ライフサイエンスコーパス: Aldrich syndrome

1 ng chronic granulomatous disease and Wiskott-Aldrich syndrome.

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

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

4 rited immunodeficiency disorder, the Wiskott-Aldrich syndrome.

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

6 nificantly to the immunopathology of Wiskott-Aldrich Syndrome.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

24 Wiskott-Aldrich syndrome family proteins act downstream of these

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

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

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

28 Wiskott-Aldrich syndrome is a rare primary immunodeficiency asso

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

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

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

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

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

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

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

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

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

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

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

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

41 and temporal regulation of neuronal Wiskott-Aldrich syndrome protein (N-WASP) activity in living cel

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

60 tion of the Arp2/3 complex by neural Wiskott-Aldrich Syndrome protein (N-WASP) via Grb2 and Nck2.

61 Neural Wiskott-Aldrich syndrome protein (N-WASP), a ubiquitous member o

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

103 d XLT are caused by mutations of the Wiskott-Aldrich syndrome protein (WASP) gene which encodes a 502

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

105 defects related to deficiency of the Wiskott-Aldrich Syndrome protein (WASp) have been described in o

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

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

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

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

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

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

112 this study, we demonstrate that the Wiskott-Aldrich syndrome protein (WASp) is an essential componen

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

141 o such adaptor proteins, Nck and the Wiskott-Aldrich syndrome protein (WASp), were recruited to the T

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

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

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

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

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

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

148 Wiskott-Aldrich syndrome protein (WASP)-deficient T cells exhibi

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

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

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

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

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

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

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

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

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

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

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

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

161 signaling pathways that include the Wiskott-Aldrich syndrome protein (WASP).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

179 regulate the activation of neuronal Wiskott-Aldrich syndrome protein and the actin related protein c

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

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

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

183 binant Arc40 bound the VCA domain of Wiskott-Aldrich syndrome protein family activators at a K(d) of

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

185 Wiskott-Aldrich syndrome protein family verprolin homologous (WA

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

202 C. parvum activates the Cdc42/neural Wiskott-Aldrich syndrome protein network in host cells resulting

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

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

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

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

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

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

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

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

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

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

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

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

215 ner, bound actin monomer via a WASP (Wiskott-Aldrich syndrome protein) homology 2 domain, bound profi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

231 Wiskott-Aldrich syndrome protein-deficient neutrophils are unabl

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

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

234 Wiskott-Aldrich syndrome protein-interacting protein (WIP) stabi

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

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

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

238 domain along with Arp2/3 complex and Wiskott-Aldrich syndrome protein.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

277 ty to be reduced on lymphocytes from Wiskott-Aldrich syndrome (WAS) patient, we find no such deficien

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

297 n of blood-cell disorders, including Wiskott-Aldrich syndrome (WAS).

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

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

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