ライフサイエンスコーパス: VCP

1 VCP is an ubiquitously expressed, highly abundant protei

2 VCP mutations should thus be considered for genetically

3 VCP recruitment coincides temporally with mitochondrial

4 VCP/p97 increases BMP signaling by accelerating ubiquiti

5 VCP/p97 inhibition also results in the accumulation of C

6 VCP/p97 is readily recruited to DNA damage sites and col

7 VCP/p97 regulates numerous cellular functions by mediati

8 VCP/p97, an enzyme critical to proteostasis, is regulate

9 yers including TDP-43, FUS/TLS, ubiquilin-2, VCP, and expanded hexanucleotide repeats within the C9OR

10 ms of ALS, including those caused by TDP-43, VCP and SOD1 mutations, supporting the concept that mult

11 rged as common FTD genes, and TARDBP/TDP-43, VCP, FUS, and CHMP2B have been identified as less common

12 e surveyed a stratified random sample of 500 VCPs, 404 of whom completed the survey (response rate, 8

13 ng and respiration analysis we demonstrate a VCP mutation/knockdown-induced dysregulation in the aden

14 nd targeted for proteasomal degradation in a VCP/p97-dependent manner, which allows survival of the c

15 c transgenic mice overexpressing WT VCP or a VCP(K524A) mutant with deficient ATPase activity.

16 catalytically inactive VCP or treated with a VCP inhibitor also failed to activate mTOR upon nutrient

17 interaction with a peptide, HV-3, abolishes VCP translocation to the mitochondria, corrects excessiv

18 rposed FDA-approved VCP inhibitors abrogated VCP-mediated repression of NIS function, resulting in si

19 Mitochondria-accumulated VCP elicits excessive mitophagy, causing neuronal cell d

20 cumulation, at least in part through the AKT/VCP axis.

21 (n = 2), VPS13A (n = 1), UBQLN2 (n = 1), and VCP (n = 1).

22 These findings show that ARF4 and VCP are involved in NIS trafficking to the plasma membra

23 ned action of SQSTM1-dependent autophagy and VCP-mediated dislocation and presentation of ubiquitinat

24 ERAD and VCP/p97 have been implicated in a multitude of human dis

25 s temporally with mitochondrial fission, and VCP is required for proteasome-dependent degradation of

26 sis and functions in concert with Parkin and VCP for Marf degradation to promote damaged mitochondria

27 Compromising proteasome and VCP/p97 function allows accumulation of both native and

28 D by showing an interaction between RFFL and VCP in vitro We conclude that RFFL is an important regul

29 The Arg/N-end rule and VCP/p97UFD1-NPL4 segregase cooperate to promote phosphor

30 Two repurposed FDA-approved VCP inhibitors abrogated VCP-mediated repression of NIS

31 itin chains) that recruit p97 (also known as VCP) and the proteasome, which ensures the rapid express

32 ts as NPL4, an adaptor of p97 (also known as VCP) segregase, which is essential for the turnover of p

33 t peptides to degradation mechanisms such as VCP and the 26S proteasome.

34 The AAA+ ATPase, p97, also referred to as VCP, plays an essential role in cellular homeostasis by

35 These findings suggest that p.Asp395Gly VCP is an autosomal-dominant genetic mutation associated

36 tau aggregates in mice in which p.Asp395Gly VCP mice was knocked in, as compared with injected wild-

37 The survey assessed VCPs' attitudes and behaviors in addressing driving conc

38 orting of CAV1 requires the AAA+-type ATPase VCP and its cofactor UBXD1.

39 n transitional endoplasmic reticulum ATPase (VCP/p97) protein.

40 ough interactions with the RMA1-Derlin-BAP31-VCP pathway.

41 ghlight an important pathologic link between VCP and cognition.

42 o-cytoplasmic mislocalization of FUS in both VCP-mutation related ALS and, crucially, in sporadic ALS

43 of RNA synthesis following UVR, whereas both VCP/p97 and proteasome inhibitions decrease cell viabili

44 on and activity of iNOS in cardiomyocytes by VCP is an essential mechanistic link of VCP-mediated pre

45 ; this myopathy is similar to that caused by VCP/p97 mutations, the most common cause of familial IBM

46 iquitination is linked to sorting of CAV1 by VCP-UBXD1.

47 nd the transcriptomic alterations induced by VCP under the cardiac stress caused by pressure overload

48 led a novel molecular regulation mediated by VCP under pressure overload that may bring new insight i

49 ion of reductase marks it for recognition by VCP/p97, an ATPase that mediates subsequent dislocation

50 tress signalling and cell death triggered by VCP/p97 inhibition and nutrient shortages and modulated

51 nd behaviors in discussing driving varied by VCP characteristics, particularly provider type.

52 th diverse cellular activities), also called VCP (valosin-containing protein), is an important therap

53 7, a valosin-containing protein (also called VCP), plays an essential role in the postubiquitinationa

54 eins in the heart, and impairment of cardiac VCP activity resulted in aggregation of large ribosomal

55 together, our data identify a role for Cdc48/VCP and endocytic function in regulating TDP-43 and FUS

56 Here we report that the p97/Cdc48/VCP segregase plays a critical role in ICL repair by unl

57 Cellular VCP/p97 dependency to maintain proteostasis was increase

58 We show that common VCP disease mutants act as hyperactive alleles with resp

59 e have previously shown that patient-derived VCP mutant fibroblasts exhibit lower mitochondrial membr

60 , we identify tracer compounds for different VCP categories: decamethylcyclopentasiloxane (D5-siloxan

61 teracts and colocalizes with TDP-43, as does VCP, in ALS patient tissue.

62 ues the defects caused by loss of Drosophila VCP and overexpression of disease relevant VCP transgene

63 Educating VCPs on useful resources, tests, and questions is needed

64 aled overwhelming interactions of endogenous VCP with ribosomal, ribosome-associated, and RNA-binding

65 We show that endogenous VCP negatively regulates Mitofusin, which is required fo

66 e ER degradation cluster that included FAF1, VCP, BAP31, and Derlin-1.

67 tes FAF1 at Ser 582, which disrupts the FAF1-VCP complex and reduces FAF1 at the plasma membrane.

68 issions and volatile chemical products (FIVE-VCP) inventory, we identify tracer compounds for differe

69 hese findings establish sequential roles for VCP/p97 and the 19 S regulatory particle in the sterol-a

70 Contributions from VCP emissions (e.g., personal care products) are highest

71 isoform of nitric oxide synthase (iNOS) from VCP TG mouse and by pharmacological inhibition of iNOS i

72 When proteasome function, VCP, or gp78 activity is compromised, BOK is stabilized

73 olymerization of a variety of functionalized VCP monomers, where high monomer conversions and spatial

74 Further, VCP and its adaptor Npl4/Ufd1 are required for clearance

75 Furthermore, VCP mutations are causative of some neurodegenerative di

76 Furthermore, VCP/p97 and UBXD7 associate with the Cockayne syndrome g

77 -causing genes, driven by SOD1, TARDBP, FUS, VCP, OPTN and UBQLN2.

78 However, how VCP functions in the heart has not been carefully examin

79 or cardiac homeostasis, suggesting how human VCP mutations negatively affect the heart.

80 We show that human VCP rescues the defects caused by loss of Drosophila VCP

81 inking tubular lysosome dysfunction to human VCP-related diseases.

82 Importantly, VCP inhibitors suppress mitochondrial defects, muscle ti

83 underlying altered mitochondrial function in VCP-related degeneration, and this new insight may infor

84 chondrial uncoupling and lower ATP levels in VCP mutation-bearing neurons via reduced ADP availabilit

85 Decreased ATP levels in VCP-deficient cells lower their energy capacity, making

86 We found that a p.Asp395Gly mutation in VCP (valosin-containing protein) was associated with dem

87 studies indicate that specific mutations in VCP are sufficient to produce resistance to CB-5083 sugg

88 reported target alterations via mutations in VCP as the primary mechanism of resistance, discrepancie

89 Mutations in VCP cause multisystem degeneration impacting the nervous

90 ned despite the fact that human mutations in VCP cause Paget disease of bone and frontotemporal demen

91 IBMPFD/ALS mutations in VCP disrupt autophagosome and endosome maturation result

92 ing the importance of on-target mutations in VCP for resistance.

93 Mutations in VCP have been reported to account for a spectrum of phen

94 s from patients with pathogenic mutations in VCP Using fluorescent live cell imaging and respiration

95 a (IBMPFD) that harbor germline mutations in VCP, the levels of Shoc2 ubiquitination and ERK1/2 phosp

96 this is impaired by pathogenic mutations in VCP.

97 TOR activity and increased the fiber size in VCP-IBM mouse skeletal muscle.

98 ser extent by amino acid (AA) stimulation in VCP-IBM muscle.

99 astened weakness, atrophy and vacuolation in VCP-IBM mice.

100 Cells expressing catalytically inactive VCP or treated with a VCP inhibitor also failed to activ

101 reover, glutamine depletion led to increased VCP/p97 expression, whereas VCP/p97 inhibition perturbed

102 es and phosphorylate VCP, thereby increasing VCP's activity and ability to disassemble stress granule

103 Gene expression analysis indicated VCP expression was particularly induced in aggressive th

104 s demonstrate a causal role of mtHtt-induced VCP mitochondrial accumulation in HD pathogenesis and su

105 that all trans retinoic acid (ATRA) induces VCP expression, creating a positive feedback loop that e

106 Here we showed that inhibiting VCP using Eeyarestatin I reduces the endoplasmic reticul

107 UBR5-dependent ubiquitylation also involves VCP/p97, an AAA ATPase regulating the folding of various

108 a deubiquitinating XPC and by preventing its VCP/p97-regulated proteolysis.

109 ty particularly for an oligomer protein like VCP.

110 e in governing protein homoeostasis has made VCP/p97 an appealing anticancer drug target.

111 Moreover, VCP appeared to exhibit tau disaggregase activity in vit

112 Moreover, VCP overexpression restored pro-survival signaling throu

113 Moreover, VCP/p97 interacts with both native and ubiquitin-conjuga

114 Blocking mtHtt/VCP mitochondrial interaction with a peptide, HV-3, abol

115 pulation density and originate from multiple VCP sources.

116 Mutant VCP produced more T-intracellular antigen-1-positive gra

117 differentiated C2C12 cells expressing mutant VCP.

118 el selectively overexpressing a human mutant VCP in neurons to study pathogenic mechanisms of mutant

119 Mechanistically, mutant VCP-overexpressing hearts up-regulate ERAD complex compo

120 The hearts of mutant VCP transgenic mice also exhibit profound defects in car

121 ons to study pathogenic mechanisms of mutant VCP-mediated neurodegeneration and cognitive impairment.

122 r granule components, indicating that mutant VCP delayed clearance of stress granules.

123 The mixed results indicate that mutant VCP together with aging lead to higher oxidative stress

124 rdiac structure and function, whereas mutant VCP-overexpressing mice develop cardiomyopathy.

125 To address whether mutant VCP triggers dysregulation of the stress granule pathway

126 However, the mechanisms by which mutant VCP triggers degeneration remain unknown.

127 r, the pathogenic mechanisms by which mutant VCP triggers neurodegeneration remain unknown.

128 We identified a novel VCP mutation (p.Glu185Lys) segregating in an autosomal d

129 97 inhibition and siRNA-mediated ablation of VCP/p97 and its cofactors UFD1 and UBXD7 impair CSB degr

130 ression, function and mechanism of action of VCP in the mammalian heart in vivo in both normal and st

131 The ATPase activity of VCP modulates the stoichiometry of HUWE1 in the Shoc2 co

132 Chemical inhibition of the activity of VCP/p97 ATPase causes an increase in ubiquitinated XPC o

133 biochemical inhibition and genetic defect of VCP/p97 enhance the recovery of RNA synthesis following

134 Conversely and consistently, depletion of VCP or UBXD1 led to accumulation of ubiquitinated CAV1,

135 Altered expression of VCP has been detected in many cancer types sometimes ass

136 ardiac-specific overexpression (3.5-fold) of VCP, we demonstrate that VCP is a new and powerful media

137 mechanism for achieving the homozygosity of VCP mutant responsible for the resistance to VCP inhibit

138 Pharmacological inhibition of VCP significantly delayed the process of sperm mitophagy

139 Inhibition of VCP/p97 induces proteotoxic ER stress and cell death in

140 ( 40% true hit rate) as direct inhibitors of VCP/p97 and ERAD.

141 d identified several candidate inhibitors of VCP/p97 ATPase.

142 Knockdown of VCP resulted in decreased RVFV replication, reduced Gn G

143 s by VCP is an essential mechanistic link of VCP-mediated preservation of mitochondrial function.

144 However, manifestation of VCP/p97 foci is independent of CSB and UBXD7.

145 s, we did not detect METTL21C methylation of VCP and HSPA8.

146 We developed a Drosophila model of VCP mutation-dependent degeneration.

147 importantly, strongly reduced recruitment of VCP-UBXD1 to endocytic compartments.

148 Here, we investigated the role of VCP in cellular stress and found that the oxidative stre

149 We also identify a novel role of VCP in preserving mitochondrial respiration and in preve

150 a mechanistic basis for the critical role of VCP in the regulation of the ERK1/2 pathway and reveals

151 d highlight the possible therapeutic role of VCP inhibitors in enhancing radioiodine effectiveness in

152 cts in mRNA metabolism and that this role of VCP is linked to dendrite pruning.

153 our data point to an interconnected role of VCP/p97 and GCN2 in maintaining cancer cell metabolic an

154 Our findings reveal a new role of VCP/p97 segregase in the timely processing of ubiquitina

155 ied on (performed always or often by >80% of VCPs), but other ocular test results and nonocular infor

156 eveal large differences in SOA potentials of VCPs, implying the need for further characterization of

157 More than one-third of VCPs (35.6%) report sometimes, often, or always communic

158 nes underlying ALS, SOD1, TARDBP, FUS, OPTN, VCP, UBQLN2, C9ORF72 and PFN1, and evaluate the informat

159 rence-mediated knockdown of either Insigs or VCP/p97.

160 The AAA+ Cdc48 ATPase (alias p97 or VCP) is a key player in multiple ubiquitin-dependent cel

161 to methylate valosin-containing protein/p97 (VCP) and heat shock 70-kDa protein 8 (HSPA8).

162 p97/VCP is an essential, abundant AAA+ ATPase that is conser

163 p97/VCP, a member of the AAA+ (ATPases associated with diver

164 omplex with ubiquitinated substrates and p97/VCP (valosin-containing protein), a major driver of ER-a

165 by which the interplay between SIK2 and p97/VCP contributes to the regulation of ERAD in mammalian c

166 functional interactions between SIK2 and p97/VCP underlie the regulation of endoplasmic reticulum (ER

167 a manner that depends on the AAA-ATPase p97/VCP [3].

168 ity of the proteasome and the AAA ATPase p97/VCP in a similar manner to infectious viruses.

169 e E3 ubiquitin ligase MARCH4, the ATPase p97/VCP, the deubiquitinating enzyme USP8, the cullin-RING l

170 s physically and functionally with Cdc48/p97/VCP, a component of UPS required for degradation of RNAP

171 tion subunits by the ubiquitin-dependent p97/VCP/Cdc48 segregase complex, leads to impaired DNA excis

172 in-binding domain, the AAA ATPase factor p97/VCP mediates rapid inactivation of HSF1, precluding late

173 In these cells, knockdown of p97/VCP rescues HSF1 from this rapid inactivation and restor

174 show that UBXD8-mediated recruitment of p97/VCP to LDs increases LD size by inhibiting the activity

175 The degradation of GM130 is dependent on p97/VCP and 26S proteasomes, and required for Golgi dispersa

176 2 or mutation of the SIK2 target site on p97/VCP led to impaired degradation of ERAD substrates and d

177 the membrane in a manner that depends on p97/VCP.

178 mbly of the active helicase dependent on p97/VCP/Cdc48.

179 tors and inhibitors of ubiquitination or p97/VCP.

180 tion of Cdc48 and its mammalian ortholog p97/VCP.

181 ch protein, demonstrating that ataxin3's p97/VCP-binding motif interacts with the inter-lobe cleft in

182 We targeted p97/VCP, the ubiquitin proteasome pathway (UPP), and autopha

183 of PAX4 or its target gene encoding the p97/VCP ATPase reduced myofibril disassembly and degradation

184 rane-embedded recruitment factor for the p97/VCP segregase that has been previously linked to endopla

185 the cellular machinery, composed of the p97/VCP ubiquitin-dependent unfoldase/segregase and the Atax

186 ating forks because of the action of the p97/VCP/Cdc48 protein remodeler.

187 horylation modifies binding of RHBDL4 to p97/VCP and Lys(63)-linked ubiquitinated proteins.

188 SIK2 co-localizes with p97/VCP in the ER membrane and stimulates its ATPase activit

189 R, including proteins that interact with p97/VCP.

190 Using this vertical cell pairing (VCP) system, we investigated the dynamics of the inhibit

191 Paradoxically, VCP complements PINK1 deficiency but not parkin deficien

192 s of clu leads to the recruitment of Parkin, VCP/p97, p62/Ref(2)P and Atg8a to depolarized swollen mi

193 ings propose a mechanism by which pathogenic VCP mutations lead to cell death.

194 ocalize to stress granules and phosphorylate VCP, thereby increasing VCP's activity and ability to di

195 mporal control were achieved to produce poly(VCPs) with predictable molecular weight and low dispersi

196 egories, such as volatile chemical products (VCPs), have become more apparent in urban air.

197 se models based on tau, TDP-43, progranulin, VCP, and CHMP2B.

198 eam of and binds to VCP in vivo and promotes VCP-dependent Marf degradation in vitro Marf accumulates

199 A visual cortical prosthesis (VCP) has long been proposed as a strategy for restoring

200 ERAD), including valosin-containing protein (VCP) and Hrd1.

201 lysis identifies valosin-containing protein (VCP) as an mtHtt-binding protein on the mitochondria.

202 act with the p97/valosin-containing protein (VCP) ATPase.

203 nse mutations of valosin-containing protein (VCP) cause an autosomal dominant disease known as inclus

204 Mutations in valosin-containing protein (VCP) cause inclusion body myopathy (IBM) associated with

205 sistance towards valosin-containing protein (VCP) inhibitors.

206 Valosin-containing protein (VCP) is a highly expressed member of the type II AAA+ AT

207 he gene encoding valosin-containing protein (VCP) lead to multisystem proteinopathies including front

208 Valosin-containing protein (VCP) mutations cause inclusion body myopathy with Paget

209 e AAA ATPase p97/valosin-containing protein (VCP) or the proteasome results in a >1,000-fold increase

210 The valosin-containing protein (VCP) participates in signaling pathways essential for ce

211 or inhibition of Valosin-Containing Protein (VCP), a ubiquitin-dependent ATPase whose human homolog i

212 Valosine-containing protein (VCP), also known as p97 or cdc48 in yeast, is a highly a

213 Valosine containing protein (VCP), also known as p97, is a member of AAA ATPase famil

214 Valosin-containing protein (VCP), also known as p97, is an ATPase with diverse cellu

215 Valosin-containing protein (VCP), also named p97, is an essential hexameric AAA+ ATP

216 eported that the valosin-containing protein (VCP), an ATPase-associated protein newly identified in t

217 core component, valosin-containing protein (VCP), in 293A cells partially abolished RFFL-mediated hE

218 otein dislocase, valosin-containing protein (VCP), may act in concert during mammalian sperm mitophag

219 teracts with the valosin-containing protein (VCP), resulting in the degradation of IkappaBalpha and s

220 p97/valosin-containing protein (VCP), which is involved in membrane remodeling in the se

221 tor 4 (ARF4) and valosin-containing protein (VCP)-controlling NIS trafficking.

222 l (MQC) requires valosin-containing protein (VCP)-dependent Mitofusin/Marf degradation to prevent dam

223 y the AAA-ATPase valosin-containing protein (VCP)/p97 and augmented by the nonsterol isoprenoid geran

224 um ATPase (TERA)/valosin-containing protein (VCP)/p97 directly binds to multiple polyglutamine diseas

225 Presumably, valosin-containing protein (VCP)/p97 extracts misfolded subunits from the endoplasmi

226 urther show that valosin-containing protein (VCP)/p97 is involved in UV light-induced XPC degradation

227 , we report that valosin-containing protein (VCP)/p97 promotes the degradation of ubiquitylated GS, r

228 demonstrate that valosin-containing protein (VCP)/p97 segregase functions in ultraviolet radiation (U

229 Valosin-containing protein (VCP/p97) ATPase (a.k.a. Cdc48) is a key member of the ER

230 ne extraction by valosin-containing protein (VCP/p97) or proteasomal degradation was inhibited.

231 cognition by the valosin-containing protein (VCP/p97/Cdc48).

232 tified in a HTS campaign against recombinant VCP, has been progressively expanded and manipulated to

233 a VCP and overexpression of disease relevant VCP transgenes dismantles tubular lysosomes, linking tub

234 ysis of the parental and previously reported VCP inhibitor (CB-5083) resistant cells and found additi

235 y of this tubular lysosomal network requires VCP, an AAA-ATPase that, when mutated, causes degenerati

236 ines, representing a new class of reversible VCP inhibitors.

237 prevents excessive SUMOylation and its RNF4-VCP mediated clearance from DSBs, thereby promoting NHEJ

238 The enhancement ratios of several VCP compounds to benzene correlate well with population

239 This study used a cardiac-specific VCP transgenic mouse model to understand the transcripto

240 es a disruption in viral egress by targeting VCP and the secretory pathway, resulting in a buildup of

241 ed in cells transfected with siRNA targeting VCP.

242 in polyglutamine disease fly models by TERA/VCP/p97 corresponds well to the improvement of double-st

243 97, we reveal that functional defect of TERA/VCP/p97 in DNA double-stranded break repair is critical

244 Among multiple functions of TERA/VCP/p97, we reveal that functional defect of TERA/VCP/p9

245 t is mediated by DNA repair function of TERA/VCP/p97.

246 only mutant proteins affect dynamism of TERA/VCP/p97.

247 l for the pathology of neurons in which TERA/VCP/p97 is located dominantly in the nucleus in vivo.

248 nt polyglutamine proteins interact with TERA/VCP/p97, only mutant proteins affect dynamism of TERA/VC

249 rough a gain-of-function mechanism, and that VCP inhibitors have therapeutic value.

250 ssion (3.5-fold) of VCP, we demonstrate that VCP is a new and powerful mediator of cardiac protection

251 Here we demonstrate that VCP is critical in controlling signals transmitted via t

252 These data together demonstrate that VCP may represent a novel therapeutic avenue for the pre

253 We previously demonstrated that VCP/Cdc48-associated mitochondrial stress responsive 1 (

254 Here, we provide evidence that VCP/p97 acts as a regulator of cellular metabolism.

255 Specifically, we find that VCP inhibition causes an altered splicing pattern of the

256 We found that VCP/p97 was tied to multiple metabolic processes on the

257 disaggregation, raising the possibility that VCP may represent a therapeutic target for the treatment

258 We propose that VCP sustains sarcoplasmic proteostasis, in part, by cont

259 enic mutations in the VCP gene, we show that VCP deficiency causes profound mitochondrial uncoupling

260 Here we show that VCP is selectively translocated to the mitochondria, whe

261 We show that VCP/p97 inhibition and siRNA-mediated ablation of VCP/p9

262 by mechanistic studies in vitro showing that VCP recruitment to damaged mitochondria requires Parkin-

263 These results suggest that VCP disease mutants cause IBMPFD through a gain-of-funct

264 These data suggest that VCP dysregulation and defective stress granule disassemb

265 Our data suggest that VCP inactivation might lead to specific gain-of-function

266 Our findings suggest that VCP inhibition without stress induction, together with f

267 These studies suggest that VCP mutations may disrupt mTOR signaling and contribute

268 ation of ubiquitinated CAV1, suggesting that VCP acts downstream of ubiquitination and is required fo

269 highest in this environment, suggesting that VCPs are an important missing source of precursors that

270 ioning, and identified new drugs against the VCP/p97/ERAD pathway in human diseases.

271 ed-pluripotent stem cell model caused by the VCP mutation.

272 hree independent pathogenic mutations in the VCP gene, we show that VCP deficiency causes profound mi

273 utation at codon 616 (N616fs*) in one of the VCP alleles in HCT116 cells, and we showed that this mut

274 nalysis, we found that overexpression of the VCP in the heart was able to normalize the pressure over

275 s-5-57 to arginines prevented binding of the VCP-UBXD1 complex and, importantly, strongly reduced rec

276 itioning of drugs as novel inhibitors of the VCP/p97 ATPase.

277 etaRII on the cell surface by recruiting the VCP/E3 ligase complex, thereby limiting excessive TGF-be

278 equently, the modified receptor binds to the VCP chaperone and both proteins are degraded by the prot

279 The VCPs cite liability risk (for reporting [24.2%] and for

280 monstrated novel biological findings by this VCP device, including novel distribution of F-actin and

281 Furthermore, Clu is upstream of and binds to VCP in vivo and promotes VCP-dependent Marf degradation

282 e findings suggest a novel KLF8 to EPSTI1 to VCP to NF-kappaB signaling mechanism potentially critica

283 The localized cellular UVR exposures lead to VCP/p97 accumulation at DNA damage spots, forming distin

284 VCP mutant responsible for the resistance to VCP inhibitors while resolving the discrepancies among p

285 zation of the C-C double bond giving rise to VCPs.

286 In trans-VCP, the cyclopropane cleavage is intrinsically favored

287 rs of protein turnover, including ubiquitin, VCP/p97 and proteasomes.

288 high-throughput, cost-effective, easy-to-use VCP system, along with conventional imaging techniques,

289 ing basis for mitochondrial uncoupling using VCP knockdown neuroblastoma cell lines, induced pluripot

290 Vinylcyclopropanes (VCPs) can be polymerized through radical ring-opening po

291 tion and ene reaction of vinylcyclopropanes (VCPs) and alkynes have been studied using density functi

292 ecyclopropanes (MCPs) to vinylcyclopropanes (VCPs).

293 + 2) cycloadditions with vinylcyclopropanes (VCPs).

294 led to increased VCP/p97 expression, whereas VCP/p97 inhibition perturbed metabolic processes and int

295 om the Golgi to the plasma membrane, whereas VCP-a principal component of endoplasmic reticulum (ER)-

296 ial functions and diverse mechanisms whereby VCP regulates cardiomyocyte protein and RNA quality cont

297 t abundant and reactive VOCs associated with VCP emissions.

298 d intermolecular (5 + 2) cycloadditions with VCPs.

299 Transgenic mice overexpressing WT VCP exhibit normal cardiac structure and function, where

300 t-specific transgenic mice overexpressing WT VCP or a VCP(K524A) mutant with deficient ATPase activit