ライフサイエンスコーパス: ESCRT

1 ESCRT knockout mutants showed that the release enhanceme

2 ESCRT proteins are implicated in myriad cellular process

3 ESCRT-I is the most upstream complex and bridges the sys

4 ESCRT-III assembly is highly dynamic and spatiotemporall

5 ESCRT-III components accumulate at the opening but are n

6 ESCRT-III executes membrane scission during the budding

7 ESCRT-III hetero-polymers adopt variable architectures,

8 ESCRT-III proteins assemble into ubiquitous membrane-rem

9 ESCRT-IIIs polymerize into membrane-binding filaments, b

10 nctional cooperation of HD-PTP with ESCRT-0, ESCRT-I and ESCRT-III and support a model for regulation

11 virus abscission by scaffolding early-acting ESCRT-I within the head of the budding virus.

12 tive dynamics of both early- and late-acting ESCRT components at MVEs under multiple growth condition

13 teracting protein X) to recruit and activate ESCRT-III.

14 This step may activate ESCRT proteins and thereby coordinate ESCRT function wit

15 (CHMP7), work together to recruit additional ESCRT-III proteins to holes in the nuclear membrane.

16 ESCRT-III complex is a critical step in all ESCRT-dependent events.

17 ssitates the re-evaluation of an alternative ESCRT-independent cell division mechanism.

18 with ALG-2 INTERACTING PROTEIN-X (ALIX), an ESCRT-III-associated protein, although the functional re

19 mer with its cofactor Vta1, ADP.BeFx, and an ESCRT-III substrate peptide.

20 iescent cells remove old nuclear pores in an ESCRT-dependent manner.

21 8-VPS37B-MVB12A was determined, revealing an ESCRT-I helical assembly with a 12-molecule repeat.

22 report a 3.2 A structure of Vps4 bound to an ESCRT-III peptide substrate.

23 or perturbation to NPC assembly triggers an ESCRT-dependent surveillance system that seals nuclear p

24 s showed that the release enhancement was an ESCRT-dependent effect.

25 synthesis in embryos deleted for CNEP-1 and ESCRT components rescued NE permeability defects.

26 Our data indicate that this ALIX- and ESCRT-III-dependent pathway promotes the sorting and del

27 primary neural progenitors require Cep55 and ESCRT for survival and abscission.

28 primary fibroblasts occurs without Cep55 and ESCRT-III at the midbody and is not affected by ESCRT de

29 peration of HD-PTP with ESCRT-0, ESCRT-I and ESCRT-III and support a model for regulation of ESCRT fu

30 nce (RNAi) assays, we found that ESCRT-I and ESCRT-III complexes are required for efficient entry of

31 this study, we demonstrated that ESCRT-I and ESCRT-III complexes are required for efficient entry of

32 -function mutation implicated a membrane and ESCRT-III regulator, Alx1, in this alternate pathway.

33 by the membrane fusion protein Comt/NSF and ESCRT-III components Shrub/CHMP4B and CHMP2B, facilitate

34 vivo and assayed the ability of retromer and ESCRT microdomains to regulate one another.

35 ed in tetraspanins, BST-2, TCR signaling and ESCRT proteins.

36 -II presumably involved in cargo sorting and ESCRT-III in membrane deformation and fission.

37 components of ESCRT-I (Tsg101 and Vps28) and ESCRT-III (Vps2B, Vps20, Vps24, Snf7, Vps46, and Vps60)

38 Further, we identify the archaeal ESCRT-III homolog, CdvB, as a key target of the proteaso

39 -I) component ELCH (ELC) and is localized at ESCRT-I-positive late endosomes likely through its PI3P

40 assembly into rings and disassembles before ESCRT-III rings expand into helices and spirals.

41 tol 3-kinase (PI3K) and the membrane-bending ESCRT factors, are required for reconstitution of the ac

42 ied a previously unknown interaction between ESCRT proteins and the Gag N-terminal protein region.

43 esults suggest that the interactions between ESCRT-III filaments and the membrane could proceed throu

44 ition of epidermal growth factor (EGF), both ESCRT-I and Vps4 are retained at endosomes for dramatica

45 embrane tubes that are scaffolded by bundled ESCRT-III filaments.

46 RT-III at the midbody and is not affected by ESCRT depletion.

47 are sorted into the lumen for degradation by ESCRT-dependent microautophagy.

48 lar membrane fission reactions are driven by ESCRT pathways, which culminate in disassembly of ESCRT-

49 echanism for membrane invagination driven by ESCRT-III.

50 is thought to be exclusively facilitated by ESCRT-dependent lysosomal degradation.

51 for NE sealing independent of the canonical ESCRT pathway.

52 xchange of the filament subunits to catalyze ESCRT-III activity.

53 by allowing constriction of the CdvB1:CdvB2 ESCRT-III division ring.

54 Cellular ESCRT machinery plays pivotal role in HIV-1 budding and

55 thought to involve the late-acting cellular ESCRT (endosomal sorting complex required for transport)

56 rus-encoded proteins and the normal cellular ESCRT machinery to drive the construction of its envelop

57 CRT components and which subsets of cellular ESCRT proteins are utilized by the virus remain largely

58 ultiple viral proteins and also the cellular ESCRT apparatus.

59 , has been used to characterize the cellular ESCRT function.

60 that Vps4, the key regulator of the cellular ESCRT machinery, is necessary for efficient entry and eg

61 ld link enveloping herpesviruses to cellular ESCRT components.

62 d in vitro that the Saccharomyces cerevisiae ESCRT-III subunit Snf7 uses a conserved acidic helix to

63 We show that in Saccharomyces cerevisiae, ESCRT-III complexes are stabilized and ILV membrane scis

64 To learn how certain ESCRT-IIIs shape positively curved membranes, we determi

65 ever, recent work has indicated that certain ESCRT-IIIs also participate in positive-curvature membra

66 s recruitment of VPS25 (ESCRT-II) and CHMP6 (ESCRT-III).

67 However, prior work has hinted at CHMP7/ESCRT-independent mechanisms.

68 ans coelomocyte, we visualized complementary ESCRT-0 and RME-8/SNX-1 microdomains in vivo and assayed

69 e formation of ILVs requires four complexes, ESCRT-0, -I, -II, and -III, with ESCRT-0, -I, and -II pr

70 g complex required for transport) components ESCRT-III and VPS4 (vacuolar protein sorting 4).

71 discovery and characterization of conserved ESCRT-like machinery across all three domains of life.

72 case in eukaryotes, and that two contractile ESCRT-III polymers perform distinct roles to ensure that

73 tivate ESCRT proteins and thereby coordinate ESCRT function with virion assembly.

74 ng cytosolic lectin, unifies and coordinates ESCRT and autophagy responses to lysosomal damage.

75 R/Cas9-mediated knock-in to tag the critical ESCRT-I component tumor susceptibility 101 (Tsg101) with

76 Under conditions of necroptotic cell death, ESCRT-III controls the duration of plasma membrane integ

77 solateral domains and suggest that defective ESCRT function may contribute to disease states through

78 of a conserved yet mechanistically divergent ESCRT-mediated lentivirus budding process in general, an

79 tor that recruits Cmp7p/CHMP7 and downstream ESCRT factors to the nuclear envelope.

80 interactions between ALIX and the downstream ESCRT-III effector CHMP4 during lysosomal repair.

81 ells prevented the recruitment of downstream ESCRTs, compromised spindle disassembly, and led to defe

82 er, the spatiotemporal pattern of endogenous ESCRT complex assembly and disassembly in mammalian cell

83 ring RNA (siRNA) to knock down the essential ESCRT-II subunit EAP20/VPS25 (ELL-associated protein 20/

84 SCRT-III component CHMP4B, thereby favouring ESCRT-mediated repair.

85 ur findings underscore essential actions for ESCRT-III in membrane remodeling, cargo selection, and c

86 Loss of NE adaptors for ESCRT-III exacerbates ER invasion and nuclear permeabili

87 autophagosome completion but dispensable for ESCRT-I complex formation and the degradation of epiderm

88 These findings offer a minimal mechanism for ESCRT-III-mediated membrane remodeling and point to a co

89 We developed a yeast model for ESCRT-dependent Gag release.

90 s to provide a range of potential models for ESCRT-mediated virus abscission.

91 hat the best-understood viral strategies for ESCRT recruitment, those adopted by the retroviruses and

92 (ESCRT)-III component CHMP4B and pUL51 forms ESCRT-III-like filaments, suggesting a direct role for p

93 brane-binding matrix domain that reduced Gag-ESCRT binding increased Gag-plasma membrane binding and

94 enetics and Gag mutational analysis with Gag-ESCRT binding studies and the characterization of Gag-pl

95 ruses, examines what is known of herpesvirus ESCRT utilization in the nucleus and cytoplasm, and iden

96 How ESCRTs bind and deform cellular membranes and ultimately

97 portant for efficient HIV-1 release, but how ESCRTs contribute to the budding process and how their a

98 emporal organization of the endogenous human ESCRT machinery.

99 r interrogating dynamics of the native human ESCRT machinery.

100 crystal structure of the headpiece of human ESCRT-I comprising TSG101-VPS28-VPS37B-MVB12A was determ

101 AL SORTING COMPLEX REQUIRED FOR TRANSPORT I (ESCRT-I) component ELCH (ELC) and is localized at ESCRT-

102 AL SORTING COMPLEX REQUIRED FOR TRANSPORT-I (ESCRT-I) complexes.

103 reveal that septins function in the ESCRT-I-ESCRT-II-CHMP6 pathway of ESCRT-III assembly and provide

104 -helix domain of LEM2 activates the ESCRT-II/ESCRT-III hybrid protein CHMP7 to form co-oligomeric rin

105 nuclear membrane proteins, and the ESCRT-II/ESCRT-III hybrid protein Cmp7p (CHMP7), work together to

106 orting complexes required for transport III (ESCRT-III) proteins have been implicated in sealing the

107 sorting complex required for transport III (ESCRT-III) subunit CHMP2A and the AAA ATPase VPS4, but t

108 sorting complex required for transport-III (ESCRT-III) catalyzes membrane fission from within membra

109 s suggest a mechanism of stepwise changes in ESCRT-III filament structure and mechanical properties v

110 he ensuing accumulation of Orm2 at the ER in ESCRT mutants necessitated TORC2 signaling through its d

111 ed in essential cellular processes including ESCRT-mediated membrane remodeling, cell adhesion, and a

112 mage elicits homeostatic responses including ESCRT-dependent membrane repair and autophagic removal o

113 to the midbody of telophase cells initiates ESCRT-III assembly into two rings, which subsequently ex

114 We suggest that a transient matrix-ESCRT interaction is replaced when Gag binds to the plas

115 ARMMs, including ARRDC1, TSG101 and multiple ESCRT complex proteins.

116 l for concomitant interactions with multiple ESCRTs, which contrasts with the compact conformation of

117 part of or associated with the multiprotein ESCRT complex participating in exosome biogenesis.

118 body (MVB) pathway using a dominant negative ESCRT (endosomal sorting complexes required for transpor

119 nery to ruptures; however, neither LEMD2 nor ESCRT-III is required to repair ruptures.

120 We found that ESCRT-III components (but not ESCRT-I components) are required for efficient nuclear e

121 -Nur1 complex as a substrate for the nuclear ESCRT machinery and explains how the dynamic tethering o

122 Surprisingly, in the absence of ESCRT function in C. elegans, cytokinetic abscission is

123 As a consequence of the action of ESCRT-III, cells undergoing necroptosis can express chem

124 urements and electron microscopy analysis of ESCRT-III-depleted cells with a mathematical model, we s

125 Self-assembly of ESCRT-III complex is a critical step in all ESCRT-depend

126 sed of Vps32 protomers, a major component of ESCRT-III complexes.

127 In this study, the core components of ESCRT-I (Tsg101 and Vps28) and ESCRT-III (Vps2B, Vps20,

128 ound to interact with Vps4 and components of ESCRT-III, and these interactions may suggest the format

129 Ac146) interact with Vps4 and components of ESCRT-III.

130 The composition of ESCRT complexes in exosomes from VCaP versus LNCaP cells

131 to the cycle of assembly and disassembly of ESCRT-III complexes at membranes.

132 pathways, which culminate in disassembly of ESCRT-III polymers by the AAA ATPase Vps4.

133 ulation of ESCRT function by displacement of ESCRT subunits, which is crucial in determining the fate

134 ith the ubiquitin E2 variant (UEV) domain of ESCRT-I protein TSG101 through two N-terminal PTAP motif

135 ved, we used siRNA to suppress expression of ESCRT (endosomal sorting complex required for transport)

136 Failure of ESCRT-III/Vps4 to release Lem2-Nur1 from heterochromatin

137 at controls the organization and function of ESCRT-III.

138 In turn, the growth of ESCRT mutants strongly depended on TORC2-mediated homeos

139 cargo deubiquitination at the initiation of ESCRT-III complex assembly.

140 Loss of ESCRT function in Drosophila imaginal discs is known to

141 tative microscopic assays to confirm loss of ESCRT-II and HD-PTP function.

142 5 and CHMP6, and the spatial organization of ESCRT-III (CHMP4B and CHMP2B) into functional rings.

143 namely artifacts caused by overexpression of ESCRT subunits, obstruct our understanding of the spatio

144 ion in the ESCRT-I-ESCRT-II-CHMP6 pathway of ESCRT-III assembly and provide a framework for the spati

145 characterize a sequential polymerization of ESCRT-III subunits that, driven by a recruitment cascade

146 r dependent on the downstream recruitment of ESCRT-I.

147 Recruitment of ESCRT-I/II complexes to the midbody of telophase cells i

148 RT-III and support a model for regulation of ESCRT function by displacement of ESCRT subunits, which

149 ver a unique Cdc42 function in regulation of ESCRT proteins at the nuclear envelope and sites of ER t

150 An all-or-none step led to final release of ESCRT-III and Vps4.

151 gest that formation of a 12-membered ring of ESCRT-I molecules is a geometry-dependent checkpoint dur

152 ordinates the recruitment of a unique set of ESCRT machinery components for phagophore closure in mam

153 Coarse-grained (CG) simulations of ESCRT assembly at HIV-1 budding sites suggest that forma

154 e septin double ring demarcates the sites of ESCRT-III assembly into rings and disassembles before ES

155 a4 binding to Vps20, which is the subunit of ESCRT-III that initiates assembly of the complex.

156 view summarizes our current understanding of ESCRT association by enveloped viruses, examines what is

157 se on microtubules governs the activation of ESCRTs and coordinated spindle disassembly.

158 We found that only ESCRT-III components are synthetic lethal, indicating th

159 her coclustering with these host proteins or ESCRT-dependent particle release failed to reduce PSGL-1

160 Mutations affected other ESCRT-dependent cellular processes, including regulation

161 hetic lethal, indicating that Vps4 and other ESCRT complexes do not function in this pathway.

162 is recruitment occurs independently of other ESCRTs but requires lysobisphosphatidic acid (LBPA) in v

163 ress complex" that is involved in recruiting ESCRT-III components to a virus egress domain on the nuc

164 thering LDs to peroxisomes and in recruiting ESCRT-III components to LD-peroxisome contact sites for

165 associated protein ALIX efficiently recruits ESCRT-III proteins to endosomes.

166 regulator of abscission, because it recruits ESCRT-III to the midbody (MB), the site of abscission.

167 nt in HIV-1C, and ALIX protein that recruits ESCRT III complex.

168 ar mechanisms that enable HD-PTP to regulate ESCRT function are unknown.

169 ealing and ER remodeling, where it regulates ESCRT disassembly to maintain nuclear envelope integrity

170 nabling plasma membrane repair by regulating ESCRT III-mediated shedding of injured plasma membrane.

171 omain of VPS4A, a critical enzyme regulating ESCRT function.

172 s that are known to be capable of regulating ESCRT-III function include the ESCRT-II complex and othe

173 with the compact conformation of the related ESCRT regulator Alix.

174 These typically require ESCRT-III proteins to stabilize negatively curved membra

175 The reformation of sealed nuclei requires ESCRTs (endosomal sorting complexes required for transpo

176 ph as an exosomal cargo, a process requiring ESCRT components in exosome biogenesis and Rab11 and Syx

177 nd, M1 Spastin recruits the membrane-shaping ESCRT-III proteins IST1 and CHMP1B to LDs via its MIT do

178 Here we have analysed the role of specific ESCRT components in HPV infection, and we find an essent

179 Strikingly, ESCRT-III subunits (CHMP4B and CHMP2A/B) accumulate to t

180 olecular machinery of multiple subcomplexes (ESCRT-I/II/III) that promotes membrane remodeling and sc

181 Gag assembly and HIV-1 budding and templates ESCRT-III assembly for membrane scission.

182 Electron microscopy confirmed that ESCRT-I subcomplexes form helical filaments in solution.

183 RNAi depletion studies confirmed that ESCRT-III proteins, particularly CHMP2A, function in eHA

184 ents bound to helical bicelles confirms that ESCRT-III filaments can interact with the membrane throu

185 In this study, we demonstrated that ESCRT-I and ESCRT-III complexes are required for efficie

186 uired for transport) proteins and found that ESCRT II and IV significantly control exosome release.

187 NA interference (RNAi) assays, we found that ESCRT-I and ESCRT-III complexes are required for efficie

188 We found that ESCRT-III components (but not ESCRT-I components) are re

189 Specifically, our data indicate that ESCRT-0 accumulates quickly on endosomes, typically in l

190 We show that ESCRT function is required for apical localization and m

191 These data show that ESCRT-I is not merely a bridging adaptor; it has an esse

192 e light-sheet microscopy, we have shown that ESCRT-III subunits polymerize rapidly on yeast endosomes

193 Current models suggest that ESCRT-III complexes surround ubiquitinated cargoes to tr

194 These data suggest that ESCRT-III proteins and ER-PM contact sites act in indepe

195 Our model predicts that ESCRTs do not become part of the ILV, but localize with

196 y defects in cnep-1 mutants, suggesting that ESCRTs restrict excess ER membranes during NE closure.

197 The ESCRT complexes drive membrane scission in HIV-1 release

198 The ESCRT is recruited through interactions with PTAP and LY

199 The ESCRT machinery is also hijacked by retroviruses, such a

200 The ESCRT machinery mediates reverse membrane scission.

201 The ESCRT-III core protein Shrub has a central role in endos

202 The ESCRT-III membrane fission machinery maintains the integ

203 he winged-helix domain of LEM2 activates the ESCRT-II/ESCRT-III hybrid protein CHMP7 to form co-oligo

204 ytokinesis, mediated by both dynamin and the ESCRT (endosomal sorting complex required for transport)

205 ents of the PtdIns 3-kinase complex, and the ESCRT machinery.

206 proteins flotillin-1 and flotillin-2 and the ESCRT-associated proteins ALIX and syntenin-1 in membran

207 of inner nuclear membrane proteins, and the ESCRT-II/ESCRT-III hybrid protein Cmp7p (CHMP7), work to

208 ab8A to damaged endolysosomes as well as the ESCRT-III component CHMP4B, thereby favouring ESCRT-medi

209 ALG-2 and ALIX assemble the ESCRT III complex, which helps excise and shed the damag

210 ntal structure-function relationships at the ESCRT-HIV-1 interface.

211 s reveal compensatory cross-talk between the ESCRT machinery, calcineurin/TORC2 signaling, and the EG

212 t the INM are remodeled in interphase by the ESCRT-III/Vps4 machinery.

213 d stomatal closure, unveiling a role for the ESCRT machinery in the control of water loss through sto

214 al membranes, consistent with a role for the ESCRT pathway in endolysosomal membrane repair.

215 Saccharomyces cerevisiae) to explore how the ESCRT machinery contributes to plasma membrane (PM) home

216 genome-wide CRISPR library and identify the ESCRT-I subunit VPS37A as a critical component for phago

217 ectosomes, thereby generally implicating the ESCRT machinery in EV biogenesis.

218 omain on the nuclear membrane.IMPORTANCE The ESCRT system is hijacked by many enveloped viruses to me

219 results reveal that septins function in the ESCRT-I-ESCRT-II-CHMP6 pathway of ESCRT-III assembly and

220 of regulating ESCRT-III function include the ESCRT-II complex and other members of the Bro1 family.

221 Here, we study the effects of inhibiting the ESCRT-associated AAA+ ATPase VPS4 on EV release from cul

222 During their 3-45 s lifetimes, the ESCRT-III assemblies accumulated 75-200 Snf7 and 15-50 V

223 somes via interaction with components of the ESCRT (endosomal sorting complex required for transport)

224 rth of candidates for the acquisition of the ESCRT complex and the control of envelope scission.

225 The strongest hits were components of the ESCRT complexes.

226 re required for efficient recruitment of the ESCRT component ALIX during lysosomal damage.

227 ion stabilizes late-acting components of the ESCRT machinery at endosomes to accelerate the rate of I

228 mework for the spatiotemporal control of the ESCRT machinery of cytokinetic abscission.

229 are revealing how the core machinery of the ESCRT pathway constricts membranes to promote fission.

230 structures with abnormal accumulation of the ESCRT protein IST1 on the limiting membrane.

231 determined that Vps27, a key protein of the ESCRT-0 complex, is required for the transport of the vi

232 Here, we report that an active form of the ESCRT-associated protein ALIX efficiently recruits ESCRT

233 Similarly, levels of the ESCRT-I complex also fluctuate on endosomes, but its ave

234 interaction between Tsg101, a member of the ESCRT-I complex, and ubiquitin.

235 abrogates the phagophore recruitment of the ESCRT-I subunit VPS28 and CHMP2A, whereas inhibition of

236 monstrate that an essential component of the ESCRT-II complex and two ESCRT-associated Bro1 proteins

237 dosomes by controlling ubiquitination of the ESCRT-III (endosomal sorting complex required for transp

238 ng imaginal discs temporally depleted of the ESCRT-III core component Shrub.

239 LEMD2 is required for recruitment of the ESCRT-III membrane repair machinery to ruptures; however

240 gene coding for an ATPase that regulates the ESCRT-III machinery in a variety of cellular processes i

241 oped viruses, does not appear to require the ESCRT-I subunit TSG101 or the Bro1 domain-containing pro

242 sing a budding yeast model, we show that the ESCRT Chm7 and the integral inner nuclear membrane (INM)

243 -1 particles, supporting the notion that the ESCRT machinery initiates virus abscission by scaffoldin

244 udy links the BAR protein superfamily to the ESCRT pathway for MP biogenesis in mammalian cardiac ven

245 n into Rab5-positive early endosomes via the ESCRT machinery.

246 The crucial roles of the ESCRTs in cellular physiology and viral disease make it

247 Our findings demonstrate that the ESCRTs can function at both the late endosome and the va

248 protein LEM2 recruiting CHMP7/Cmp7 and then ESCRT-III.

249 EVs generated through ESCRT-independent pathways are also beneficial to virus

250 geting through ubiquitination and binding to ESCRT (Endosomal Sorting Complexes Required for Transpor

251 ion and inhibition of TOR complex 2 (TORC2), ESCRT-III/Vps4 assemblies form at the PM and help mainta

252 red for transport) and LEM2, a transmembrane ESCRT adaptor(2-4).

253 omal sorting complex required for transport (ESCRT) complex.

254 al sorting complexes required for transport (ESCRT) function.

255 omal sorting complex required for transport (ESCRT) III.

256 omal sorting complex required for transport (ESCRT) machinery as mediators of intracellular propagati

257 omal sorting complex required for transport (ESCRT) machinery carries out the membrane scission react

258 al sorting complexes required for transport (ESCRT) machinery drives membrane scission for diverse ce

259 omal sorting complex required for transport (ESCRT) machinery into endosome intralumenal vesicles (IL

260 omal sorting complex required for transport (ESCRT) machinery is necessary for budding of many envelo

261 omal sorting complex required for transport (ESCRT) machinery plays a key role in MVE biogenesis, ena

262 al sorting complexes required for transport (ESCRT) machinery, causes frontotemporal dementia linked

263 al sorting complexes required for transport (ESCRT) machinery, including charged multivesicular body

264 al sorting complexes required for transport (ESCRT) mediate evolutionarily conserved membrane remodel

265 omal sorting complex required for transport (ESCRT) plays a crucial role in the transportation and de

266 EndoSomal Complexes Required for Transport (ESCRT) proteins, but how they are regulated in this proc

267 ar endosomal complex required for transport (ESCRT) proteins.

268 omal sorting complex required for transport (ESCRT) proteins.

269 omal sorting complex required for transport (ESCRT), a cellular machinery that coats the inside of bu

270 ytic sorting complex required for transport (ESCRT), a molecular machinery of multiple subcomplexes (

271 omal sorting complex required for transport (ESCRT)-associated factor ALG-2-interacting protein X (AL

272 ar endosomal complex required for transport (ESCRT)-III component CHMP4B and pUL51 forms ESCRT-III-li

273 omal sorting complex required for transport (ESCRT)-III mediates abscission, the process that physica

274 al sorting complexes required for transport (ESCRT-0 to -III/VPS4) sequester receptors at the endosom

275 omal-sorting-complex-required-for-transport (ESCRT) protein CHMP5, known to be required for the forma

276 al sorting complexes required for transport (ESCRTs) are essential for multiple membrane modeling and

277 al sorting complexes required for transport (ESCRTs) mediate diverse membrane remodeling events.

278 al sorting complexes required for transport (ESCRTs).

279 ne in the Gaussian curvature likely triggers ESCRT-III/VPS4 assembly to enable neck constriction and

280 Two ESCRT proteins, TSG101 and ALIX, bind to the Gag C-termi

281 al component of the ESCRT-II complex and two ESCRT-associated Bro1 proteins are dispensable for HSV-1

282 erved functional differences between the two ESCRT-III proteins implicated in cytokinesis, CdvB1 and

283 better understand the mechanisms underlying ESCRT-mediated formation of ILVs, we exploited the rapid

284 This causes unrestrained ESCRT-III accumulation, which drives extensive membrane

285 ation and facilitate ILV formation: Upstream ESCRT-driven budding does not require ATP consumption as

286 a mathematical model, we show that upstream ESCRT-induced alteration of the Gaussian bending rigidit

287 ction in ILV formation, the role of upstream ESCRTs (0 to II) in membrane shape remodeling is not und

288 internal vesicles accumulate over time, use ESCRT (endosomal sorting complexes required for transpor

289 es abscission, impairs recruitment of VPS25 (ESCRT-II) and CHMP6 (ESCRT-III).

290 from yeast spheroplasts, but Gag release was ESCRT-independent.

291 Whereas ESCRT-III/VPS4 have an established function in ILV forma

292 dramatically extended periods of time, while ESCRT-0 dynamics are only modestly affected.

293 is more than fivefold shorter compared with ESCRT-0.

294 nding domain of Raf also coprecipitates with ESCRT (endosomal sorting complex required for transport)

295 complexes, ESCRT-0, -I, -II, and -III, with ESCRT-0, -I, and -II presumably involved in cargo sortin

296 How HSV-1 structural proteins interact with ESCRT components and which subsets of cellular ESCRT pro

297 med aggregates that appear to interfere with ESCRT-independent NE sealing.

298 cell imaging a novel Cdc42 localization with ESCRT proteins at sites of nuclear envelope and ER fissi

299 se the functional cooperation of HD-PTP with ESCRT-0, ESCRT-I and ESCRT-III and support a model for r

300 A dynamic interplay of pyroptosis with ESCRT-mediated plasma membrane repair also occurs.

301 of ER membranes into NE holes together with ESCRT-mediated remodeling is required for nuclear closur