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 arises from somatic mutations in hematopoietic stem

3 CHIP binding to Hsc70 binding was also stimulated by the

4 CHIP carriers with these mutations also had increased co

5 CHIP is also shown to regulate PTEN-dependent transcript

6 CHIP is associated with a variety of adverse outcomes, i

7 CHIP is associated with increased risk of incident CVD.

8 CHIP knockdown in HEK-293T cells using CRISPR-Cas9 led t

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 transfection in HIV-1 reporter TZM-bl cells resulte

14 CHIP's implications for stem cell transplantation have b

15 CHIP-dependent effects on AMPK activity were accompanied

16 CHIP-S20E knock-in mice better clear ubiquitinated prote

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

18 ds ratio, 1.73 [95% CI, 1.23-2.44]; P=0.001; CHIP with variant allele frequency >0.1: odds ratio, 1.9

19 : odds ratio, 1.36 [95% 1.10-1.68]; P=0.004; CHIP with variant allele frequency >0.1: odds ratio, 1.4

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

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

22 A CHIP mutant lacking the U-box domain, which is responsib

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

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

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

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

27 Co-transfection of Tat with a CHIP-expressing plasmid decreased the levels of Tat prot

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

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

30 was independently associated with CHIP (all CHIP: odds ratio, 1.36 [95% 1.10-1.68]; P=0.004; CHIP wi

31 larger for natural premature menopause (all CHIP: odds ratio, 1.73 [95% CI, 1.23-2.44]; P=0.001; CHI

32 ry disease (hazard ratio associated with all CHIP: 1.36 [95% CI, 1.07-1.73]; P=0.012; hazard ratio as

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

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

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

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

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

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

39 y outcomes were the presence of any CHIP and CHIP with variant allele frequency >0.1.

40 signal for predilection to develop CHIP and CHIP-associated cardiovascular disease.

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

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

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

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

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

46 [95% CIs]), children insured by Medicaid and CHIP were significantly more likely to receive a prevent

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

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

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

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

51 Co-primary outcomes were the presence of any CHIP and CHIP with variant allele frequency >0.1.

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

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

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

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

56 ed Cox models tested the association between CHIP and incident coronary artery disease.

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

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 cting protein) promoted SIRT6 stability, but CHIP expression was reduced in human and mouse plaque VS

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

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

63 polypeptides, contributes to recognition by CHIP.

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

65 plaque VSMCs and is positively regulated by CHIP.

66 t interference from direct ubiquitination by CHIP, as evidenced by Bcl-2 associated athanogene 1-M co

67 in the efficiency of Hsc70 ubiquitination by CHIP.

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

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

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

71 Across cohorts, CHIP prevalence in postmenopausal women with versus with

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

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

74 -Farber Cancer Institute (2003-2011) detects CHIP in 136/629 patients (21.6%).

75 as a risk signal for predilection to develop CHIP and CHIP-associated cardiovascular disease.

76 matory traits that are specific to different CHIP driver genes.

77 In gene-specific analyses, only DNMT3A CHIP was significantly associated with premature menopau

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

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

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

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

82 Engineered CHIP enhanced KCNQ1 ubiquitination, eliminated KCNQ1 sur

83 While enhancing CHIP functionality has broad therapeutic potential, prio

84 This review explains CHIP, explores the clinical quandaries, strives to provi

85 PKG-mediated CHIP-pS20 or expressing CHIP-S20E (phosphomimetic) reduces ischemic proteo- and

86 In pairs discordant for CHIP mutations, we tested if the affected twin died befo

87 on among twin pairs that were discordant for CHIP mutations.

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

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

90 models have supported a mechanistic role for CHIP in promoting vascular disease.

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

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

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

94 Furthermore, CHIP overexpression caused a proteasome-dependent reduct

95 Furthermore, CHIP promoted ubiquitination of Tat by both WT as well a

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

97 1,853 (13.6%) had Medicaid, 9554 (18.4%) had CHIP, and 8125 (10.8%) were uninsured.

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

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

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

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

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

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

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

105 is increases CHIP binding affinity to Hsc70, CHIP protein half-life, and consequent clearance of stre

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

107 cence polarization to characterize the Hsc70-CHIP interaction.

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

109 Thus, the finding that enhancing Hsp70:CHIP-mediated ubiquitination does not affect native prot

110 opment of a facile in vitro method for Hsp70:CHIP-mediated ubiquitination will be beneficial for test

111 ed a highly sensitive ELISA to measure Hsp70:CHIP-dependent nNOS ubiquitination without interference

112 assay to assess the selectivity of the Hsp70:CHIP complex for inactivated nNOS.

113 ing this assay, we have shown that the Hsp70:CHIP complex preferentially ubiquitinates heme-deficient

114 ers ubiquitination of holo-nNOS by the Hsp70:CHIP complex.

115 In humans, CHIP associates with prevalent myocardial infarction.

116 monstrated by chromatin immunoprecipitation (CHIP).

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

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

119 e hypothesis that IL-6 pathway antagonism in CHIP carriers would decrease cardiovascular disease (CVD

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

121 While TP53 mutations have been identified in CHIP, the molecular mechanisms by which mutant p53 promo

122 e among the most commonly found mutations in CHIP, lead to increased expression of inflammatory genes

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

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

125 This increases CHIP binding affinity to Hsc70, CHIP protein half-life,

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

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

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

129 .56], P=0.019), with greater risk from large CHIP clones (hazard ratio, 1.59 [95% CI, 1.21-2.09], P<0

130 Among carriers of large CHIP clones, genetically reduced IL-6 signaling abrogate

131 CVD event risk among participants with large CHIP clones (hazard ratio, 0.46 [95% CI, 0.29-0.73], P<0

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

133 The ubiquitin ligase CHIP (C terminus of HSC70-interacting protein) promoted

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

135 r attention on host cell E3 ubiquitin ligase CHIP (C terminus of HSP70-binding protein).

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

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

138 sines 317 and 545 by the E3 ubiquitin ligase CHIP and prevented proteasomal degradation.

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

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

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

142 ough the activity of the E3 ubiquitin ligase CHIP.

143 of bound clients by the E3 ubiquitin ligase CHIP.

144 Hsc70 and Hsp90 and by the ubiquitin ligase CHIP.

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

146 In vivo, depressing PKG activity lowers CHIP-S20 phosphorylation and protein, exacerbating prote

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

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

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

150 In those not receiving IMiD maintenance, CHIP is associated with decreased overall survival (OS)

151 The hsp90B-MAST1-CHIP signaling axis and its relationship with cisplatin

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

153 Meanwhile, CHIP assay demonstrated the binding of c-Myc to KPNB1 pr

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

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

156 PKG-mediated CHIP-pS20 or expressing CHIP-S20E (phosphomimetic) reduc

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

158 In mice, CHIP accelerates atherosclerosis and increases IL-6/IL-1

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

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

161 previously described negative association of CHIP mutations on survival could not be confirmed in a d

162 We tested the association of CHIP status with incident CVD events (myocardial infarct

163 independent participants, the association of CHIP status with myocardial infarction similarly varied

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

165 e the opportunity to identify root causes of CHIP.

166 Despite the potential contribution of CHIP to myriad cardiovascular and aging-related diseases

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

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

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

170 ng to the tetratricopeptide repeat domain of CHIP.

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

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

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

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

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

176 Because the implication of CHIP with ASCVD, genetic loss-of-function studies of Tet

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

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

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

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

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

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

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

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

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

186 chase assay was increased in the presence of CHIP.

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

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

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

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

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

192 The recognition of CHIP as a nontraditional risk factor challenges speciali

193 However, regardless of CHIP status, the use of IMiD maintenance associates with

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

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

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

197 In order to gain a better understanding of CHIP and the impact of clonal dynamics on transplantatio

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

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

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

201 %-67%]) than children insured by Medicaid or CHIP.

202 as found for any specific gene, subgroup, or CHIP mutations overall, and no significant heritability

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

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

205 [67%] of six patients) cases for whom paired CHIP and therapy-related myeloid neoplasm samples were a

206 l haematopoiesis of indeterminate potential (CHIP) and clonal cytopenias of undetermined significance

207 al hematopoiesis of indeterminate potential (CHIP) and is associated with adverse outcomes.

208 al hematopoiesis of indeterminate potential (CHIP) increases with age and is associated with increase

209 al hematopoiesis of indeterminate potential (CHIP) is a recently identified process where older patie

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

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

212 matopoiesis (CH) of indeterminate potential (CHIP) is defined by mutations in myeloid cancer-associat

213 al hematopoiesis of indeterminate potential (CHIP) refers to clonal expansion of hematopoietic stem c

214 l haematopoiesis of indeterminate potential (CHIP)(6).

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

216 l haematopoiesis of indeterminate potential (CHIP), occurs most commonly as a result of mutations in

217 al hematopoiesis of indeterminate potential (CHIP), the age-related expansion of hematopoietic cells

218 al hematopoiesis of indeterminate potential (CHIP), was associated with hematologic malignancy as wel

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

220 al hematopoiesis of indeterminate potential (CHIP).

221 al hematopoiesis of indeterminate potential (CHIP).

222 as a novel therapeutic target for preventing CHIP progression and treating hematological malignancies

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

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

225 ulated CHIP binding to Hsc70 while promoting CHIP oligomerization.

226 ole of host cell E3 ubiquitin ligase protein CHIP in regulating HIV-1 replication through ubiquitin-d

227 ase c-terminus of Hsp70-interacting protein (CHIP) and subsequent degradation in cells.

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

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

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

231 70):c-terminus of Hsp70-interacting protein (CHIP) complex facilitates the ubiquitination and subsequ

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

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

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

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

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

237 boxyl terminus of Hsc70-interacting protein (CHIP) is an important regulator of proteostasis in many

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

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

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

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

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

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

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

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

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

247 Rather CHIP recruitment involves reciprocal allosteric interact

248 and cytotoxicity, whereas a phospho-silenced CHIP-S20A amplifies both.

249 rgical premature menopause and gene-specific CHIP subtypes.

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

251 Surprisingly, CHIP is also associated with a doubling of the risk of a

252 to identify participants with DNMT3A or TET2 CHIP.

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

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

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

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

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

258 Here we report that CHIP-mediated protein turnover is markedly post-translat

259 Importantly, we highlight the risk that CHIP poses in leading to dominance of precancerous mutan

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

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

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

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

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

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

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

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

268 ibody (iDAb) fused to the UBOX domain of the CHIP E3 ligase.

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

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

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

272 aematopoietic stem cell function, leading to CHIP through mechanisms that are specific to clonal haem

273 we did not find a genetic predisposition to CHIP mutations in this twin study.

274 During 6.9-year median follow-up, CHIP associated with increased incident CVD event risk (

275 l enhancement of protein quality control via CHIP.

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

277 yeloid neoplasm and the primary exposure was CHIP.

278 While CHIP is downregulated in ovarian carcinoma, induced expr

279 menopause was independently associated with CHIP (all CHIP: odds ratio, 1.36 [95% 1.10-1.68]; P=0.00

280 menopause, is independently associated with CHIP among postmenopausal women.

281 ether premature menopause is associated with CHIP is unknown.

282 cation of three genetic loci associated with CHIP status, including one locus at TET2 that was specif

283 1.73]; P=0.012; hazard ratio associated with CHIP with variant allele frequency >0.1: 1.48 [95% CI, 1

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

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

286 Individuals with CHIP have a doubled risk of coronary heart disease and i

287 t of cardiovascular risk in individuals with CHIP, and highlights current knowledge gaps.

288 We identified 1079 (3.0%) individuals with CHIP, including 432 (1.2%) with large clones (allele fra

289 ogramme, and identify 4,229 individuals with CHIP.

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

291 adation pathway through its interaction with CHIP.

292 the association of premature menopause with CHIP, adjusted for age, race, the first 10 principal com

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

294 Patients with CHIP had significantly inferior overall survival compare

295 we assess cardiovascular risk in people with CHIP?

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

297 73], P<0.001) but not in individuals without CHIP (hazard ratio, 0.95 [95% CI, 0.89-1.01], P=0.08; P(

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

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

300 Among postmenopausal middle-aged women, CHIP was independently associated with incident coronary