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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 bute significantly to the immunopathology of Wiskott-Aldrich Syndrome.
7 nce contributes to the bleeding diathesis of Wiskott-Aldrich syndrome.
8 of the use of gene therapy in patients with Wiskott-Aldrich syndrome.
10 We have focused on a murine model of the Wiskott-Aldrich syndrome, an immunodeficiency in which a
11 uccessfully used to treat conditions such as Wiskott-Aldrich syndrome and chronic granulomatous disea
12 ress in understanding the molecular basis of Wiskott-Aldrich syndrome and its ramifications for the c
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 forms of severe combined immune deficiency, Wiskott-Aldrich syndrome, and chronic granulomatous dise
17 for severe combined immunodeficiency (SCID), Wiskott-Aldrich syndrome, and chronic granulomatous dise
18 acute myelogenous leukemia, Paris-Trousseau, Wiskott-Aldrich syndrome, and the May-Hegglin, Sebastian
19 glycosylated IgA were found in patients with Wiskott-Aldrich syndrome, and these abnormal antibodies
20 with human immunodeficiency virus infection, Wiskott-Aldrich syndrome, and vasculopathy with capillar
21 In this issue of the JCI, Lexmond et al. use Wiskott-Aldrich syndrome as a model disease and establis
27 ne defects that result from mutations in the Wiskott-Aldrich syndrome gene (WAS), which have a broad
29 logical disorder associated with compromised Wiskott-Aldrich Syndrome Interacting Protein (WIP) funct
32 nfused in 7 consecutive patients with severe Wiskott-Aldrich syndrome lacking HLA antigen-matched rel
33 protein (N-WASP), the ubiquitously expressed Wiskott-Aldrich syndrome-like (WASL) protein, in mouse s
35 at monocytes/macrophages from WASP-deficient Wiskott-Aldrich syndrome patients are severely defective
37 ified up to 4 years after transplant in four Wiskott-Aldrich syndrome patients treated with HSPC gene
38 me platelets, which lack alpha-granules, and Wiskott-Aldrich syndrome platelets, which have cytoskele
39 utoimmune disorders in patients with classic Wiskott-Aldrich syndrome, possibly caused by immune dysr
41 as the levels of F-actin and phosphorylated Wiskott Aldrich syndrome protein, an actin nucleation pr
43 tein c-Abl interactor 1 (Abi1) with neuronal Wiskott-Aldrich syndrome protein (N-WASP) (an actin-regu
44 complex was necessary for cdc42 and neuronal Wiskott-Aldrich syndrome protein (N-WASP) activation, ac
45 spatial and temporal regulation of neuronal Wiskott-Aldrich syndrome protein (N-WASP) activity in li
46 nts in the actin regulatory protein neuronal Wiskott-Aldrich syndrome protein (N-WASP) and an SH2 dom
47 474/1 leads to recruitment of Nck and neural Wiskott-Aldrich syndrome protein (N-WASP) and strong act
48 c42), the nucleation-promoting factor neural Wiskott-Aldrich syndrome protein (N-WASP) and the actin
49 zation is mediated by activation of neuronal Wiskott-Aldrich syndrome protein (N-WASp) and the Arp (a
50 iprotein compound containing CrkII, neuronal Wiskott-Aldrich Syndrome Protein (N-WASP) and the Arp2/3
51 gulators of actin cytoskeleton dynamics, the Wiskott-Aldrich syndrome protein (N-WASP) and the Arp2/3
52 ole of the actin nucleation promoters neural Wiskott-Aldrich syndrome protein (N-WASP) and WAVE2 in c
53 and Src family tyrosine kinases, and neural Wiskott-Aldrich syndrome protein (N-WASP) but not the Ar
54 indicates that the nuclear localized neural Wiskott-Aldrich syndrome protein (N-WASP) can induce de
56 we showed that S. flexneri relies on neural Wiskott-Aldrich Syndrome protein (N-WASP) in HT-29 cells
57 f hyaluronan (HA) and CD44 with the neuronal Wiskott-Aldrich syndrome protein (N-WASP) in regulating
58 f the actin-regulatory protein called neural Wiskott-Aldrich syndrome protein (N-WASP) interacting wi
62 er suggests that the actin-regulatory neural Wiskott-Aldrich syndrome protein (N-WASP) mediates the e
64 actin nucleating endocytic protein neuronal Wiskott-Aldrich syndrome protein (N-WASP) to facilitate
65 n activation of the Arp2/3 complex by neural Wiskott-Aldrich Syndrome protein (N-WASP) via Grb2 and N
67 -mediated EGFR signaling up-regulated neural Wiskott-Aldrich syndrome protein (N-WASP), an actin nucl
68 ched in actin-related protein 3 and neuronal Wiskott-Aldrich syndrome protein (N-WASP), and their ass
69 in-binding and -polymerizing proteins neural Wiskott-Aldrich syndrome protein (N-WASP), cortactin, an
70 ockout approach to assess the role of neural Wiskott-Aldrich syndrome protein (N-WASP), the ubiquitou
71 s, we have analysed the dynamics of neuronal Wiskott-Aldrich syndrome protein (N-WASP), WASP-interact
73 nce microscopy, we demonstrate that neuronal Wiskott-Aldrich syndrome protein (N-WASP), which is coex
75 M. avium led to the recruitment of neuronal Wiskott-Aldrich syndrome protein (N-WASp), which was not
84 ctivation, when it is able to associate with Wiskott-Aldrich syndrome protein (WASp) and the actin fi
87 in polymerization through Arp2/3 nucleation, Wiskott-Aldrich syndrome protein (WASP) and WASP family
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
93 which are caused by WAS mutations affecting Wiskott-Aldrich syndrome protein (WASp) expression or ac
94 rimary immunodeficiency caused by absence of Wiskott-Aldrich syndrome protein (WASP) expression, resu
99 d by different human proteins, including the Wiskott-Aldrich syndrome protein (WASp) family members.
100 w that mycolactone operates by hijacking the Wiskott-Aldrich syndrome protein (WASP) family of actin-
102 , and acidic (VCA) region of proteins in the Wiskott-Aldrich syndrome protein (WASp) family, Arp2/3 c
106 WAS and XLT are caused by mutations of the Wiskott-Aldrich syndrome protein (WASP) gene which encod
108 No defects related to deficiency of the Wiskott-Aldrich Syndrome protein (WASp) have been descri
109 f formins, known filament nucleators use the Wiskott-Aldrich syndrome protein (WASP) homology 2 (WH2
120 previously that tyrosine phosphorylation of Wiskott-Aldrich syndrome protein (WASP) is important for
123 utation (Leu270Pro) in the gene encoding the Wiskott-Aldrich syndrome protein (WASp) resulting in an
125 fic mutations in the human gene encoding the Wiskott-Aldrich syndrome protein (WASp) that compromise
126 LN) is caused by activating mutations in the Wiskott-Aldrich syndrome protein (WASP) that result in a
127 Here we have used cells deficient in the Wiskott-Aldrich syndrome protein (WASp) to demonstrate t
128 etal dysfunction caused by deficiency of the Wiskott-Aldrich syndrome protein (WASp) to explore the c
129 r receptor-bound protein 2 (Grb2) and to the Wiskott-Aldrich syndrome protein (WASp) to form a hetero
131 ds through its BAR domain and interacts with Wiskott-Aldrich Syndrome Protein (WASP) via its SRC homo
132 roteins involved in actin dynamics including Wiskott-Aldrich syndrome protein (WASp) were regulated b
133 ed via the phagocyte-specific kinase Hck and Wiskott-Aldrich syndrome protein (WASP), 2 major regulat
134 we demonstrated that ACK1 phosphorylates the Wiskott-Aldrich syndrome protein (WASP), a Cdc42 effecto
135 s, develop in patients and mice deficient in Wiskott-Aldrich syndrome protein (WASP), a hematopoietic
136 tients bearing inactivating mutations in the Wiskott-Aldrich syndrome protein (WASP), a key regulator
137 onsisting of WASp-interacting protein (WIP), Wiskott-Aldrich syndrome protein (WASp), actin, and myos
138 f, required an activating factor such as the Wiskott-Aldrich syndrome protein (WASP), and might exhib
139 rcent of natural killer (NK) cells expressed Wiskott-Aldrich syndrome protein (WASP), and NK cells co
141 teractions with a wide network of molecules: Wiskott-Aldrich syndrome protein (WASp), Grb2, ribosomal
142 se pulldown analyses show Robo4 binding to a Wiskott-Aldrich syndrome protein (WASP), neural Wiskott-
143 we provide evidence that Kit signals through Wiskott-Aldrich syndrome protein (WASP), the central hem
144 e B (PhyB) and fused the Cdc42 effector, the Wiskott-Aldrich Syndrome Protein (WASP), to the light-de
147 hat branching occurs when Arp2/3 is bound to Wiskott-Aldrich syndrome protein (WASP), which is in tur
149 edly reduced in macrophages deficient in the Wiskott-Aldrich syndrome protein (WASP), which still con
151 tients with the Wiskott-Aldrich syndrome and Wiskott-Aldrich syndrome protein (WASP)-deficient mice,
154 P) intracellular domain (AICD) downregulates Wiskott-Aldrich syndrome protein (WASP)-family verprolin
157 s, where it was activated by p78/83, a viral Wiskott-Aldrich syndrome protein (WASP)-like protein.
165 inhibit the ability of Nwk-SH3a to activate Wiskott-Aldrich syndrome protein (WASp)/actin related pr
166 mparable to podosomes in the localization of Wiskott-Aldrich syndrome protein (WASP)/matrix metallopr
167 Nucleation-promoting factors (NPFs) of the Wiskott-Aldrich syndrome protein (WASP)/Scar family are
168 lex must bind ATP, protein activators [e.g., Wiskott-Aldrich syndrome protein (WASp)], and the side o
170 /3 complex activation domain (WCA) of Las17 (Wiskott-Aldrich syndrome protein [WASp] homologue) fused
171 ngagement increases actin polymerization and Wiskott-Aldrich syndrome protein activation in a Btk-dep
172 achment but inhibits ingestion by decreasing Wiskott-Aldrich syndrome protein activation, and hence a
173 contractility, independent of its effects on Wiskott-Aldrich syndrome protein and p21-activated kinas
174 t complex and the endosomal Arp2/3 activator Wiskott-Aldrich syndrome protein and Scar homolog (WASH)
175 l. and Gomez and Billadeau reveal that WASH (Wiskott-Aldrich syndrome protein and SCAR homolog) activ
179 FAM21, which also binds retromer, within the Wiskott-Aldrich syndrome protein and SCAR homologue (WAS
180 w that the COMMD/CCDC22/CCDC93 (CCC) and the Wiskott-Aldrich syndrome protein and SCAR homologue (WAS
182 dc42 may regulate the activation of neuronal Wiskott-Aldrich syndrome protein and the actin related p
183 ptor that replaces toca-1 to mobilize neural Wiskott-Aldrich syndrome protein and the Arp2/3 complex.
185 ely in hematopoietic stem cells, and because Wiskott-Aldrich syndrome protein exerts a strong selecti
186 Recombinant Arc40 bound the VCA domain of Wiskott-Aldrich syndrome protein family activators at a
192 drich syndrome is caused by mutations of the Wiskott-Aldrich syndrome protein gene, which codes for a
193 he discovery of unique functional domains of Wiskott-Aldrich syndrome protein has been instrumental i
194 ress made in dissecting the functions of the Wiskott-Aldrich syndrome protein has direct implications
195 g a proline-rich domain and an actin-binding Wiskott-Aldrich syndrome protein homology 2 (WH2) domain
196 y relies on a cluster of three actin-binding Wiskott-Aldrich syndrome protein homology 2 (WH2) domain
197 length short (SALS) is a recently identified Wiskott-Aldrich syndrome protein homology 2 (WH2) domain
198 despite having only a single G-actin-binding Wiskott-Aldrich syndrome protein Homology 2 (WH2) domain
199 autoregulatory domain (DAD) that resembles a Wiskott-Aldrich syndrome protein homology 2 (WH2) sequen
200 variable was the presence or absence of the Wiskott-Aldrich syndrome protein in the lymphoid cells f
204 mphiphysin-RVS-domain protein Rvs167 and the Wiskott-Aldrich syndrome protein Las17 at the point of p
205 ed that C. parvum activates the Cdc42/neural Wiskott-Aldrich syndrome protein network in host cells r
208 ve studies of patients with mutations of the Wiskott-Aldrich syndrome protein unequivocally demonstra
210 The direct interaction of Skap2 with the Wiskott-Aldrich syndrome protein via its SH3 domain is c
211 ctin dynamics and Ag transport by activating Wiskott-Aldrich syndrome protein via Vav and phosphatidy
213 hat drive actin polymerization such as WASp (Wiskott-Aldrich syndrome protein) and HS1 (hematopoietic
214 mbly protein Las17 (a yeast homolog of human Wiskott-Aldrich syndrome protein) and participate in the
215 for actin binding (profilin or the WH2 from Wiskott-Aldrich syndrome protein) decrease full-length I
216 EspF(U) potently activates the host WASP (Wiskott-Aldrich syndrome protein) family of actin-nuclea
217 proteins 2/3) complex is activated by WASP (Wiskott-Aldrich syndrome protein) family proteins to nuc
218 tant manner, bound actin monomer via a WASP (Wiskott-Aldrich syndrome protein) homology 2 domain, bou
219 nucleation-promoting protein N-WASP (Neural Wiskott-Aldrich syndrome protein) is up-regulated in bre
221 ctin dynamics through the Nck/N-WASp (neural Wiskott-Aldrich syndrome protein)/Arp2/3 pathway is esse
222 exists in a macromolecular complex with the Wiskott-Aldrich syndrome protein, an actin nucleation-pr
223 kott-Aldrich syndrome protein (WASP), neural Wiskott-Aldrich syndrome protein, and WASP-interacting p
224 cell division cycle 42, which, together with Wiskott-Aldrich syndrome protein, coordinates F-actin re
225 such as integrin beta1, cortactin, neuronal Wiskott-Aldrich syndrome protein, membrane type 1 metall
226 sion required actin polymerization, neuronal Wiskott-Aldrich syndrome protein, myosin II and Rho GTPa
227 the microtubule-organizing center, F-actin, Wiskott-Aldrich syndrome protein, nor proline rich tyros
228 became more tightly associated with neuronal Wiskott-Aldrich syndrome protein, promoting actin-relate
232 ition, Arp3-silenced cells expressing neural Wiskott-Aldrich syndrome protein-derived peptides that i
235 s includes Wiskott-Aldrich syndrome protein, Wiskott-Aldrich syndrome protein-interacting protein, co
242 onse to signals that locally activate neural Wiskott-Aldrich-syndrome protein (N-WASP) and the Arp2/3
245 ycolactone-mediated activation of neural (N) Wiskott-Aldrich syndrome proteins (WASP) induces defects
246 to which we apply these ideas is that of the Wiskott-Aldrich Syndrome Proteins as activators of actin
247 cytoskeletal regulator WASP, mutated in the Wiskott-Aldrich syndrome, provides selective advantage f
251 cluding common variable immunodeficiency and Wiskott-Aldrich syndrome, to explain the occurrence of a
254 nsitization in patients with food allergy or Wiskott-Aldrich syndrome (WAS) and defined whether spont
257 Scar/WAVE proteins, members of the conserved Wiskott-Aldrich syndrome (WAS) family, promote actin pol
260 dividuals with the X-linked immunodeficiency Wiskott-Aldrich syndrome (WAS) have opposite alterations
277 sequences of immunodeficiency, patients with Wiskott-Aldrich syndrome (WAS) often suffer from poorly
278 al allospecific T-cell clones derived from a Wiskott-Aldrich syndrome (WAS) patient identified by flo
279 ar density to be reduced on lymphocytes from Wiskott-Aldrich syndrome (WAS) patient, we find no such
282 all Rho GTPase Cdc42, known to interact with Wiskott-Aldrich syndrome (WAS) protein, is an important
283 rich syndrome gene (WAS) are responsible for Wiskott-Aldrich syndrome (WAS), a disease characterized
285 y affected in macrophages from patients with Wiskott-Aldrich syndrome (WAS), an X chromosome-linked i
286 ng severe combined immune deficiency (SCID), Wiskott-Aldrich syndrome (WAS), and chronic granulomatou
289 f consanguineous parents, showed features of Wiskott-Aldrich syndrome (WAS), including recurrent infe
290 ysis of the French Registry of patients with Wiskott-Aldrich Syndrome (WAS), Mahlaoui et al have iden
291 f a nationwide database of 160 patients with Wiskott-Aldrich syndrome (WAS), we identified a subset o
292 e precisely identify the B-cell phenotype in Wiskott-Aldrich syndrome (WAS), we used 3 distinct murin
300 tanding of the distinct clinical phenotypes (Wiskott-Aldrich syndrome/X-linked thrombocytopenia; inte
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