ライフサイエンスコーパス: VCP

1 VCP inhibition by si/shRNA or small-molecule (Eeyarestat

2 VCP is an ubiquitously expressed, highly abundant protei

3 VCP is necessary for protein degradation via the proteas

4 VCP is required concurrently with the proteasome, as add

5 VCP mutations are the cause of inclusion body myopathy,

6 VCP mutations should thus be considered for genetically

7 VCP participates in diverse cellular functions by associ

8 VCP recruitment coincides temporally with mitochondrial

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

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

11 VCPs with terminal substitution on the alkene reacted wi

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

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

14 y was conducted among a random sample of 500 VCPs who were active members of their Michigan professio

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

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

17 cellularly expressed IgG Fc is degraded in a VCP-independent manner.

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

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

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

21 ound that mutation of cysteine 162 abrogated VCP cell surface expression.

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

23 triazoles, a new class of potent, allosteric VCP inhibitors, are described.

24 Although VCP has been described as a virulence factor, the mechan

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

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

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

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

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

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

31 e switch in species selectivity of SPICE and VCP is the presence of oppositely charged residues in th

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 survey assessed VCPs' attitudes and behaviors in addressing driving conc

35 associated degradation (ERAD) pathway ATPase VCP/p97 leads to the Nrdp1-dependent accumulation of ubi

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

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

38 Thus, aberrant interactions between VCP and NF1 may explain the dementia phenotype and cogni

39 ghlight an important pathologic link between VCP and cognition.

40 nd devising communication strategies between VCPs and other members of the health care team.

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

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

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

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

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

46 Resources endorsed by VCPs as helpful or very helpful include driving assessme

47 ly identified genetic forms of ALS (C9ORF72, VCP, UBQLN2, and PFN1), underscores the central role of

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

49 7, a valosin-containing protein (also called VCP), plays an essential role in the postubiquitinationa

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

51 nd mammalian Vms1 stably interact with Cdc48/VCP/p97, a component of the ubiquitin/proteasome system

52 In cultured cells, VCP binds to DIAP1 in a ubiquitin- and BIR domain-depend

53 ame intrinsic preferences occur with the cis-VCP, an unfavorable rotation is required in order to gen

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

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

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

57 o bind VACV A56, the ectromelia virus (ECTV) VCP homolog is only able to bind the ECTV homolog of A56

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

59 Transient expression of either VCP/p97 or PP2Ac was sufficient to elevate levels of the

60 Endogenous VCP/p97 and PP2Ac were co-immunoprecipitated from primar

61 Although overexpressed or endogenous VCP did not seem to focally aggregate inside neurons, TD

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

63 surface expression, we transiently expressed VCP and A56 in eukaryotic cell lines and found that they

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

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

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

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

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

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

70 Furthermore, VCP mutations are causative of some neurodegenerative di

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

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

73 GST-VCP/p97 bound purified PP2A in pulldown assays, showing

74 d-type and disease-causing versions of human VCP/p97.

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

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

77 ation and used mass spectrometry to identify VCP/p97 as a novel partner for PP2Ac.

78 These results implicate VCP as an important host factor in antiviral immunity.

79 Importantly, VCP inhibitors suppress mitochondrial defects, muscle ti

80 To understand the regulation of autophagy in VCP-IBM muscle, we examined the AKT/FOXO3 and mammalian

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

82 nd autophagosome biogenesis was increased in VCP-IBM muscle.

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

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

85 Mutations in VCP cause multisystem degeneration impacting the nervous

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

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

88 Because mutations in VCP predispose humans to amyotrophic lateral sclerosis,

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

90 this is impaired by pathogenic mutations in VCP.

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

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

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

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

95 Indeed, VCP interacts genetically with the PINK1/parkin pathway

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

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

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

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

100 ld-type virus (vv-VCPwt) and a virus lacking VCP (vv-VCPko).

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

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

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

104 differentiated C2C12 cells expressing mutant VCP.

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

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

107 In vitro studies indicate that mutant VCP causes inappropriate activation of the NF-kappaB sig

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

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

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

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

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

113 terized a Drosophila model of IBMPFD (mutant-VCP-related degeneration).

114 identifying neurofibromin-1 (NF1) as a novel VCP interactor in the CNS.

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

116 97 inhibition and siRNA-mediated ablation of VCP/p97 and its cofactors UFD1 and UBXD7 impair CSB degr

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

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

119 MPFD-associated mutations disrupt binding of VCP to NF1, resulting in reduced synaptogenesis.

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

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

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

123 This suggests that surface expression of VCP may contribute to poxvirus pathogenesis.

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

125 While the smallpox homolog of VCP is able to bind VACV A56, the ectromelia virus (ECTV

126 Depletion or catalytic inhibition of VCP prevents capsid degradation and reduces neutralizati

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

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

129 ( 40% true hit rate) as direct inhibitors of VCP/p97 and ERAD.

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

131 a substrate that necessitates involvement of VCP, since intracellularly expressed IgG Fc is degraded

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

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

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

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

136 y, we evaluated the therapeutic potential of VCP inhibition and observed significantly reduced NSCLC

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

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

139 ngs but also identified the specific role of VCP in NSCLC pathogenesis and progression.

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

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

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

143 More than 80% of VCPs are confident in their ability to determine whether

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

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

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

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

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

149 p97/VCP is a hexameric ATPase that is coupled to diverse cel

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

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

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

153 These data indicate that UBXD8 and p97/VCP play central integrative roles in cellular energy ho

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

155 mal interaction between ATP7A(T994I) and p97/VCP, an ubiquitin-selective chaperone which is mutated i

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

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

158 related DMN and establish a link between p97/VCP and genetically distinct forms of motor neuron degen

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

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

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

162 ing review will discuss the evidence for p97/VCP in autophagy and how a disruption in this process co

163 One particularly important role for p97/VCP is facilitating intracellular protein degradation.

164 ex, we demonstrate that the Sel1L, Hrd1, p97/VCP, and importin beta proteins are required for the dis

165 dominant disorder caused by mutations in p97/VCP (valosin-containing protein).

166 In addition, IBMPFD mutations in p97/VCP lead to accumulation of autophagic structures in pat

167 This is likely due to a defect in p97/VCP-mediated autophagosome maturation.

168 all-interfering RNA (SiRNA) knockdown of p97/VCP corrected ATP7A(T994I) mislocalization.

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

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

171 xpression of a dominant negative form of p97/VCP, a protein essential for dislocation of ERAD substra

172 2 or mutation of the SIK2 target site on p97/VCP led to impaired degradation of ERAD substrates and d

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

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

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

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

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

178 The p97/VCP ATPase complex facilitates the extraction and degrad

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

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

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

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

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

184 Paradoxically, VCP complements PINK1 deficiency but not parkin deficien

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

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

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

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

189 Common situations that prompted VCPs to ask patients about driving included poor visual

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

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

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

193 Mutations in valosin-containing protein (VCP) cause a rare, autosomal dominant disease called inc

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

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

196 id change in the valosin-containing protein (VCP) gene in an Italian family with autosomal dominantly

197 mutations in the valosin-containing protein (VCP) gene.

198 mutations in the valosin-containing protein (VCP) gene.

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

200 p97/valosin-containing protein (VCP) is a type II ATPase associated with various cellula

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

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

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

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

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

206 the function of Valosin-containing protein (VCP), a ubiquitin-selective AAA chaperone involved in en

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

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

209 y the ATPase p97/valosin-containing protein (VCP), an enzyme with segregase and unfoldase activity, a

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

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

212 nic mutations in valosin-containing protein (VCP), the human ortholog of CDC48.

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

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

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

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

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

218 Valosin-containing protein (VCP)/p97 is an AAA ATPase molecular chaperone that regul

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

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

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

222 mutant SOD1 and valosin-containing protein (VCP)/p97.

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

224 d vaccinia virus complement control protein (VCP), respectively, to subvert the host complement syste

225 e vaccinia virus complement control protein (VCP).

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

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

228 We show that Ydr049 (renamed VCP/Cdc48-associated mitochondrial stress-responsive--Vm

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

230 In this respect, VCP has recently received a great deal of attention as a

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

232 identified as FABP1, Sar1b, Sec13, and small VCP/p97-interactive protein by immunoblot, LC-MS/MS, and

233 Strong VCP inhibition is cell lethal, but milder inhibition int

234 tudying the reactions of several substituted VCPs with a range of unsymmetrical alkynes.

235 s a virus that does not express cell surface VCP is attenuated in vivo.

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

237 ed in cells transfected with siRNA targeting VCP.

238 CONCLUSIONS/SIGNIFICANCE: Thus, targeting VCP in NSCLC may provide a novel strategy to restore p53

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

240 utamine proteins impair accumulation of TERA/VCP/p97 and interaction of related double-stranded break

241 97, we reveal that functional defect of TERA/VCP/p97 in DNA double-stranded break repair is critical

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

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

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

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

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

247 wn to be more human complement-specific than VCP, and in this study we show that VCP is more bovine c

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

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

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

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

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

253 We also found that VCP directly regulates p53 and NFkappaB protein levels a

254 A recent study indicated that VCP expression levels are correlated with prognosis and

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

256 We propose that VCP/p97-mediated Tyr nitration of PP2A increases the lev

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

258 fic than VCP, and in this study we show that VCP is more bovine complement-specific than SPICE.

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

260 GY/PRINCIPAL FINDINGS: Our results show that VCP is significantly overexpressed in non-small cell lun

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 cytometry verified this data and shows that VCP inhibition significantly (p<0.001, p<0.003) induced

264 These results suggest that VCP contributes to virulence by dampening both antibody

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

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

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

268 lude motor neuron degeneration, suggest that VCP mutations may account for approximately 1%-2% of fam

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

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

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

272 ang and colleagues have further expanded the VCP interactome by identifying neurofibromin-1 (NF1) as

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

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

275 uitination and subsequent recruitment of the VCP-UFD1L-NPL4 dislocase complex.

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 ce of this ubiquitination for binding to the VCP-UBXD1 complex and for sorting into lysosomes.

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

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

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

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

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

289 The human selenoprotein VIMP (VCP-interacting membrane protein)/SelS (selenoprotein S)

290 ) cycloadditions between vinylcyclopropanes (VCPs) and alkynes have been conducted experimentally and

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

292 nd homo-ene reactions of vinylcyclopropanes (VCPs) and alkynes have been studied using density functi

293 ecyclopropanes (MCPs) to vinylcyclopropanes (VCPs).

294 + 2) cycloadditions with vinylcyclopropanes (VCPs).

295 a virulence factor, the mechanisms by which VCP enhances VACV pathogenesis have not been fully defin

296 While VCPs view that advising patients about driving is an imp

297 sults show that degeneration associated with VCP mutations is mediated in part by toxic gain of funct

298 3-nitrotyrosine in the PP2Ac associated with VCP/p97, a response severely reduced in macrophages from

299 could therefore form a disulfide bridge with VCP.

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