ライフサイエンスコーパス: Wiskott-Aldrich syndrome

1 including chronic granulomatous disease and Wiskott-Aldrich syndrome.

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

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

4 ked inherited immunodeficiency disorder, the Wiskott-Aldrich syndrome.

5 ct of the gene defective in an Xid disorder, Wiskott-Aldrich syndrome.

6 nce contributes to the bleeding diathesis of Wiskott-Aldrich syndrome.

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

8 The Wiskott-Aldrich syndrome, a primary human immunodeficien

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

10 uccessfully used to treat conditions such as Wiskott-Aldrich syndrome and chronic granulomatous disea

11 ress in understanding the molecular basis of Wiskott-Aldrich syndrome and its ramifications for the c

12 cluding severe combined immunodeficiency and Wiskott-Aldrich syndrome and metabolic conditions such a

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

14 eatures of immunodeficient patients with the Wiskott-Aldrich syndrome and Wiskott-Aldrich syndrome pr

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

16 for severe combined immunodeficiency (SCID), Wiskott-Aldrich syndrome, and chronic granulomatous dise

17 forms of severe combined immune deficiency, Wiskott-Aldrich syndrome, and chronic granulomatous dise

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

19 with human immunodeficiency virus infection, Wiskott-Aldrich syndrome, and vasculopathy with capillar

20 In this issue of the JCI, Lexmond et al. use Wiskott-Aldrich syndrome as a model disease and establis

21 cal study in paediatric patients with severe Wiskott-Aldrich syndrome, defined by either WAS gene mut

22 Humans with Wiskott-Aldrich syndrome display a progressive immunolog

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

24 of Rho1 with its downstream effector Wash, a Wiskott-Aldrich syndrome family protein.

25 Wiskott-Aldrich syndrome family proteins act downstream

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

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

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

29 logical disorder associated with compromised Wiskott-Aldrich Syndrome Interacting Protein (WIP) funct

30 Wiskott-Aldrich syndrome is a rare primary immunodeficie

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

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

33 nfused in 7 consecutive patients with severe Wiskott-Aldrich syndrome lacking HLA antigen-matched rel

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

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

36 le treatment option for patients with severe Wiskott-Aldrich syndrome, particularly for those who do

37 at monocytes/macrophages from WASP-deficient Wiskott-Aldrich syndrome patients are severely defective

38 Macrophages from WASP-deficient Wiskott-Aldrich syndrome patients lack podosomes, result

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

40 me platelets, which lack alpha-granules, and Wiskott-Aldrich syndrome platelets, which have cytoskele

41 study, we investigated the role of neuronal Wiskott Aldrich syndrome protein (N-WASP) in modulating

42 The actin cytoskeletal regulator Wiskott Aldrich syndrome protein (WASp) has been implica

43 actin-nucleating machine activated by WASp (Wiskott Aldrich syndrome protein).

44 as the levels of F-actin and phosphorylated Wiskott Aldrich syndrome protein, an actin nucleation pr

45 The constitutively active mutant of the Wiskott-Aldrich Syndrome protein (CA-WASp) is the cause

46 tein c-Abl interactor 1 (Abi1) with neuronal Wiskott-Aldrich syndrome protein (N-WASP) (an actin-regu

47 complex was necessary for cdc42 and neuronal Wiskott-Aldrich syndrome protein (N-WASP) activation, ac

48 nts in the actin regulatory protein neuronal Wiskott-Aldrich syndrome protein (N-WASP) and an SH2 dom

49 474/1 leads to recruitment of Nck and neural Wiskott-Aldrich syndrome protein (N-WASP) and strong act

50 c42), the nucleation-promoting factor neural Wiskott-Aldrich syndrome protein (N-WASP) and the actin

51 zation is mediated by activation of neuronal Wiskott-Aldrich syndrome protein (N-WASp) and the Arp (a

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

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

54 ole of the actin nucleation promoters neural Wiskott-Aldrich syndrome protein (N-WASP) and WAVE2 in c

55 and Src family tyrosine kinases, and neural Wiskott-Aldrich syndrome protein (N-WASP) but not the Ar

56 indicates that the nuclear localized neural Wiskott-Aldrich syndrome protein (N-WASP) can induce de

57 Neuronal Wiskott-Aldrich syndrome protein (N-WASP) has an essenti

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

59 f hyaluronan (HA) and CD44 with the neuronal Wiskott-Aldrich syndrome protein (N-WASP) in regulating

60 f the actin-regulatory protein called neural Wiskott-Aldrich syndrome protein (N-WASP) interacting wi

61 Neuronal Wiskott-Aldrich syndrome protein (N-WASP) is a member of

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

63 Co et al. now show that the neural Wiskott-Aldrich syndrome protein (N-WASP) mediates dynam

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

65 actin nucleating endocytic protein neuronal Wiskott-Aldrich syndrome protein (N-WASP) to facilitate

66 -mediated EGFR signaling up-regulated neural Wiskott-Aldrich syndrome protein (N-WASP), an actin nucl

67 ched in actin-related protein 3 and neuronal Wiskott-Aldrich syndrome protein (N-WASP), and their ass

68 in-binding and -polymerizing proteins neural Wiskott-Aldrich syndrome protein (N-WASP), cortactin, an

69 ockout approach to assess the role of neural Wiskott-Aldrich syndrome protein (N-WASP), the ubiquitou

70 s, we have analysed the dynamics of neuronal Wiskott-Aldrich syndrome protein (N-WASP), WASP-interact

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

72 nce microscopy, we demonstrate that neuronal Wiskott-Aldrich syndrome protein (N-WASP), which is coex

73 Here, we demonstrate that neuronal Wiskott-Aldrich syndrome protein (N-WASP), which promote

74 M. avium led to the recruitment of neuronal Wiskott-Aldrich syndrome protein (N-WASp), which was not

75 Neuronal Wiskott-Aldrich syndrome protein (N-WASP)-activated acti

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

77 Nck and the actin nucleation promoter neural Wiskott-Aldrich syndrome protein (N-WASP).

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

79 the actin polymerization catalyst, neuronal Wiskott-Aldrich syndrome protein (N-WASP).

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

81 The Wiskott-Aldrich syndrome protein (WASP) and neural WASP

82 The WIP C-terminal domain binds to Wiskott-Aldrich syndrome protein (WASp) and regulates it

83 ctivation, when it is able to associate with Wiskott-Aldrich syndrome protein (WASp) and the actin fi

84 Actin polymerization mediated by Wiskott-Aldrich syndrome protein (WASp) and the actin-re

85 Nodule formation is dependent on Wiskott-Aldrich syndrome protein (WASp) and the ARP2/3 c

86 in polymerization through Arp2/3 nucleation, Wiskott-Aldrich syndrome protein (WASP) and WASP family

87 In T lymphocytes, the Wiskott-Aldrich Syndrome protein (WASP) and WASP-interac

88 actin polymerization in pseudopods, whereas Wiskott-Aldrich syndrome protein (WASP) assembles actin

89 the SRC homology 3 (SH3) domain and impairs Wiskott-Aldrich syndrome protein (WASP) binding, but it

90 tative model of allosteric regulation of the Wiskott-Aldrich syndrome protein (WASP) by the Rho GTPas

91 the formation of endogenous Lck-Dlgh1-Zap70-Wiskott-Aldrich syndrome protein (WASp) complexes in whi

92 w that the actin nucleation-promoting factor Wiskott-Aldrich syndrome protein (WASP) contributes to m

93 Wiskott-Aldrich syndrome protein (WASP) deficiency in mi

94 ry immune deficiency disorder resulting from Wiskott-Aldrich syndrome protein (WASp) deficiency.

95 efined by either WAS gene mutation or absent Wiskott-Aldrich syndrome protein (WASP) expression or a

96 which are caused by WAS mutations affecting Wiskott-Aldrich syndrome protein (WASp) expression or ac

97 rimary immunodeficiency caused by absence of Wiskott-Aldrich syndrome protein (WASP) expression, resu

98 The proteins of the Wiskott-Aldrich syndrome protein (WASP) family are activ

99 Members of the Wiskott-Aldrich syndrome protein (WASP) family control a

100 Members of the Wiskott-Aldrich syndrome protein (WASP) family control c

101 We recently showed that the Wiskott-Aldrich syndrome protein (WASP) family member, W

102 w that mycolactone operates by hijacking the Wiskott-Aldrich syndrome protein (WASP) family of actin-

103 Wiskott-Aldrich syndrome protein (WASP) family verprolin

104 , and acidic (VCA) region of proteins in the Wiskott-Aldrich syndrome protein (WASp) family, Arp2/3 c

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

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

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

108 f formins, known filament nucleators use the Wiskott-Aldrich syndrome protein (WASP) homology 2 (WH2

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

110 The role of the Wiskott-Aldrich syndrome protein (WASp) in platelet func

111 Wiskott-Aldrich Syndrome protein (WASp) is a hematopoiet

112 The Wiskott-Aldrich syndrome protein (WASP) is a key cytoske

113 The Wiskott-Aldrich syndrome protein (WASP) is a product of

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

115 Wiskott-Aldrich syndrome protein (WASp) is essential for

116 The Wiskott-Aldrich syndrome protein (WASp) is important for

117 previously that tyrosine phosphorylation of Wiskott-Aldrich syndrome protein (WASP) is important for

118 Wiskott-Aldrich syndrome protein (WASP) is in a complex

119 The Wiskott-Aldrich syndrome protein (WASp) regulates actin

120 utation (Leu270Pro) in the gene encoding the Wiskott-Aldrich syndrome protein (WASp) resulting in an

121 The Wiskott-Aldrich Syndrome protein (WASp) serves as a cruc

122 fic mutations in the human gene encoding the Wiskott-Aldrich syndrome protein (WASp) that compromise

123 LN) is caused by activating mutations in the Wiskott-Aldrich syndrome protein (WASP) that result in a

124 etal dysfunction caused by deficiency of the Wiskott-Aldrich syndrome protein (WASp) to explore the c

125 r receptor-bound protein 2 (Grb2) and to the Wiskott-Aldrich syndrome protein (WASp) to form a hetero

126 Defects in Wiskott-Aldrich Syndrome protein (WASp) underlie develop

127 ds through its BAR domain and interacts with Wiskott-Aldrich Syndrome Protein (WASP) via its SRC homo

128 roteins involved in actin dynamics including Wiskott-Aldrich syndrome protein (WASp) were regulated b

129 ed via the phagocyte-specific kinase Hck and Wiskott-Aldrich syndrome protein (WASP), 2 major regulat

130 s, develop in patients and mice deficient in Wiskott-Aldrich syndrome protein (WASP), a hematopoietic

131 tients bearing inactivating mutations in the Wiskott-Aldrich syndrome protein (WASP), a key regulator

132 onsisting of WASp-interacting protein (WIP), Wiskott-Aldrich syndrome protein (WASp), actin, and myos

133 ynapse through focal nucleation of actin via Wiskott-Aldrich syndrome protein (WASP), and contraction

134 f, required an activating factor such as the Wiskott-Aldrich syndrome protein (WASP), and might exhib

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

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

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

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

139 we provide evidence that Kit signals through Wiskott-Aldrich syndrome protein (WASP), the central hem

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

141 Podosome formation requires the Wiskott-Aldrich syndrome protein (WASP), which is a prod

142 hat branching occurs when Arp2/3 is bound to Wiskott-Aldrich syndrome protein (WASP), which is in tur

143 Here we show that deficiency of Wiskott-Aldrich syndrome protein (WASp), which signals t

144 edly reduced in macrophages deficient in the Wiskott-Aldrich syndrome protein (WASP), which still con

145 WAVE1--the Wiskott-Aldrich syndrome protein (WASP)--family verproli

146 tients with the Wiskott-Aldrich syndrome and Wiskott-Aldrich syndrome protein (WASP)-deficient mice,

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

148 P) intracellular domain (AICD) downregulates Wiskott-Aldrich syndrome protein (WASP)-family verprolin

149 Wiskott-Aldrich syndrome protein (WASP)-homology domain

150 Here, we demonstrate that Wiskott-Aldrich syndrome protein (WASp)-interacting prot

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

152 recognize other motility proteins, like the Wiskott-Aldrich syndrome protein (WASP).

153 r of the actin cytoskeleton and activator of Wiskott-Aldrich syndrome protein (WASP).

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

155 ematopoietic-specific cytoskeletal regulator Wiskott-Aldrich syndrome protein (WASP).

156 lex by the actin nucleation-promoting factor Wiskott-Aldrich Syndrome protein (WASp).

157 inase (ACK), p21-activated kinase (PAK), and Wiskott-Aldrich syndrome protein (WASP).

158 inhibit the ability of Nwk-SH3a to activate Wiskott-Aldrich syndrome protein (WASp)/actin related pr

159 mparable to podosomes in the localization of Wiskott-Aldrich syndrome protein (WASP)/matrix metallopr

160 Nucleation-promoting factors (NPFs) of the Wiskott-Aldrich syndrome protein (WASP)/Scar family are

161 lex must bind ATP, protein activators [e.g., Wiskott-Aldrich syndrome protein (WASp)], and the side o

162 Wiskott-Aldrich syndrome protein (WASPs) control actin d

163 /3 complex activation domain (WCA) of Las17 (Wiskott-Aldrich syndrome protein [WASp] homologue) fused

164 ngagement increases actin polymerization and Wiskott-Aldrich syndrome protein activation in a Btk-dep

165 achment but inhibits ingestion by decreasing Wiskott-Aldrich syndrome protein activation, and hence a

166 Fusion of macrophages deficient in Wiskott-Aldrich syndrome protein and Cdc42, key molecule

167 contractility, independent of its effects on Wiskott-Aldrich syndrome protein and p21-activated kinas

168 t complex and the endosomal Arp2/3 activator Wiskott-Aldrich syndrome protein and Scar homolog (WASH)

169 lled strumpellin, is a core component of the Wiskott-Aldrich syndrome protein and SCAR homolog (WASH)

170 l. and Gomez and Billadeau reveal that WASH (Wiskott-Aldrich syndrome protein and SCAR homolog) activ

171 WASH (Wiskott-Aldrich Syndrome Protein and SCAR Homolog) is an

172 Wiskott-Aldrich syndrome protein and SCAR homologue (WAS

173 The Arp2/3-activator Wiskott-Aldrich syndrome protein and Scar homologue (WAS

174 FAM21, which also binds retromer, within the Wiskott-Aldrich syndrome protein and SCAR homologue (WAS

175 w that the COMMD/CCDC22/CCDC93 (CCC) and the Wiskott-Aldrich syndrome protein and SCAR homologue (WAS

176 JIPs are recruited by Wiskott-Aldrich syndrome protein and scar homologue (WAS

177 ptor that replaces toca-1 to mobilize neural Wiskott-Aldrich syndrome protein and the Arp2/3 complex.

178 Mutations of the Wiskott-Aldrich syndrome protein can result in highly va

179 ely in hematopoietic stem cells, and because Wiskott-Aldrich syndrome protein exerts a strong selecti

180 The scaffolding protein WAVE-1 (Wiskott-Aldrich syndrome protein family member 1) direct

181 et breast cancer development and metastasis, Wiskott-Aldrich syndrome protein family member 3 (Wasf3)

182 Wiskott-Aldrich syndrome protein family verprolin homolo

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

184 NK cell function relies on Wiskott-Aldrich syndrome protein for filamentous actin (

185 Wiskott-Aldrich syndrome protein gene mutations result i

186 drich syndrome is caused by mutations of the Wiskott-Aldrich syndrome protein gene, which codes for a

187 he discovery of unique functional domains of Wiskott-Aldrich syndrome protein has been instrumental i

188 ress made in dissecting the functions of the Wiskott-Aldrich syndrome protein has direct implications

189 y relies on a cluster of three actin-binding Wiskott-Aldrich syndrome protein homology 2 (WH2) domain

190 g a proline-rich domain and an actin-binding Wiskott-Aldrich syndrome protein homology 2 (WH2) domain

191 despite having only a single G-actin-binding Wiskott-Aldrich syndrome protein Homology 2 (WH2) domain

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

193 autoregulatory domain (DAD) that resembles a Wiskott-Aldrich syndrome protein homology 2 (WH2) sequen

194 variable was the presence or absence of the Wiskott-Aldrich syndrome protein in the lymphoid cells f

195 Wiskott-Aldrich syndrome protein is a signaling molecule

196 Since Wiskott-Aldrich syndrome protein is expressed exclusivel

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

198 mphiphysin-RVS-domain protein Rvs167 and the Wiskott-Aldrich syndrome protein Las17 at the point of p

199 Neuronal Wiskott-Aldrich syndrome protein regulates TGF-beta1-med

200 WASH is an Arp2/3 activator of the Wiskott-Aldrich syndrome protein superfamily that functi

201 ASH is an endosomal protein belonging to the Wiskott-Aldrich syndrome protein superfamily that partic

202 ve studies of patients with mutations of the Wiskott-Aldrich syndrome protein unequivocally demonstra

203 The actin-modulating protein Wiskott-Aldrich syndrome protein verprolin homologous-1

204 The direct interaction of Skap2 with the Wiskott-Aldrich syndrome protein via its SH3 domain is c

205 ctin dynamics and Ag transport by activating Wiskott-Aldrich syndrome protein via Vav and phosphatidy

206 Finally, the Wiskott-Aldrich syndrome protein was shown to play an im

207 Neural Wiskott-Aldrich syndrome protein(N-Wasp) is an actin nuc

208 hat drive actin polymerization such as WASp (Wiskott-Aldrich syndrome protein) and HS1 (hematopoietic

209 mbly protein Las17 (a yeast homolog of human Wiskott-Aldrich syndrome protein) and participate in the

210 belson tyrosine kinase) and N-WASP (neuronal Wiskott-Aldrich Syndrome Protein) at the cell edge witho

211 for actin binding (profilin or the WH2 from Wiskott-Aldrich syndrome protein) decrease full-length I

212 EspF(U) potently activates the host WASP (Wiskott-Aldrich syndrome protein) family of actin-nuclea

213 proteins 2/3) complex is activated by WASP (Wiskott-Aldrich syndrome protein) family proteins to nuc

214 nucleation-promoting protein N-WASP (Neural Wiskott-Aldrich syndrome protein) is up-regulated in bre

215 n with the nucleation-promoting factor Wasp (Wiskott-Aldrich syndrome protein).

216 ctin dynamics through the Nck/N-WASp (neural Wiskott-Aldrich syndrome protein)/Arp2/3 pathway is esse

217 exists in a macromolecular complex with the Wiskott-Aldrich syndrome protein, an actin nucleation-pr

218 kott-Aldrich syndrome protein (WASP), neural Wiskott-Aldrich syndrome protein, and WASP-interacting p

219 cell division cycle 42, which, together with Wiskott-Aldrich syndrome protein, coordinates F-actin re

220 such as integrin beta1, cortactin, neuronal Wiskott-Aldrich syndrome protein, membrane type 1 metall

221 sion required actin polymerization, neuronal Wiskott-Aldrich syndrome protein, myosin II and Rho GTPa

222 the microtubule-organizing center, F-actin, Wiskott-Aldrich syndrome protein, nor proline rich tyros

223 became more tightly associated with neuronal Wiskott-Aldrich syndrome protein, promoting actin-relate

224 This includes Wiskott-Aldrich syndrome protein, Wiskott-Aldrich syndro

225 Studies of Wiskott-Aldrich syndrome protein-deficient cell lines an

226 Wiskott-Aldrich syndrome protein-deficient neutrophils a

227 ition, Arp3-silenced cells expressing neural Wiskott-Aldrich syndrome protein-derived peptides that i

228 The Wiskott-Aldrich syndrome protein-family verprolin-homolo

229 Further, CYFIP2 is part of the Wiskott-Aldrich syndrome protein-family verprolin-homolo

230 s includes Wiskott-Aldrich syndrome protein, Wiskott-Aldrich syndrome protein-interacting protein, co

231 fining mechanisms that control activation of Wiskott-Aldrich syndrome protein.

232 se 1, Grb2-associated protein 2 (Grap2), and Wiskott-Aldrich syndrome protein.

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

234 e cytoskeleton by binding and activating the Wiskott-Aldrich syndrome protein.

235 suring vector copy numbers and expression of Wiskott-Aldrich syndrome protein.

236 onse to signals that locally activate neural Wiskott-Aldrich-syndrome protein (N-WASP) and the Arp2/3

237 The Src family kinase Hck, Wiskott-Aldrich-syndrome protein, and phospholipase Cgam

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

239 ycolactone-mediated activation of neural (N) Wiskott-Aldrich syndrome proteins (WASP) induces defects

240 Wiskott-Aldrich syndrome proteins (WASPs), the prototypi

241 to which we apply these ideas is that of the Wiskott-Aldrich Syndrome Proteins as activators of actin

242 cytoskeletal regulator WASP, mutated in the Wiskott-Aldrich syndrome, provides selective advantage f

243 The Wiskott-Aldrich syndrome-related protein WAVE2 promotes

244 The activity of the Wiskott-Aldrich syndrome-related WAVE3 protein is critic

245 m patients with X-linked thrombocytopenia or Wiskott-Aldrich syndrome, respectively.

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

247 Wiskott Aldrich syndrome (WAS) is caused by mutations in

248 Wiskott Aldrich syndrome (WAS), an X-linked immunodefici

249 ng in patients treated with gene therapy for Wiskott-Aldrich syndrome (WAS) and beta-hemoglobinopathi

250 nsitization in patients with food allergy or Wiskott-Aldrich syndrome (WAS) and defined whether spont

251 erious issue for all patients with classical Wiskott-Aldrich syndrome (WAS) and X-linked thrombocytop

252 Because Wiskott-Aldrich syndrome (WAS) and X-linked thrombocytop

253 Wiskott-Aldrich Syndrome (WAS) family proteins are Arp2/

254 Scar/WAVE proteins, members of the conserved Wiskott-Aldrich syndrome (WAS) family, promote actin pol

255 Patients with the immunodeficiency Wiskott-Aldrich syndrome (WAS) frequently develop system

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

257 dividuals with the X-linked immunodeficiency Wiskott-Aldrich syndrome (WAS) have opposite alterations

258 The Wiskott-Aldrich syndrome (WAS) interacting protein (WIP)

259 Wiskott-Aldrich syndrome (WAS) is a platelet/immunodefic

260 Wiskott-Aldrich syndrome (WAS) is a primary immunodefici

261 Wiskott-Aldrich syndrome (WAS) is a primary immunodefici

262 Wiskott-Aldrich syndrome (WAS) is a rare X-linked primar

263 Wiskott-Aldrich syndrome (WAS) is a severe X-linked immu

264 Wiskott-Aldrich syndrome (WAS) is an inherited immunodef

265 Wiskott-Aldrich syndrome (WAS) is an X-linked disease ca

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

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

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

269 Wiskott-Aldrich syndrome (WAS) is an X-linked primary im

270 Wiskott-Aldrich syndrome (WAS) is an X-linked primary im

271 Wiskott-Aldrich syndrome (WAS) is associated with mutati

272 Wiskott-Aldrich syndrome (WAS) is caused by loss-of-func

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

274 The Wiskott-Aldrich syndrome (WAS) is characterized by defec

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

276 sequences of immunodeficiency, patients with Wiskott-Aldrich syndrome (WAS) often suffer from poorly

277 al allospecific T-cell clones derived from a Wiskott-Aldrich syndrome (WAS) patient identified by flo

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

279 Mutations in Wiskott-Aldrich syndrome (WAS) protein (WASp), a regulat

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

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

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

283 y affected in macrophages from patients with Wiskott-Aldrich syndrome (WAS), an X chromosome-linked i

284 cordingly, hematolymphoid cancers develop in Wiskott-Aldrich syndrome (WAS), an X-linked primary immu

285 ng severe combined immune deficiency (SCID), Wiskott-Aldrich syndrome (WAS), and chronic granulomatou

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

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

288 f consanguineous parents, showed features of Wiskott-Aldrich syndrome (WAS), including recurrent infe

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

290 f a nationwide database of 160 patients with Wiskott-Aldrich syndrome (WAS), we identified a subset o

291 e precisely identify the B-cell phenotype in Wiskott-Aldrich syndrome (WAS), we used 3 distinct murin

292 Wiskott-Aldrich syndrome (WAS), X-linked thrombocytopeni

293 tions thereof contribute to the pathology of Wiskott-Aldrich syndrome (WAS).

294 ts with a genetic immunodeficiency disorder, Wiskott-Aldrich syndrome (WAS).

295 etic and immunologic symptoms reminiscent of Wiskott-Aldrich syndrome (WAS).

296 splantation was the only curative option for Wiskott-Aldrich syndrome (WAS).

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

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

299 an interim analysis of patients with severe Wiskott-Aldrich syndrome who received lentiviral vector-

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