ライフサイエンスコーパス: WASP

1 WASP and WAVE also colocalize to dynamic signaling struc

2 WASP CRIB mutants are no longer able to restrict Rac act

3 WASP depletion from human neutrophils confirms that both

4 WASP exerts its effects on actin dynamics through a mult

5 WASP homolog associated with actin, membranes, and micro

6 WASP recruits actin monomers to the complex and stimulat

7 WASP's Cdc42 and Rac interacting binding ("CRIB") motif

8 WASP-33b displays a large heat differential between its

9 WASP-deficient animals displayed an adjuvant-free IgE-se

10 WASP-deficient lymphoma showed increased mitogen-activat

11 WASP-family proteins are known to promote assembly of br

12 ed action of two regulatory sequences: (i) a WASP homology 2 (WH2) domain that binds actin, and (ii)

13 Specimens from 3 sites were processed on a WASP instrument (Copan) and incubated on the WASPLab pla

14 formin cooperates with profilin and Spire, a WASP homology domain 2 (WH2) repeat protein, to stimulat

15 Accordingly, WASP inhibition reverses the elevated F-actin content, f

16 s [7], creating seed filaments that activate WASP-bound Arp2/3 complex [8].

17 Upon BCR activation, WASP is activated first, followed by N-WASP in mouse and

18 Following T-cell activation, WASP is degraded, leading to cytoskeletal unraveling and

19 During activation, WASP limits nucleation rates by releasing slowly from na

20 , chemical inhibition of Rac does not affect WASP localization or activation at sites of endocytosis.

21 lastic lymphoma kinase-positive (ALK+) ALCL, WASP and WIP expression is regulated by ALK oncogenic ac

22 inear filament nucleation in cells; although WASP must be released for nucleation, Dip1 stays associa

23 thways include endocytosis through SID-3 and WASP; a uridylyltransferase that destabilizes viral RNAs

24 ymerization upstream of the WAVE complex and WASP, respectively.

25 key biochemical difference between Dip1 and WASP that may limit linear filament nucleation in cells;

26 ctors (NEPFs) such as Ena/VASP, formins, and WASP-family proteins recruit profilin:actin for filament

27 s, the interaction between small GTPases and WASP is more complex than previously thought-Rac regulat

28 Our studies also show that Hck and WASP are required for passage through a dense three-dime

29 We use structure-based mutations and WASP-Arp fusion chimeras to determine how WASP stimulate

30 Our data show that Nck and WASP form a clutch between LAT condensates and actin in

31 aration of LAT, Grb2, Sos1, SLP-76, Nck, and WASP.

32 results uncover a novel role for PSTPIP1 and WASP in orchestrating different types of actin-based pro

33 out to show that cells lacking both SCAR and WASP are unable to grow, make pseudopods or, unexpectedl

34 Loss of SCAR and WASP causes excessive dDia2 activity, maintaining F-acti

35 Wiskott-Aldrich syndrome protein (WASP) and WASP family verprolin-homologous 2 (WAVE2) proteins are

36 Wiskott-Aldrich Syndrome protein (WASP) and WASP-interacting-protein (WIP) regulate T cell antigen r

37 nucleation promoting factors (NPFs) such as WASP, plays an important role in many actin-mediated cel

38 Our data indicate that synergy between WASP proteins and cortactin may play a general role in a

39 g a proline-rich domain and an actin-binding WASP-Homology 2 domain.

40 ated a double conditional mouse lacking both WASP and N-WASP selectively in B lymphocytes (B/DcKO).

41 eals a clear trend: only organisms with both WASP and SCAR/WAVE-activators of branched actin assembly

42 ac regulates a subset of WASP functions, but WASP reciprocally restricts active Rac through its CRIB

43 elated proteins 2/3) complex is activated by WASP (Wiskott-Aldrich syndrome protein) family proteins

44 m discoideum, loss of SCAR is compensated by WASP moving to the leading edge to generate morphologica

45 al synaptic F-actin selectively generated by WASP in the form of distinct F-actin 'foci'.

46 The cross-linked complex is inhibited by WASP's CA region, even though CA potently stimulates cro

47 n our understanding of the events connecting WASP and calcium ion signaling.

48 BMMs and cells expressing phospho-deficient WASP have reduced ability to promote carcinoma cell inva

49 orrected HSPCs, expression of vector-derived WASP, improved T-cell function, antigen-specific respons

50 Here we describe WASP, a suite of tools for unbiased allele-specific read

51 d activities of Arp2/3 complex and different WASP/WAVE proteins.

52 This ensures WASP-activated Arp2/3 complex only nucleates branched ac

53 For example, WASP-33 is an A-type star with a temperature of about 7,

54 ations") for the highly irradiated exoplanet WASP-43b spanning three full planet rotations using the

55 and functional surrogate of mycolactone for WASP/N-WASP-dependent effects.

56 -linked Arp2/3 complex bypasses the need for WASP in activation and is more active than WASP-activate

57 nucleation but is a specific requirement for WASP-mediated activation.

58 Our results reveal a Treg-specific role for WASP that is required for prevention of Th2 effector cel

59 has been shown to drive pseudopod formation, WASP's role in this process is controversial.

60 tactin has structural features distinct from WASP acidic regions (A) that are required for synergy be

61 thermal spectrum for the ultrahot gas giant WASP-121b, which has an equilibrium temperature of appro

62 ation than that observed in mice with global WASP deficiency, indicating that allergic responses to f

63 reover, Nef points out podosomes and the Hck/WASP signaling pathway as good candidates to control tis

64 ure binding N-WASP and hematopoietic homolog WASP, where the number and configuration of hydroxyl gro

65 nd WASP-Arp fusion chimeras to determine how WASP stimulates movement toward the short-pitch conforma

66 However, WASP without a functional CRIB domain localizes normally

67 ALK+ lymphomas were accelerated in WASP- and WIP-deficient mice.

68 nd determine the biochemical requirements in WASP proteins for synergy.

69 ix-protein WASP/Myosin complex that includes WASP, class I myosins (Myo3 and Myo5), WIP (Vrp1), and t

70 ppressed by Bruton's tyrosine kinase-induced WASP activation, and is restored by the activation of SH

71 taining inositol 5-phosphatase that inhibits WASP activation.

72 nt with a role for this pathway in invasion, WASP(-/-) BMMs do not invade into tumor spheroids with t

73 Dictyostelium cells lacking WASP inappropriately activate Rac at the rear, which aff

74 ever, the specific tyrosine kinase mediating WASP phosphorylation is still unclear.

75 Finally, we demonstrate that multiple WASP family proteins synergistically activate Arp2/3 com

76 N-WASP constructs with and without the native polyproline

77 N-WASP depletion increased the width of cell-cell junction

78 N-WASP was not present at cell-cell junctions in monolayer

79 N-WASP-depleted cells do not recognize lysophosphatidic ac

80 In addition to activating Arp2/3, N-WASP binds actin-filament barbed ends, and both N-WASP a

81 er proteins can bind and possibly activate N-WASP, but it remains unclear how such binding events rel

82 eptide motifs that allosterically activate N-WASP, leading to localized actin nucleation on cellular

83 42guanosine triphosphate and SNX9 activate N-WASP-WIP- and Arp2/3-mediated actin nucleation.

84 hermore, contractile stimulation activated N-WASP in live smooth muscle cells as evidenced by changes

85 resonance energy transfer efficiency of an N-WASP sensor.

86 oteins c-Abl (Abelson tyrosine kinase) and N-WASP (neuronal Wiskott-Aldrich Syndrome Protein) at the

87 Colocalization of endothelial actin and N-WASP at sites of C. parapsilosis internalization was obs

88 r, our data support a model where IcsA and N-WASP form a tight complex releasing the N-WASP VCA domai

89 er an interaction of Nck with both WIP and N-WASP is required for their recruitment to vaccinia durin

90 whereas F-actin assembly factors Dia2 and N-WASP reside on phosphoinositide-rich membranes for longe

91 le conditional mouse lacking both WASP and N-WASP selectively in B lymphocytes (B/DcKO).

92 e also identify Cdc42 effectors Pak2/4 and N-WASP, as well as the actomyosin machinery, to be crucial

93 ates cell migration by affecting Pfn-1 and N-WASP, but not pVASP, cortactin and focal adhesions.

94 ocalized Src homology 3 (SH3) adapters and N-WASP, resulting in the assembly of dynamic actin network

95 Unlike profilin, cofilin, Dia2, and N-WASP, they do not require high "stimulus-responsive" pho

96 volved in metastasis, namely RhoA-ROCK and N-WASP.

97 hrin and its cytoplasmic partners, Nck and N-WASP.

98 hrough influences from both E-cadherin and N-WASP.

99 tream factors, including FBP17, Cdc42, and N-WASP.

100 We found that basic regions of Nck and N-WASP/WASP promote association and co-movement of LAT con

101 ctin nucleation-promoting factors, such as N-WASP and WAVE2, as well as isolated WH2 domains, includi

102 otein recruits cytosolic effectors such as N-WASP that induce localized actin polymerization.

103 catenin, but increased association between N-WASP and VE-cadherin, suggesting a role for N-WASP in pr

104 rn chain was the minimal structure binding N-WASP and hematopoietic homolog WASP, where the number an

105 ion by N-WASP-Y256F overexpression blocked N-WASP effects in P aeruginosa-induced actin stress fiber

106 binds actin-filament barbed ends, and both N-WASP and barbed ends are tightly clustered in these inva

107 nly partially reduces MRTF-A activation by N-WASP and WAVE2.

108 tion, WASP is activated first, followed by N-WASP in mouse and human primary B cells.

109 of branched Arp2/3-mediated nucleation by N-WASP overexpression caused loss of the typical actin com

110 hibition of N-WASP-Y256 phosphorylation by N-WASP-Y256F overexpression blocked N-WASP effects in P ae

111 e fine tuning of p53-induced senescence by N-WASP.

112 ilament imaging to determine how clustered N-WASP affects Arp2/3-independent barbed-end assembly.

113 In vivo, compared with controls, N-WASP down-regulation increases survival and prevents lun

114 (ABPs), including profilin, cofilin, Dia2, N-WASP, ezrin, and moesin, but the underlying molecular me

115 ial actin-based motility by downregulating N-WASP.

116 inly by Cdc42 and its downstream effectors N-WASP and PAK3, although DOCK10 is also able to activate

117 uits the actin nucleation-promoting factor N-WASP to tight junctions.

118 e Wiskott-Aldrich syndrome protein family, N-WASP.

119 ASP and VE-cadherin, suggesting a role for N-WASP in promoting P aeruginosa-induced adherens junction

120 ether, our results reveal a novel role for N-WASP in remodeling EC junctions, which is critical for m

121 ts show that the Cdc42-binding domain from N-WASP is able to displace TOCA1 HR1 from Cdc42, whereas t

122 Furthermore, N-WASP down-regulation blocked TGF-beta1 activation mediat

123 lamentous actin, involving ATP hydrolysis, N-WASP and formin, mediates Omega-profile merging by provi

124 s to a loss of Cdc42 activation, impairing N-WASP-driven Arp2/3-mediated actin polymerization.

125 ion of the senescence marker, p16Ink4a, in N-WASP-deficient epidermis.

126 nescence, was not significantly altered in N-WASP-null keratinocytes.

127 Increased N-WASP-Y256 phosphorylation promotes N-WASP and integrin a

128 P aeruginosa increased N-WASP-Y256 phosphorylation, which required the activation

129 Mechanistically, N-WASP regulated senescence by preventing p53-dependent de

130 RP2/3) actin polymerization complex member N-WASP.

131 e actin polymerization-promoting molecule, N-WASP, display cyclic hair loss and skin inflammation.

132 ase occurs because LLPS of the Nephrin-Nck-N-WASP signaling pathway on lipid bilayers increases membr

133 monstrate that proteins in the nephrin/Nck/N-WASP actin-regulatory pathway cluster into micron-scale

134 ns of Nck enhances phase separation of Nck/N-WASP/nephrin assemblies.

135 We propose that this novel N-WASP assembly activity provides an Arp2/3-independent fo

136 weak NPF, can displace a more potent NPF, N-WASP, from nascent branch junctions to synergistically a

137 in the interactions of two mammalian NPFs, N-WASP and WAVE2, with Arp2/3 complex.

138 s of this interaction and the mechanism of N-WASP activation remain poorly understood.

139 a novel role for Pak in the regulation of N-WASP activation, actin dynamics and cell contractility.

140 bilayers increases membrane dwell time of N-WASP and Arp2/3 complex, consequently increasing actin a

141 podosome, TH12 precedes the recruitment of N-WASP and Arp2/3 in the initial phase of podosome formati

142 ain and the GTPase binding domain (GBD) of N-WASP and no binding to the verprolin homology/cofilin/ac

143 h density and turnover similar to those of N-WASP in Nck comets, did not reconstitute dynamic, elonga

144 An inactive conformation of N-WASP is stabilized by intramolecular contacts between th

145 The activation of N-WASP is suppressed by Bruton's tyrosine kinase-induced W

146 Furthermore, loss of N-WASP reduces the diffusivity of CD19, a stimulatory co-r

147 Depletion of N-WASP resulted in an increase in transendothelial electri

148 F-beta1-induced phosphorylation of Y256 of N-WASP via activation of small Rho GTPase and focal adhesi

149 WASP coordinately with the associations of N-WASP with cortactin and actin.

150 eation-promoting factor (the VCA domain of N-WASP), with density and turnover similar to those of N-W

151 We studied the role of N-WASP, a key regulator of Arp2/3 complex and actin assemb

152 ading to recruitment of Nck, activation of N-WASP, and actin polymerization via the Arp2/3 complex.

153 sted, Nck was the most potent activator of N-WASP-driven actin assembly.

154 Inhibition of N-WASP-Y256 phosphorylation by N-WASP-Y256F overexpression

155 of IcsA bind to the WH1 and GBD domains of N-WASP.

156 erization of microtubules or inhibition of N-WASP.

157 ic fibroblasts (MEFs) lacking Nck, WIP, or N-WASP, we have investigated whether an interaction of Nck

158 trikingly different networks from WAVE2 or N-WASP, which comprised unexpectedly short filaments.

159 dimerized VCA regions of WAVE1, WAVE2, or N-WASP.

160 This pathway collaborated with other N-WASP-independent, senescence-promoting signaling downstr

161 Moreover, primary N-WASP-null keratinocytes displayed a premature senescence

162 WRC depletion promoted N-WASP/Arp2/3 complex activation and recruitment to leadin

163 eased N-WASP-Y256 phosphorylation promotes N-WASP and integrin alphaVbeta6 association as well as TGF

164 he BIN1 isoform BIN1+13+17, which promotes N-WASP-dependent actin polymerization to stabilize the T-t

165 neuronal Wiskott-Aldrich syndrome protein (N-WASP) activation, actin polymerization and contraction i

166 neuronal Wiskott-Aldrich syndrome protein (N-WASP) and an SH2 domain that binds to multiple phosphoty

167 e neural Wiskott-Aldrich-syndrome protein (N-WASP) and the Arp2/3 complex.

168 Neuronal Wiskott-Aldrich syndrome protein (N-WASP) has an essential role in actin structure dynamics.

169 neuronal Wiskott Aldrich syndrome protein (N-WASP) in modulating P aeruginosa-induced vascular permea

170 s neural Wiskott-Aldrich syndrome protein (N-WASP), cortactin, and ARP2/3 subunits.

171 Neuronal Wiskott-Aldrich syndrome protein (N-WASP)-activated actin polymerization drives extension of

172 neuronal Wiskott-Aldrich syndrome protein (N-WASP).

173 es through balanced activation of the Rac1/N-WASP/Arp2/3 and Rho/formins pathways.

174 dium assembly, whereas WICH/WIRE regulates N-WASP activation to control invadopodium maturation and d

175 A, which recruits the host actin regulator N-WASP.

176 acute inhibition of the Arp2/3 regulator, N-WASP, which is associated with enhanced signaling, incre

177 in the phase-separated clusters, rendering N-WASP and Arp2/3 activity stoichiometry dependent.

178 lthough it is clear that Shigella requires N-WASP for this process, the molecular details of this int

179 th cadherin at the apical ZA also requires N-WASP.

180 Collectively, these data reveal N-WASP as an inhibitor of p53-induced senescence, which mi

181 B-cell-specific N-WASP gene deletion causes enhanced and prolonged BCR sig

182 thin a single cortactin molecule, but that N-WASP antagonizes cortactin-mediated bundling.

183 hese cell monolayers, we demonstrated that N-WASP down-regulation by short hairpin RNA prevented TGF-

184 lar epithelial cells, we demonstrated that N-WASP downregulation attenuated P aeruginosa-induced acti

185 We show that N-WASP drives pancreatic cancer metastasis, with roles in

186 These results demonstrate that N-WASP expression in B lymphocytes is required for the dev

187 wiskostatin, we further demonstrated that N-WASP is required for localized F-actin polymerization, G

188 We hypothesized that N-WASP plays a critical role in these TGF-beta1-induced re

189 Our data indicate that N-WASP plays a crucial role in the development of TGF-beta

190 Together, our data demonstrate that N-WASP plays an essential role in P aeruginosa-induced vas

191 We report that N-WASP regulates endothelial monolayer integrity by affect

192 These findings demonstrate that N-WASP regulates p53-dependent senescence in keratinocytes

193 the senescence phenotype, indicating that N-WASP was an inhibitor of p53-induced senescence.

194 of the ARP2/3 complex by expression of the N-WASP (V)CA domain or application of two ARP2/3 inhibitor

195 displace TOCA1 HR1 from Cdc42, whereas the N-WASP domain but not the TOCA1 HR1 domain inhibits actin

196 contrast to the nanomolar affinity of the N-WASP G protein-binding region for Cdc42.

197 al virulence factors, directly engages the N-WASP GBD and competes with VCA binding.

198 Using the N-WASP inhibitor wiskostatin, we further demonstrated that

199 N-WASP form a tight complex releasing the N-WASP VCA domain to recruit the host cell machinery for a

200 maging approaches, we demonstrate that the N-WASP-interactors WIP and WICH/WIRE play non-redundant ro

201 ectors facilitate a handover from TOCA1 to N-WASP, which can then drive recruitment of the actin-modi

202 g cascade and connecting PAK1 signaling to N-WASP-cortactin-mediated actin polymerization and GLUT4 v

203 of the cytoplasmic domain of p14 triggers N-WASP-mediated assembly of a branched actin network.

204 In vivo, N-WASP knockdown attenuated the development of pulmonary e

205 Neural WASP (N-WASP) is a broadly expressed homolog of WASP, and regula

206 molecule imaging revealed that unlike WASP/N-WASP, cortactin remains bound to junctions during nuclea

207 nctional surrogate of mycolactone for WASP/N-WASP-dependent effects.

208 We describe a signaling loop whereby N-WASP and the endocytic adapter SNX18 promote lysophospha

209 This leads to recruitment of the Nck-WIP-N-WASP complex that triggers Arp2/3-dependent actin polyme

210 of Nck are not required to recruit the WIP:N-WASP complex but are essential to stimulate actin assemb

211 of focal adhesion components together with N-WASP and Arp2/3 complex at leading invasive edges in 3D.

212 WIP interacts with N-WASP and cortactin and is essential for invadopodium ass

213 ylation and increases its association with N-WASP coordinately with the associations of N-WASP with c

214 We use nanofibers coated with N-WASP WWCA domains as model cell surfaces and single-acti

215 vertebrate poxviruses by interacting with N-WASP/WASP.

216 Neural WASP (N-WASP) is a broadly expressed homolog of WASP, an

217 In the absence of WASP, active GTP-bound CDC42 was increased and the genet

218 The activation of WASP constitutes a key pathway for actin filament nuclea

219 mimicked the natural toxin for activation of WASP in vitro and induced comparable alterations of epit

220 ical role played by Arp2/3 as an effector of WASP-mediated control over actin polymerization, mutatio

221 Here we show that the expression of WASP and WIP is frequently low or absent in anaplastic l

222 The fraction of WASP-positive lymphocytes increased from a median of 3.9

223 ation is the critical activating function of WASP and that monomer delivery is not a fundamental requ

224 P (N-WASP) is a broadly expressed homolog of WASP, and regulates B-cell signaling by modulating B-cel

225 upled to accumulation of threshold levels of WASP and WIP, but not to recruitment kinetics or release

226 to food allergens are dependent upon loss of WASP expression in this immune compartment.

227 Loss of WASP was phenotypically associated with increased GATA3

228 ts indicate that tyrosine phosphorylation of WASP by Hck is required for proper macrophage functions.

229 suggesting that tyrosine phosphorylation of WASP by Hck may play a role in tissue infiltration of ma

230 demonstrate that tyrosine phosphorylation of WASP in response to stimulation with CX3CL1 or via Fcgam

231 Moreover, retention of WASP together with SCAR correctly predicts alpha-motilit

232 previously thought-Rac regulates a subset of WASP functions, but WASP reciprocally restricts active R

233 t attachment studies are used to parametrize WASP for simulation of MWCNTs transport in Brier Creek,

234 In particular, WASP phosphorylation was primarily mediated by the p61 i

235 ed in leukocytes, can tyrosine phosphorylate WASP and regulates WASP-mediated macrophage functions.

236 in the atmosphere of the hot-Jupiter planet WASP-19b.

237 h hosts the hottest known transiting planet, WASP-33b; the planet is itself as hot as a red dwarf sta

238 Platelet WASP deficiency accelerates random consumption, and a tr

239 cted using the Walk-Away specimen processor (WASP).

240 blish that the Wiskott-Aldrich gene product (WASP) serves an essential role in T regulatory cells to

241 n Water Quality Analysis Simulation Program (WASP) was updated to incorporate particle collision rate

242 s triggered and coordinated by a six-protein WASP/Myosin complex that includes WASP, class I myosins

243 ucleation, Wiskott-Aldrich syndrome protein (WASP) and WASP family verprolin-homologous 2 (WAVE2) pro

244 cytes, the Wiskott-Aldrich Syndrome protein (WASP) and WASP-interacting-protein (WIP) regulate T cell

245 nd impairs Wiskott-Aldrich syndrome protein (WASP) binding, but it does not affect interaction with p

246 ing factor Wiskott-Aldrich syndrome protein (WASP) contributes to maintenance of front-rear polarity

247 Wiscott Aldrich Syndrome protein (WASP) deficiency results in defects in calcium ion signa

248 or absent Wiskott-Aldrich syndrome protein (WASP) expression or a Zhu clinical score of 3 or higher.

249 Wiskott-Aldrich syndrome protein (WASP) family verprolin homologous protein 1 (WAVE1) regu

250 ylation of Wiskott-Aldrich syndrome protein (WASP) is important for diverse macrophage functions incl

251 se Hck and Wiskott-Aldrich syndrome protein (WASP), 2 major regulators of podosomes.

252 ons in the Wiskott-Aldrich syndrome protein (WASP), a key regulator of actin dynamics.

253 actin via Wiskott-Aldrich syndrome protein (WASP), and contraction of the resultant actin filaments

254 nregulates Wiskott-Aldrich syndrome protein (WASP)-family verprolin homologous protein 1 (WAVE1 or WA

255 (PAK), and Wiskott-Aldrich syndrome protein (WASP).

256 ve revealed a critical role for WAS protein (WASP) expression in B lymphocytes in the maintenance of

257 patients and mice deficient in WAS protein (WASP) frequently develop IgE-mediated reactions to commo

258 eural (N) Wiskott-Aldrich syndrome proteins (WASP) induces defects in cell adhesion underpinning cyto

259 Wiskott-Aldrich syndrome proteins (WASPs), the prototypical Arp2/3 complex activators, acti

260 consumption, and a trans effect of recipient WASP deficiency contributes to this.

261 Consistent with reduced WASP tyrosine phosphorylation, phagocytosis, chemotaxis,

262 an tyrosine phosphorylate WASP and regulates WASP-mediated macrophage functions.

263 rf, and Rab G-protein families in regulating WASP homologue associated with actin, membranes, and mic

264 od driver suppressor of cAR mutations (SCAR)/WASP and verprolin homologue (WAVE) is not recruited to

265 This work shows that SCAR, WASP, and dDia2 compete for actin.

266 Pseudopods are replaced in double SCAR/WASP mutants by aberrant filopods, induced by the formin

267 imulates cross-linking, suggesting that slow WASP detachment masks the activating potential of the sh

268 When clustered on a surface, WASP-family proteins can drive branched actin networks t

269 ocomotion and endocytosis, membrane-tethered WASP proteins stimulate actin filament nucleation by the

270 r WASP in activation and is more active than WASP-activated Arp2/3 complex.

271 velengths shorter than 91.2 nanometres) than WASP-33b, leading to a predicted range of mass-loss rate

272 We conclude that WASP generates a dynamic F-actin architecture in the con

273 Our findings demonstrate that WASP and WIP are tumor suppressors in T cell lymphoma an

274 encing (ChIP-seq) reads, we demonstrate that WASP has a low error rate and is far more powerful than

275 These studies provide evidence that WASP and WIP play central roles in establishment of a ro

276 Our data indicate that WASP displaces the autoinhibitory Arp3 C-terminal tail f

277 rk expands the number of critical roles that WASP-family proteins play in the assembly of branched ac

278 Here, we show that WASP-family proteins also function as polymerases that a

279 d actin-related protein 2/3 (Arp2/3) and the WASP-family verprolin homologous protein (WAVE) complex,

280 ing of the IcsA passenger domain to both the WASP homology 1 (WH1) domain and the GTPase binding doma

281 omplex and several proteins that compose the WASP/myosin complex generates the force necessary to def

282 ered covalent cross-link to determine if the WASP-induced conformational change is sufficient for act

283 ion by nucleation-promoting factors like the WASP/WAVE family, followed by remodeling of actin networ

284 nding to nucleation-promoting factors of the WASP and WAVE families was previously thought to be suff

285 its interaction with WAVE2, a member of the WASP family of cytoskeletal regulatory proteins required

286 ed to identify Abi1, a core component of the WASP-family verprolin homologous protein (WAVE) regulato

287 This engineered protein reveals that the WASP/Myosin complex has four essential activities: recru

288 tethering the branched actin network to the WASP-family proteins that create it.

289 pto B chromogenic medium (ChromID) using the WASP automated processor.

290 d onto CPSE agar with a 1-mul loop using the WASP.

291 Thus, WASP and the WAVE complex direct the formation of branch

292 fore need to limit Dip1 activity relative to WASP to preserve the dendritic nature of actin networks,

293 Single-molecule imaging revealed that unlike WASP/N-WASP, cortactin remains bound to junctions during

294 tionarily conserved recruitment of the WASH (WASP and SCAR homolog) complex to both macropinosomes an

295 ll levels of Rac activity also increase when WASP is unable to bind to Rac.

296 Yet, when WASP function is eliminated there is negligible effect o

297 .6) at 12 months after gene therapy, whereas WASP-positive platelets increased from 19.1% (range 4.1-

298 omplex activation and the mechanism by which WASP stimulates the conformational change have been unkn

299 active state, providing a mechanism by which WASP stimulates the short-pitch conformation and activat

300 While WASP-deficient Tregs efficiently contained Th1- and Th17

301 o show that Dip1 causes actin assembled with WASP and Arp2/3 complex to form disconnected networks wi