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 ributes to the bleeding diathesis of Wiskott-Aldrich syndrome.

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

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

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

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

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

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

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

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

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

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

25 Wiskott-Aldrich syndrome family proteins act downstream of these

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

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

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

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

30 Wiskott-Aldrich syndrome is a rare primary immunodeficiency asso

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

181 Wiskott-Aldrich syndrome protein family verprolin homologous (WA

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

228 Wiskott-Aldrich syndrome protein-deficient neutrophils are unabl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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