ライフサイエンスコーパス: CHIP

1 CHIP (c-terminal Hsp70-interacting protein) is an E3 lig

2 CHIP (carboxyl terminus of Hsc70-interacting protein) is

3 CHIP and RMA1 recognize different regions of CFTR and a

4 CHIP binding to Hsc70 binding was also stimulated by the

5 CHIP carriers with these mutations also had increased co

6 CHIP interacts with iNOS and promotes its ubiquitination

7 CHIP is a multidomain chaperone, utilizing both a tetrat

8 CHIP is also shown to regulate PTEN-dependent transcript

9 CHIP knockdown increased the plasma membrane abundance o

10 CHIP may serve as promising prognostic biomarker of angi

11 CHIP noncanonically ubiquitinates SirT6 at K170, which s

12 CHIP or Hsp70 overexpression promoted endogenous MLK3 ub

13 CHIP-dependent effects on AMPK activity were accompanied

14 CHIP-mediated iNOS targeting to the proteasome sequentia

15 CHIP-Seq analysis showed that the K218/221Q mutation gre

16 nd dental (Medicaid, 80% [78%-81%]; P < .01; CHIP, 77% [76%-79%]; P < .01) visits than were privately

17 e medical (Medicaid, 88% [86%-89%]; P < .01; CHIP, 88% [87%-89%]; P < .01) and dental (Medicaid, 80%

18 m, identified herein for the first time as a CHIP-ubiquitination substrate (unlike its AMPKalpha2-iso

19 nic transcription factors myocardin/SRF in a CHIP-dependent manner.

20 We determined that a CHIP monomer is most stable when the HH domain has an ex

21 also reduced the level of MLK3 protein via a CHIP-dependent mechanism.

22 In addition, CHIP depletion in ovarian cancer SKOV3 cells increased c

23 t the VEGFR2 protein level was reduced after CHIP overexpression.

24 Although CHIP, an E3 ubiquitin ligase, promoted NCC ubiquitinatio

25 he implementation of the Medicare Access and CHIP Reauthorization Act (MACRA) offers a time-sensitive

26 ment of value payment in Medicare Access and CHIP Reauthorization Act and will likely remain so for t

27 nalyze the impact of the Medicare Access and CHIP Reauthorization Act of 2015 (MACRA) on the field of

28 ordable Care Act and the Medicare Access and CHIP Reauthorization Act, solidified the role of value-b

29 ctivation inhibits ERK5/CHIP association and CHIP Ub ligase activity.

30 e: two ubiquitin ligases (SCF(betaTrCP2) and CHIP) determine the GH responsiveness of cells by contro

31 e degraded at the same rate in CHIP(-/-) and CHIP(+/+) mouse embryonic fibroblasts after treatment wi

32 tein) regulates protein quality control, and CHIP deletion accelerates aging and reduces the life spa

33 ivo concentrations of Hsp70, Hsp90, HOP, and CHIP under normal conditions and when client proteins ar

34 ER-associated E3 ubiquitin ligases, HRD1 and CHIP.

35 eracted more strongly with Hsp70, Hsp40, and CHIP, consistent with a role for the Hsp70/Hsp40 system

36 We also show that both Hsp70 and CHIP play a major role in the ubiquitination of C331A nN

37 ed the stoichiometries of the CHIP-Hsp70 and CHIP-Hsp90 complexes and measured the corresponding diss

38 quitination and binding of Hsp90, Hsp70, and CHIP in a manner that is specific for changes in the hem

39 taining purified E1, E2 (UbcH5a), Hsp70, and CHIP that recapitulates the ability of the cells to sele

40 quitination and binding of Hsp90, Hsp70, and CHIP.

41 ion of the inactivated nNOS by an Hsp70- and CHIP (C terminus of Hsc70-interacting protein)-dependent

42 [95% CIs]), children insured by Medicaid and CHIP were significantly more likely to receive a prevent

43 otein was rapidly ubiquitinated by MuRF1 and CHIP.

44 CHIP association, suggesting that p90RSK and CHIP competes for ERK5 binding and that p90RSK activatio

45 p90RSK and CHIP share a common binding site in the ERK5 C-terminal

46 emistry, protein chemistry, and reporter and CHIP assays.

47 ls in response to GA and stress stimuli, and CHIP-dependent regulation of MLK3 is required for suppre

48 the dimeric GHR, identifying both Ubc13 and CHIP as novel factors in the regulation of cell surface

49 ting the AR by activating E3 ligases such as CHIP represents a novel strategy for the treatment of pr

50 ting the AR by activating E3 ligases such as CHIP represents a novel strategy for the treatment of pr

51 siRNAs to myocardin or NF-kappaB, as well as CHIP overexpression prevented (while siRNA-mediated CHIP

52 In addition to betaTrCP, CHIP interacts specifically with the cytosolic tails of

53 liminary evidence for an association between CHIP and atherosclerotic cardiovascular disease, but the

54 on of Hsc70 provides for flexibility between CHIP and the chaperone, allowing the ligase to "search"

55 by Ube2w stabilizes the interaction between CHIP and ataxin-3, which through its DUB activity limits

56 trate a stress-dependent interaction between CHIP and Daxx (death domain-associated protein).

57 The interaction between CHIP and Daxx results in ubiquitination of Daxx, which i

58 he role of CHIP and the relationship between CHIP and VEGF-VEGFR2 (VEGF receptor 2) pathway in RCC.

59 creased proteasome-mediated degradation, but CHIP overexpression in these cells increases SirT6 prote

60 In vitro ubiquitination of Daxx by CHIP revealed that ubiquitin chain formation utilizes no

61 The ubiquitination of Daxx by CHIP utilizes lysines 630 and 631 and competes with the

62 phosphorylatable Slug-4SA is not degraded by CHIP.

63 mode of ubiquitination of Hsp70 and Hsp90 by CHIP, which ultimately leads to their degradation.

64 care, with caregivers of children insured by CHIP reporting the highest rates of difficulty accessing

65 polypeptides, contributes to recognition by CHIP.

66 nism that the Warburg effect is regulated by CHIP through its function as an E3 ligase, which mediate

67 e of ubiquitination of various substrates by CHIP in vitro.

68 es on human Hsp70 and Hsp90 ubiquitinated by CHIP.

69 in the efficiency of Hsc70 ubiquitination by CHIP.

70 f a modular human E3 ubiquitin ligase called CHIP (carboxyl terminus of Hsc70-interacting protein) by

71 ntegral gp78 and the cytosolic co-chaperone, CHIP (C terminus of Hsp70-interacting protein), as the r

72 inhibitor-specific microarray analyses (CLIP-CHIP) of laser-dissected leukocyte infiltrated and nonin

73 he altered nNOS by Hsp70 and its cochaperone CHIP, an E3-ubiquitin ligase, has been proposed.

74 domain and association with the cochaperone CHIP, resulting in ubiquitination and proteasomal degrad

75 al degradation in the ER through cochaperone CHIP, Hsp105 has a primary role promoting CFTR quality c

76 a purified ubiquitinating system containing CHIP (carboxyl terminus of Hsp70-interacting protein) as

77 However, molecular features that control CHIP recruitment to Hsp/c70, and hence the fate of the H

78 Compared with wild-type controls, CHIP knockout mice or novel CRISPR/Cas9 mice without CHI

79 ate ubiquitination, ataxin-3 deubiquitinates CHIP, effectively terminating the reaction.

80 HIP antisense oligonucleotides to knock down CHIP reversed the LTED-induced down-regulation of ERalph

81 In addition, we demonstrate that an E3 CHIP (carboxyl terminus of Hsp70 interacting protein) in

82 kin, APC, and SCF(betaTRCP1)), the U-box E3, CHIP, and HECT domain E3s (E6AP and Nedd4) when assayed

83 Each CHIP monomer consists of a tetratricopeptide-repeat (TPR

84 compartment-specific substrates would enable CHIP to participate in the reorganization of the respect

85 On the other hand, depletion of endogenous CHIP stabilizes PTEN.

86 Engineered CHIP enhanced KCNQ1 ubiquitination, eliminated KCNQ1 sur

87 ral aging, because aged rats showed enhanced CHIP interaction; ubiquitination and degradation of both

88 ot after LTED prevented the enhanced ERalpha-CHIP interaction and ERalpha ubiquitination/degradation

89 growth factor-1 (IGF-1) was mediated by ERK5-CHIP signal module via inducible cAMP early repressor (I

90 Both disruption of ERK5-CHIP binding with inhibitory helical linker domain fragm

91 as a novel CHIP substrate and that the ERK5-CHIP complex plays an obligatory role in inhibition of I

92 The regulatory mechanism governing ERK5/CHIP interaction is unknown.

93 K activation is critical for inhibiting ERK5/CHIP interaction.

94 p90RSK activation inhibits ERK5/CHIP association and CHIP Ub ligase activity.

95 r an ERK5 fragment (aa571-807) inhibits ERK5/CHIP association, suggesting that p90RSK and CHIP compet

96 Here, we reveal a mechanism for CHIP's influence on longevity by demonstrating that CHIP

97 Moreover, the same motif is required for CHIP-mediated ubiquitination of Hsc70 in vitro, highligh

98 MPK as the first physiological substrate for CHIP chaperone activity and establishing a link between

99 sphate enhance association of chaperone-free CHIP with liposomes.

100 ility of the XRCC1 monomer is protected from CHIP-mediated ubiquitylation by interaction with the bin

101 Furthermore, CHIP overexpression caused a proteasome-dependent reduct

102 dings provide evidence of a de novo GSK3beta-CHIP-Slug pathway that may be involved in the progressio

103 1,853 (13.6%) had Medicaid, 9554 (18.4%) had CHIP, and 8125 (10.8%) were uninsured.

104 sequencing cohort, 120 patients (29.9%) had CHIP at the time of ASCT, which was associated with an i

105 ired samples (two [33%] of six patients) had CHIP mutations that decreased in allele frequency, givin

106 herapy-treated patients with cancer who have CHIP are at increased risk of developing therapy-related

107 NTERPRETATION: Patients with cancer who have CHIP are at increased risk of developing therapy-related

108 Patients with cancer who have CHIP are at increased risk of developing therapy-related

109 ICER induction was enhanced in heterozygous CHIP(+/-) mice.

110 GM12878) obtained via ChIA-PET, Hi-C, and Hi-CHIP assays.

111 To understand how CHIP recognizes Hsp/c70, we utilized a dominant negative

112 elaxation-based NMR experiments on the Hsc70-CHIP complex determined that the two partners move indep

113 cence polarization to characterize the Hsc70-CHIP interaction.

114 Disrupting Hsp70-CHIP interaction prevents the aggresome formation, where

115 sly shown that nNOS turnover is due to Hsp70/CHIP-dependent ubiquitination and proteasomal degradatio

116 degradation, either by regulating the Hsp90/CHIP complex directly or by competing as a client protei

117 These studies implicate CHIP as a stress-dependent regulator of Daxx that counte

118 Our previous studies have implicated CHIP (carboxyl terminus of Hsp70-interacting protein) as

119 In CHIP-deficient cells, SirT6 protein half-life is substan

120 In CHIP-depleted cells, SirT6 K170 mutation increases SirT6

121 lcoholic steatohepatitis (NASH) was found in CHIP(-/-)-mice over the first 8-9-months of life.

122 scriptional portrait in CHIP(+/+) but not in CHIP(-/-) heat shocked mouse embryonic fibroblasts.

123 he p53-dependent transcriptional portrait in CHIP(+/+) but not in CHIP(-/-) heat shocked mouse embryo

124 r (AR112Q), are degraded at the same rate in CHIP(-/-) and CHIP(+/+) mouse embryonic fibroblasts afte

125 levation and injurious insulin resistance in CHIP(-/-)-livers apparently counteracts/delays rapid pro

126 nd promotes downstream gene transcription in CHIP-depleted cells.

127 Thus, increasing CHIP E3 ligase activity and blocking HSP90 chaperone act

128 and the depletion of ERK5 by siRNA inhibited CHIP Ub ligase activity, which suggests an obligatory ro

129 data suggest a role for p90RSK in inhibiting CHIP activity and promoting cardiac apoptosis through bi

130 as the E3 ligase to show that Hsp90 inhibits CHIP-dependent nNOS ubiquitination.

131 of ERK5 or overexpression of p90RSK inhibits CHIP activity and accelerates cardiac apoptosis after MI

132 ain bound directly to GATA4 and enhanced its CHIP (C terminus of Hsp70-interacting protein) E3 ligase

133 s nuclear stabilization of FOXOs, well-known CHIP-ubiquitination targets.

134 Cells lacking CHIP are hypersensitive to DNA-damaging agents, but DNA

135 cells involving activation of the E3 ligase CHIP (C-terminus of Hsp70-interacting protein) and degra

136 event Hsp70 association and ubiquitin ligase CHIP (C terminus of Hsc70-interacting protein)-mediated

137 The E3 ubiquitin ligase CHIP (C-terminus of Hsc70 Interacting Protein, a 70 kDa

138 The ubiquitin ligase CHIP (carboxyl terminus of Hsp70-interacting protein) re

139 upon both Hsp70 and the E3 ubiquitin ligase CHIP and is blocked by methylene blue.

140 The Hsp90-related ubiquitin ligase CHIP is able to interact and destabilize FGFR3.

141 aches, we found that the E3 ubiquitin ligase CHIP is highly expressed throughout the collecting duct;

142 The HSP90-associated E3 ubiquitin ligase CHIP mediates the ensuing proteasome-dependent MIF degra

143 containing Hsp70 and the E3 ubiquitin ligase CHIP requires the interaction of Bag1 with Hsp70, but th

144 inding interface for the E3-ubiquitin ligase CHIP within the major disordered domain of IRF-1 led us

145 ted and degraded by the tau ubiquitin ligase CHIP, and this largely depends on the Hsp90 complex.

146 to recruit the cochaperone ubiquitin ligase CHIP, which is known to facilitate the ubiquitination of

147 of bound clients by the E3 ubiquitin ligase CHIP.

148 Hsc70 and Hsp90 and by the ubiquitin ligase CHIP.

149 not uniquely rely on the E3 ubiquitin ligase CHIP.

150 targeted the catalytic domain of E3 ligase, CHIP, to YFP-tagged KCNQ1 +/- KCNE1 subunits with a GFP-

151 , the cochaperone HOP, and ubiquitin ligase, CHIP.

152 y Hsp70-dependent ubiquitin E3 ligases, like CHIP, is inhibited.

153 em-cell transplantation (ASCT) for lymphoma, CHIP at the time of ASCT would be associated with an inc

154 on In patients undergoing ASCT for lymphoma, CHIP at the time of transplantation is associated with i

155 inal residues are necessary both to maintain CHIP stability and function.

156 ber of E3 ubiquitin ligases, including MDM2, CHIP, and NEDD4, which can result in its proteosomal deg

157 Mechanistically, CHIP promoted LKB1-mediated phosphorylation of AMPK, inc

158 her p90RSK activation inhibits ERK5-mediated CHIP activation, and subsequently increases ICER levels

159 erexpression prevented (while siRNA-mediated CHIP disruption potentiated) high insulin-induced SR ele

160 ce types, the average wait time for Medicaid-CHIP enrollees was 22 days longer than that for privatel

161 Overall, 66% of Medicaid-CHIP callers (179 of 273) were denied an appointment as

162 sparities in provider acceptance of Medicaid-CHIP versus private insurance across all tested specialt

163 In polyglutamine disease models, CHIP has been considered a primary protection factor by

164 sion of CHIP, but not of the inactive mutant CHIP K30A, induced accumulation of AXL polyubiquitinated

165 esome formation, whereas a dominant-negative CHIP mutant sensitizes the aggregation of misfolded prot

166 We identified ICER as a novel CHIP substrate and that the ERK5-CHIP complex plays an o

167 lical linker domain fragment (aa 101-200) of CHIP and the depletion of ERK5 by siRNA inhibited CHIP U

168 crease in SirT6 expression in the absence of CHIP is associated with decreased SirT6 promoter occupan

169 rnary folding complex whereas the binding of CHIP to the chaperones has previously been shown to lead

170 es from two prospective cohorts, carriers of CHIP had a risk of coronary heart disease that was 1.9 t

171 of a Tau protein triage system consisting of CHIP/Hsp70 and other chaperones have begun to emerge.

172 Reciprocally, depletion of CHIP leads to promotion of tumor growth.

173 Depletion of CHIP, using siRNA, inhibited IGF-1-mediated reduction of

174 The distribution of CHIP-related gene mutations differs between individuals

175 The TPR domain of CHIP and parts of the N-terminal domain of PTEN are requ

176 ng to the tetratricopeptide repeat domain of CHIP.

177 We assessed the effect of CHIP at the time of ASCT on subsequent outcomes, includi

178 Moreover, low expression of CHIP is a strong and independent negative prognostic val

179 in ovarian carcinoma, induced expression of CHIP results in significant inhibition of the tumor grow

180 this study, we found that the expression of CHIP was downregulated and significantly correlated with

181 were available, the mean allele frequency of CHIP mutations had expanded by the time of the therapy-r

182 mpairs Angiotensin II-mediated inhibition of CHIP activity and subsequent increase in ICER levels.

183 a systematic analysis of the interactions of CHIP with E2 conjugating enzymes and found that only a s

184 on of CHIP protects against and knockdown of CHIP exacerbates toxicity mediated by mutant LRRK2.

185 ter channel AQP2 in vitro shRNA knockdown of CHIP in CCD cells increased AQP2 protein t1/2 and reduce

186 Knockdown of CHIP or MDM2 (mouse homolog of double minute 2 protein)

187 Knockdown of CHIP stabilizes the wtSlug protein and reduces Slug ubiq

188 Depletion or knockout of CHIP increased the glycolytic products in both tumor and

189 Monoubiquitination of CHIP by Ube2w stabilizes the interaction between CHIP an

190 Overexpression of CHIP leads to elevated ubiquitination and a shortened ha

191 Overexpression of CHIP protects against and knockdown of CHIP exacerbates

192 Overexpression of CHIP, but not of the inactive mutant CHIP K30A, induced

193 e-exome sequencing to detect the presence of CHIP in peripheral-blood cells and associated such prese

194 The presence of CHIP in peripheral-blood cells was associated with nearl

195 f-concept study to compare the prevalence of CHIP between patients with cancer who later developed th

196 The prevalence of CHIP in all patients (23 [33%] of 69 patients) was highe

197 d all-cause mortality, but the prevalence of CHIP in patients who develop therapy-related myeloid neo

198 ses had a significantly higher prevalence of CHIP than did matched controls (eight [62%] of 13 cases

199 Here we discuss the nature and prevalence of CHIP, distinction of this state from MDS, and current ar

200 tion, ELISA tests showed that restoration of CHIP inhibited, while knockdown promoted, the secreted l

201 However, little is known about the role of CHIP and the relationship between CHIP and VEGF-VEGFR2 (

202 y and Ub assay showed ICER as a substrate of CHIP Ub ligase.

203 whereas the levels of a natural substrate of CHIP were unaffected.

204 n (Ub) ligase and subsequent upregulation of CHIP ligase activity, which induces ICER ubiquitination

205 which suggests an obligatory role of ERK5 on CHIP activation.

206 ured by Medicaid (26% [23%-28%]; P < .01) or CHIP (38% [35%-40%]; P < .01).

207 ed with the increased CYP3A4 loss on gp78 or CHIP coexpression, suggests that ERAD-associated E3 Ub-l

208 Administration of a proteasomal inhibitor or CHIP antisense oligonucleotides to knock down CHIP rever

209 Children's odds of having Medicaid or CHIP coverage increased when their parents were randomly

210 Children's Medicaid or CHIP coverage, assessed monthly and in 6-month intervals

211 %-67%]) than children insured by Medicaid or CHIP.

212 ning 26S proteasomes, UbcH5, an E3 (MuRF1 or CHIP), and a protein substrate, dramatically stimulated

213 Combined RMA1 or CHIP inactivation and Corr-4a treatment enhanced CFTRDel

214 We report that inactivation of the RMA1 or CHIP ubiquitin ligase permits a pool of CFTRDeltaF508 to

215 uted ER-associated degradation system, P269A CHIP inhibited Hsc70-dependent CFTR ubiquitination and d

216 ed clonal evolution in cases for whom paired CHIP and therapy-related myeloid neoplasm samples were a

217 [67%] of six patients) cases for whom paired CHIP and therapy-related myeloid neoplasm samples were a

218 nal haemopoiesis of indeterminate potential (CHIP) is an age-associated genetic event linked to incre

219 al hematopoiesis of indeterminate potential (CHIP) is an age-related condition characterized by somat

220 al hematopoiesis of indeterminate potential (CHIP), analogous to monoclonal gammopathy of undetermine

221 al hematopoiesis of indeterminate potential (CHIP), which is defined as the presence of an expanded s

222 al hematopoiesis of indeterminate potential (CHIP).

223 ting to the proteasome sequentially precedes CHIP-mediated iNOS sequestration to the aggresome.

224 Akt also prevents CHIP-induced tau ubiquitination and its subsequent degra

225 of the Children's Health Insurance Program (CHIP) beyond 2017, merits renewed attention on the quali

226 caid or Children's Health Insurance Program (CHIP) coverage (intent-to-treat analyses).

227 and the Children's Health Insurance Program (CHIP) versus private insurance.

228 ulated CHIP binding to Hsc70 while promoting CHIP oligomerization.

229 the C terminus of Hsp70-interacting protein (CHIP) and the Hsp70/Hsp90 organizer protein, were associ

230 rboxy terminus of Hsp70-interacting protein (CHIP) and the molecular chaperone Hsp90 are implicated i

231 COOH terminus of Hsp70 interacting protein (CHIP) as being connected to this process.

232 boxyl terminus of HSP70-interacting protein (CHIP) binds, ubiquitinates, and promotes the ubiquitin p

233 The C terminus of Hsp70 interacting protein (CHIP) E3 ligase functions as a key regulator of protein

234 of C-terminus of Hsc70-interacting protein (CHIP) E3 ubiquitin-ligase impairs hepatic cytochrome P45

235 ase C-terminus of Hsc70 interacting protein (CHIP) has been shown in vitro and in vivo to associate w

236 boxyl terminus of Hsc70-interacting protein (CHIP) in the regulation of MLK3 protein levels.

237 boxyl terminus of Hsc70-interacting protein (CHIP) interacts with wild-type Slug (wtSlug).

238 C-terminus of Hsc/p70-Interacting Protein (CHIP) is a homodimeric E3 ubiquitin ligase.

239 the C terminus of Hsc70-interacting protein (CHIP) on myocytes has been reported.

240 ligase C-terminal Hsp70-interacting protein (CHIP) recognizes and marks for degradation not only a mu

241 nate protein 70 (Hsc70)-interacting protein (CHIP) that leads to its ubiquitination/proteasomal degra

242 hat C terminus of HSC70-interacting protein (CHIP), a regulator of protein quality control, influence

243 the C terminus of Hsc70-interacting protein (CHIP), an E3 ubiquitin ligase that ubiquitinates ataxin-

244 ligase C-terminal Hsp70-interacting protein (CHIP), if freed from chaperones during acute stress, can

245 f heat shock protein 70-interacting protein (CHIP), increased SRF activity, as well as beta-myosin he

246 H5a-C terminus of Hsc70-interacting protein (CHIP)-Hsc70-Hsp40) complexes, as well as protein kinases

247 COOH terminus of Hsp70-interacting protein (CHIP)-mediated ubiquitination.

248 boxyl terminus of HSC70-interacting protein (CHIP).

249 terminal of Hsp70/Hsp90 interacting protein (CHIP).

250 the plasma membrane quality control proteins CHIP and Hsc70 partially restored DeltaF508CFTR-scaffold

251 contrast to nearly all homodimeric proteins, CHIP is asymmetric.

252 Rather CHIP recruitment involves reciprocal allosteric interact

253 molecular events that coordinately regulate CHIP, a neuroprotective E3 implicated in protein quality

254 ation coupled to high-throughput sequencing (CHIP-seq) to investigate the changes that occur in mRNA

255 However, the U-box mutation stimulated CHIP binding to Hsc70 while promoting CHIP oligomerizati

256 itination competitive with Daxx sumoylation, CHIP integrates the proteotoxic stress response of the c

257 We conclude that CHIP preferentially recognizes and mediates degradation

258 influence on longevity by demonstrating that CHIP stabilizes the sirtuin family member SirT6, a lysin

259 Furthermore, we determined that CHIP forms polyubiquitin chains on Hsp70 and Hsp90 linke

260 These observations establish that CHIP does not play an exclusive role in regulating the t

261 It is established that CHIP binds to Hsp90 as well as to Hsp70, but we show her

262 Here, we present evidence that CHIP binds, ubiquitinates and regulates expression of hi

263 We found that CHIP binds tightly to two molecules of Hsc70 forming a 2

264 Simultaneously, we observed that CHIP expression inversely correlated with PKM2 levels in

265 Here, we report that CHIP, the chaperone-associated E3 ligase, induces ubiqui

266 Here, we show that CHIP (carboxyl terminus of Hsc70-interacting protein), a

267 We show that CHIP interacts with MLK3 and, together with the E2 ubiqu

268 Accordingly, we show that CHIP regulates PKM2 protein stability and thereafter the

269 In summary, these results suggest that CHIP regulates AQP2 and subsequently, renal water handli

270 or of glycolysis in tumors, as a target that CHIP mediated for degradation.

271 findings demonstrate for the first time that CHIP may be involved in RCC angiogenesis through regulat

272 enza A virus (IAV) infection, as well as the CHIP-seq data from ENCODE on transcription factor (TF) a

273 ough the importance of phosphodegrons in the CHIP targeting of its substrates is known, to our knowle

274 mice subjected to myocardial infarction, the CHIP Ub ligase activity was decreased, with an increase

275 we characterized the stoichiometries of the CHIP-Hsp70 and CHIP-Hsp90 complexes and measured the cor

276 S in vitro and regulates, in large part, the CHIP-dependent degradation of nNOS in HEK293 cells, as w

277 initiating, regulating, and terminating the CHIP ubiquitination cycle.

278 Here, we study one facet of this CHIP-mediated turnover by determining the lysine residue

279 The discovery of this CHIP-SirT6 interaction represents a novel protein-stabil

280 Thus, CHIP modulates MLK3 protein levels in response to GA and

281 vity limits the length of chains attached to CHIP substrates.

282 f in loop 7 of E2 is required for binding to CHIP but is not sufficient for activation of the E2 appr

283 PA motif provides specificity for binding to CHIP, whereas activation of the E2 approximately Ub conj

284 pendent E3 ligase Parkin acts redundantly to CHIP on some substrates.

285 Here, we show that two CHIP substrates, the glucocorticoid receptor (GR), a cla

286 revealed that mammalian UBC7/gp78 and UbcH5a/CHIP E2-E3 ubiquitin ligases were capable of ubiquitinat

287 control exerts on the aging process by using CHIP-/- mice.

288 In vitro, CHIP negatively regulated RCC cell migration, invasion a

289 yeloid neoplasm and the primary exposure was CHIP.

290 While CHIP is downregulated in ovarian carcinoma, induced expr

291 n hyperglycemic states, via association with CHIP ubiquitin (Ub) ligase and subsequent upregulation o

292 he most commonly mutated genes in cases with CHIP were TET2 (three [38%] of eight patients) and TP53(

293 PTEN shared an inverse correlation with CHIP in human prostate cancer patient samples, thereby t

294 Ubc13 activity and its interaction with CHIP precede endocytosis of GHR.

295 adation pathway through its interaction with CHIP.

296 set myocardial infarction, participants with CHIP had a risk of myocardial infarction that was 4.0 ti

297 Patients with CHIP had significantly inferior overall survival compare

298 nce, 14.1% v 4.3% for those with and without CHIP, respectively; P = .002).

299 ckout mice or novel CRISPR/Cas9 mice without CHIP E3 ligase activity had greater AQP2 abundance and a

300 overall survival compared with those without CHIP (10-year overall survival, 30.4% v 60.9%, respectiv