ライフサイエンスコーパス: Aldrich

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

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

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

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

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

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

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

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

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

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

11 0 were positive with rabbit serum (RS; Sigma-Aldrich, St. Louis, MO).

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

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

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

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

16 Wiscott-Aldrich syndrome protein (WASP) was observed in the acti

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

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

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

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

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

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

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

24 Wiskott-Aldrich syndrome (WAS) is a platelet/immunodeficiency di

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

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

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

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

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

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

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

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

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

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

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

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

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

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

39 Wiskott-Aldrich syndrome family proteins act downstream of these

40 Wiskott-Aldrich syndrome is a rare primary immunodeficiency asso

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

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

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

44 Wiskott-Aldrich syndrome protein (WASP) has emerged as a central

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

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

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

48 Wiskott-Aldrich syndrome protein (WASP)-homology domain 2 (WH2)

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

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

51 Wiskott-Aldrich syndrome protein family verprolin homologous (WA

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

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

54 Wiskott-Aldrich syndrome protein-deficient neutrophils are unabl

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

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

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

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

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

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

61 rotubule-organizing center, F-actin, Wiskott-Aldrich syndrome protein, nor proline rich tyrosine kina

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

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

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

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

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

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

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

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

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

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

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

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

74 b2-associated protein 2 (Grap2), and Wiskott-Aldrich syndrome protein.

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

76 ng chronic granulomatous disease and Wiskott-Aldrich syndrome.

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

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

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

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

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

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

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

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

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

86 e disorders in patients with classic Wiskott-Aldrich syndrome, possibly caused by immune dysregulatio

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

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

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

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

91 ytes/macrophages from WASP-deficient Wiskott-Aldrich syndrome patients are severely defective in chem

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

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

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

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

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

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

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

99 natural killer (NK) cells expressed Wiskott-Aldrich syndrome protein (WASP), and NK cells contained

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

122 n Metastasis (MIM), a Shh-inducible, Wiskott-Aldrich homology 2 domain-containing protein that potent

123 an immunodeficiency virus infection, Wiskott-Aldrich syndrome, and vasculopathy with capillary leak s

124 ex activation domain (WCA) of Las17 (Wiskott-Aldrich syndrome protein [WASp] homologue) fused to an e

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

146 rp3-silenced cells expressing neural Wiskott-Aldrich syndrome protein-derived peptides that inhibit A

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

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

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

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

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

152 s mediated by activation of neuronal Wiskott-Aldrich syndrome protein (N-WASp) and the Arp (actin-rel

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

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

155 onan (HA) and CD44 with the neuronal Wiskott-Aldrich syndrome protein (N-WASP) in regulating actin po

156 Neuronal Wiskott-Aldrich syndrome protein (N-WASP) is a member of the WAS

157 The VCA domain of the neuronal Wiskott-Aldrich syndrome protein (N-WASP) is a potent activator

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

159 actin-related protein 3 and neuronal Wiskott-Aldrich syndrome protein (N-WASP), and their assembly wa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

187 eased, while natural cytotoxicity of Wiskott-Aldrich syndrome-NK cells is maintained.

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

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

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

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

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

193 ts with X-linked thrombocytopenia or Wiskott-Aldrich syndrome, respectively.

194 of the distinct clinical phenotypes (Wiskott-Aldrich syndrome/X-linked thrombocytopenia; intermittent

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

212 of actin cytoskeleton dynamics, the Wiskott-Aldrich syndrome protein (N-WASP) and the Arp2/3 complex

213 The Wiskott-Aldrich syndrome protein (WASP) and its homolog neuronal

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

215 odel of allosteric regulation of the Wiskott-Aldrich syndrome protein (WASP) by the Rho GTPase Cdc42

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

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

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

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

220 ferent human proteins, including the Wiskott-Aldrich syndrome protein (WASp) family members.

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

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

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

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

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

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

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

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

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

230 We demonstrate that the Wiskott-Aldrich syndrome protein (WASp) is an important componen

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

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

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

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

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

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

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

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

239 strated that ACK1 phosphorylates the Wiskott-Aldrich syndrome protein (WASP), a Cdc42 effector that p

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

241 red an activating factor such as the Wiskott-Aldrich syndrome protein (WASP), and might exhibit a pre

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

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

244 uced in macrophages deficient in the Wiskott-Aldrich syndrome protein (WASP), which still contain the

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

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

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

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

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

250 Mutations of the Wiskott-Aldrich syndrome protein can result in highly variable c

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

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

253 e in dissecting the functions of the Wiskott-Aldrich syndrome protein has direct implications for our

254 e was the presence or absence of the Wiskott-Aldrich syndrome protein in the lymphoid cells from pati

255 In addition, the Wiskott-Aldrich syndrome protein is required for natural killer

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 es of patients with mutations of the Wiskott-Aldrich syndrome protein unequivocally demonstrated a st

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

260 Finally, the Wiskott-Aldrich syndrome protein was shown to play an important

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

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

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

275 ching occurs when Arp2/3 is bound to Wiskott-Aldrich syndrome protein (WASP), which is in turn bound

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

300 mation of endogenous Lck-Dlgh1-Zap70-Wiskott-Aldrich syndrome protein (WASp) complexes in which Dlgh1