protein, an actin nucleation-promoting

261 The Wiskott-Aldrich syndrome protein-family verprolin-homologous pro

262 Further, CYFIP2 is part of the Wiskott-Aldrich syndrome protein-family verprolin-homologous pro

263 eleton by binding and activating the Wiskott-Aldrich syndrome protein.

264 we apply these ideas is that of the Wiskott-Aldrich Syndrome Proteins as activators of actin polymer

265 The Wiskott-Aldrich syndrome, a primary human immunodeficiency, resu

266 ave focused on a murine model of the Wiskott-Aldrich syndrome, an immunodeficiency in which autoimmun

267 letal regulator WASP, mutated in the Wiskott-Aldrich syndrome, provides selective advantage for the d

268 The Wiskott-Aldrich syndrome-related protein WAVE2 promotes Arp2/3-d

269 The activity of the Wiskott-Aldrich syndrome-related WAVE3 protein is critical for t

270 defects in regulatory T cells in the Wiskott-Aldrich syndrome.

271 rited immunodeficiency disorder, the Wiskott-Aldrich syndrome.

272 ystem effector, VopL, encoding three Wiskott-Aldrich homology 2 domains that are interspersed with th

273 hat appeared to be a repeat of three Wiskott-Aldrich syndrome homology 2 (WH2) domains in the middle

274 de evidence that Kit signals through Wiskott-Aldrich syndrome protein (WASP), the central hematopoiet

275 The WIP C-terminal domain binds to Wiskott-Aldrich syndrome protein (WASp) and regulates its activa

276 issue of the JCI, Lexmond et al. use Wiskott-Aldrich syndrome as a model disease and establish that t

277 hrough focal nucleation of actin via Wiskott-Aldrich syndrome protein (WASP), and contraction of the

278 it was activated by p78/83, a viral Wiskott-Aldrich syndrome protein (WASP)-like protein.

279 omez and Billadeau reveal that WASH (Wiskott-Aldrich syndrome protein and SCAR homolog) activates Arp

280 WASH (Wiskott-Aldrich Syndrome Protein and SCAR Homolog) is an Arp2/3

281 e actin polymerization such as WASp (Wiskott-Aldrich syndrome protein) and HS1 (hematopoietic lineage

282 U) potently activates the host WASP (Wiskott-Aldrich syndrome protein) family of actin-nucleating fac

283 s 2/3) complex is activated by WASP (Wiskott-Aldrich syndrome protein) family proteins to nucleate br

284 he nucleation-promoting factor Wasp (Wiskott-Aldrich syndrome protein).

285 olymerization in pseudopods, whereas Wiskott-Aldrich syndrome protein (WASP) assembles actin at clath

286 g of WASp-interacting protein (WIP), Wiskott-Aldrich syndrome protein (WASp), actin, and myosin IIA t

287 ively regulates its interaction with Wiskott-Aldrich interacting protein and decreases its protein st

288 Patients with Wiskott-Aldrich syndrome (WAS) have numerous immune cell deficie

289 s of immunodeficiency, patients with Wiskott-Aldrich syndrome (WAS) often suffer from poorly understo

290 GTPase Cdc42, known to interact with Wiskott-Aldrich syndrome (WAS) protein, is an important regulato

291 ed in macrophages from patients with Wiskott-Aldrich syndrome (WAS), an X chromosome-linked immunodef

292 the French Registry of patients with Wiskott-Aldrich Syndrome (WAS), Mahlaoui et al have identified s

293 onwide database of 160 patients with Wiskott-Aldrich syndrome (WAS), we identified a subset of infant

294 Humans with Wiskott-Aldrich syndrome display a progressive immunological dis

295 n, when it is able to associate with Wiskott-Aldrich syndrome protein (WASp) and the actin filament-r

296 gh its BAR domain and interacts with Wiskott-Aldrich Syndrome Protein (WASP) via its SRC homology 3 d

297 HS1 interacts with Wiskott-Aldrich syndrome protein (WASp), another key actin-regul

298 ision cycle 42, which, together with Wiskott-Aldrich syndrome protein, coordinates F-actin reorganiza

299 ated IgA were found in patients with Wiskott-Aldrich syndrome, and these abnormal antibodies might co

300 use of gene therapy in patients with Wiskott-Aldrich syndrome.