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 depletion from human neutrophils confirms that both

3 WASP exerts its effects on actin dynamics through a mult

4 WASP homolog associated with actin, membranes, and micro

5 WASP recruits actin monomers to the complex and stimulat

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

7 WASP-activated Arp2/3 complex assembles branched actin n

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

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

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

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

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

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

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

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

16 ration of profilin-actin for elongation, and WASP-homology 2 (WH2) domains recruit actin monomers for

17 s of Arp2/3 complex with mother filament and WASP are temporally coordinated with initiation of daugh

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

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

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

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

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

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

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

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

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

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

28 Nck also binds WASP-interacting protein (WIP), which inhibits the abili

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

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

31 provides a mechanism by which membrane-bound WASP proteins can stimulate network growth without restr

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

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

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

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

36 growth cannot occur until it is triggered by WASP release.

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

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

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

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

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

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

43 dent) and actin cortex network (as known for WASP and cortical actin) to reduce the work required for

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

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

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

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

48 The WAVE/SCAR (for WASP family verprolin homologous/suppressor of cyclic AM

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

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

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

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

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

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

55 Its mammalian homolog, WASP, has also been studied extensively as an activator

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

57 deling of the consumption of WT platelets in WASP(-) recipients, and vice versa.

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

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

60 t of activators of Arp2/3 complex, including WASP and myosin-I.

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

62 taining inositol 5-phosphatase that inhibits WASP activation.

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

64 in-binding and nucleation mechanism in Las17/WASP that is required for its function in actin regulati

65 ine domain of both yeast Las17 and mammalian WASP.

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

67 namic reorganization of the plasma membrane (WASP independent) and actin cortex network (as known for

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

69 iciency of CD8(+) T-cell responses in murine WASP deficiency, in which abrogated production of IFN-I

70 N-WASP also contains two Nck-binding sites, but its recrui

71 N-WASP constructs with and without the native polyproline

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

73 N-WASP has a crucial proinvasive role in driving Arp2/3 co

74 N-WASP must be dimerized for potent synergy, and targeted

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

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

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

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

79 42guanosine triphosphate and SNX9 activate N-WASP-WIP- and Arp2/3-mediated actin nucleation.

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

81 T) probe for N-WASP activity showed active N-WASP at sites of internalization for both live and heat-

82 e in N-WASP phosphorylation which affected N-WASP recruitment to the bacterial surface, decreased the

83 cleation inhibitor (cytochalasin D) and an N-WASP inhibitor (wiskostatin) both inhibited uptake of he

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

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

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

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

88 yeast during disseminated candidiasis, and N-WASP may play a key role in the process.

89 We discovered that WRC and N-WASP play opposing roles in 3D epithelial cell migration

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

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

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

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

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

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

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

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

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

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

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

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

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

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

107 The Arp2/3 complex, N-WASP, WAVE1, cortactin, and Cdc42 regulate the secondary

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

109 Cortactin, N-WASP, cofilin, and actin arrive together to form the inv

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

111 eted mutations indicate release of dimeric N-WASP from nascent branches limits nucleation.

112 opose a model in which cortactin displaces N-WASP from nascent branches as a prerequisite for nucleat

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

114 region of the nucleation-promoting factor N-WASP is not affected by GMF, whereas nucleation activate

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

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

117 resonance energy transfer (FRET) probe for N-WASP activity showed active N-WASP at sites of internali

118 er birth, suggesting an important role for N-WASP in maintaining foot processes.

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

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

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

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

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

124 le of various tyrosine kinases involved in N-WASP activation and uncovered a previously unappreciated

125 ed that Btk depletion led to a decrease in N-WASP phosphorylation which affected N-WASP recruitment t

126 down by lentivirus-mediated RNAi inhibited N-WASP activation, actin polymerization, and contraction i

127 Mice lacking N-WASP specifically in podocytes were born with normal kid

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

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

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

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

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

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

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

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

136 ctin, and Arp2 requires phosphorylation of N-WASP at the Tyr-256 residue by focal adhesion kinase.

137 In addition, inducing deletion of N-WASP in adult mice resulted in severe proteinuria and ki

138 We show that depletion of N-WASP in endothelial cells impaired AJ adhesion and favor

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

140 3 complex (Arp2/3), to address the role of N-WASP in regulating AJ stability and thereby endothelial

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

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

143 Expression of the VCA domain of N-WASP or phosphomimicking (Y256D)-N-WASP mutant in endoth

144 Finally, we showed that the levels of N-WASP phosphorylation and Btk expression were increased i

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

146 otein (WIP), which inhibits the ability of N-WASP to activate the Arp2/3 complex until it receives an

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

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

149 The interaction of N-WASP with p120-catenin, actin, and Arp2 requires phospho

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 ion were not affected, primary cultures of N-WASP-deficient podocytes revealed significant impairment

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

155 erization of microtubules or inhibition of N-WASP.

156 short interfering RNA-mediated ablation of N-WASP.

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

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

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

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

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

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

163 neuronal Wiskott-Aldrich syndrome protein (N-WASP) (an actin-regulatory protein) in smooth muscle cel

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

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

166 r neural Wiskott-Aldrich syndrome protein (N-WASP) and the actin nucleator the actin-related protein

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 n neural Wiskott-Aldrich Syndrome protein (N-WASP) in HT-29 cells.

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

171 f neural Wiskott-Aldrich syndrome protein (N-WASP), which induces actin polymerization through actin-

172 neuronal Wiskott-Aldrich syndrome protein (N-WASP), which is coexpressed with WASP in all immune cell

173 neuronal Wiskott-Aldrich syndrome protein (N-WASP), which promotes actin nucleation, is required to s

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

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

176 the Arp2/3 complex and associated proteins N-WASP, WAVE1, cortactin, and Cdc42 regulate 3D cell migra

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

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

179 ent of the cellular process that regulates N-WASP activation, actin dynamics, and contraction in smoo

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

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

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

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

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

185 We show that N-WASP binds p120-catenin through its verprolin cofilin ac

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

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

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

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

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

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

192 Our study demonstrates that N-WASP, by mediating p120-catenin interaction with actin-p

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

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

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

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

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

198 ntly suppressed by coadministration of the N-WASP inhibitor wiskostatin.

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

200 cinia virus integrates the activity of the N-WASP-ARP2/3 and Rac1-FHOD1 pathways.

201 Vaccinia virus dissemination relies on the N-WASP-ARP2/3 pathway, which mediates actin tail formation

202 Exposure of the N-WASP-depleted endothelial cell monolayer to the permeabi

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

204 es and is recruited to the virus, bound to N-WASP, by interacting with the second SH3 domain of Nck.

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

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

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

208 3 complex weakly on its own, but with WASP/N-WASP, another class of NPFs, potently activates.

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

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

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

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

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

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

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

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

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

218 main of N-WASP or phosphomimicking (Y256D)-N-WASP mutant in endothelial cells stabilizes AJs and faci

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

220 nd it interacts with the complex using a non-WASP-like binding mode.

221 Silencing of CIP4, not WASP, expression resulted in fewer proplatelet-like exte

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

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

224 depletion results in decreased activation of WASP, but increased activation of PAK1 and p38 mitogen-a

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

226 isingly little is known about the effects of WASP deficiency on antiviral immunity.

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

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

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

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

231 Loss of WASP was phenotypically associated with increased GATA3

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

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

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

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

236 in megakaryocytic cells with reduced CIP4 or WASP protein.

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

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

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

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

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

242 Platelet WASP deficiency accelerates random consumption, and a tr

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

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

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

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

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

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

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

250 absence of Wiskott-Aldrich syndrome protein (WASP) expression, resulting in defective function of man

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

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

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

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

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

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

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

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

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

260 f its activator, suppressor of cAMP receptor/WASP-family verprolin homologous (Scar/WAVE), but the re

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

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

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

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

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

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

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

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

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

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

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

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

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

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 We found that WASP proteins dissociated from filament-bound Arp2/3 com

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

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

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

280 This suggests that CIP4 modulates both the WASP and p38 MAPK pathways to promote lamellipodium asse

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

282 ne-associated actin assembly mediated by the WASP family veroprolin homolog (WAVE) regulatory complex

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

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

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

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

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 -terminal domain (VCD) and an array of three WASP homology 2 (WH2) motifs.

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

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

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

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

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

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

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

297 These data suggest that while WASP promotes formation of pre-nucleation complexes, fil

298 s Arp2/3 complex weakly on its own, but with WASP/N-WASP, another class of NPFs, potently activates.

299 protein (N-WASP), which is coexpressed with WASP in all immune cells, is a critical negative regulat

300 e antiviral immune response in patients with WASP deficiency in vivo.