ライフサイエンスコーパス: USP7

1 and cellular ubiquitin-specific protease 7 (USP7).

2 HSV-1), binds ubiquitin-specific protease 7 (USP7).

3 nating enzyme Ubiquitin-Specific Protease 7 (USP7).

4 hysically associates with the deubiquitinase USP7.

5 e oligo-ubiquitinated and deubiquitinated by USP7.

6 UbE2E1 as well as the catalytic activity of USP7.

7 g hydrogen bonds to the allosteric pocket of USP7.

8 is for enhanced affinity and specificity for USP7.

9 ting its interaction with the deubiquitinase USP7.

10 itin-conjugating enzyme that is regulated by USP7.

11 cribed by Kategaya as specific inhibitors of USP7.

12 GNE-6640 and GNE-6776 non-covalently target USP7 12 A distant from the catalytic cysteine.

13 we identified ubiquitin specific protease 7 (USP7), a deubiquitinating enzyme, as a novel regulator o

14 of a single amino acid to abolish binding to USP7 accelerated the accumulation of viral mRNAs and pro

15 r the last decade, in the context of HAFOUS, USP7 activators may represent a more relevant approach.

16 Collectively, these USP7 activities promote the genomic deposition of H2AK11

17 summary, engineering compounds that inhibit USP7 activity by attenuating ubiquitin binding suggests

18 Our findings support the notion that USP7 activity could be potentially targeted in a substra

19 Loss of USP7 activity results in increased ubiquitination of NF-

20 Mechanistically, USP7 acts as a molecular rheostat to precisely fine-tune

21 USP7 acts on protein quality control through the SMAD2 t

22 Finally, we found that USP7 also differentially interacts with mutant Huntingti

23 ve identified ubiquitin-specific protease 7 (USP7; also known as HAUSP) as a regulator of N-Myc funct

24 g PCGF4/BMI1), modulates the localization of USP7 and bridges USP7 with PRC1.4, allowing for the stab

25 gions, including 16p13.2 (encompassing genes USP7 and C16orf72) and Cadherin 13, and implement a rigo

26 1 at S380 accelerates complex formation with USP7 and CENPF to regulate their stability, thus having

27 76, thereafter promoting the binding between USP7 and HO-1, finally leading to enhanced HO-1 deubiqui

28 ssays to probe the interaction between the C-USP7 and HSV-1 immediate-early protein ICP0 (infected ce

29 the "palm" region of the catalytic domain of USP7 and inhibit its catalytic activity.

30 re the first to identify vIRF-2 targeting of USP7 and its role in HHV-8 biology, expanding our unders

31 overexpression decreases the association of USP7 and p53 and attenuates USP7-mediated p53 deubiquiti

32 Moreover, these data support the pursuit of USP7 and PHF8 as potential targets for breast cancer int

33 g cyclin A2 and that the interaction between USP7 and PHF8 is augmented during DNA damage.

34 , specifically, were regulated negatively by USP7 and positively by vIRF-2-USP7 interaction, the latt

35 llenge in defining predictors of response to USP7 and potential patient populations that would benefi

36 xtended the UbE2E1 regulation of uH2AK119 to USP7 and showed that USP7 is also a key regulator for mo

37 o interacted with itself, whereas the TDs of USP7 and SPOP did not self-associate.

38 However, the close proximity of USP7 and telomerase binding sites on TPP1 suggest possib

39 These findings demonstrate that USP7 and USP10 are DUBs that regulate NHE3 ubiquitinatio

40 Inhibition of USP7 and USP10 by chemical inhibitors or knockdown had a

41 of PKA by forskolin decreased the binding of USP7 and USP10 to NHE3, while increasing ubiquitination

42 ary to develop inhibitors targeting the DUBs USP7 and USP10, which are involved in regulating levels

43 d by determining the effects of silencing of USP7 and USP10.

44 Mechanistically, USP7 and USP11 regulate the ubiquitination status of the

45 eport that two ubiquitin-specific proteases, USP7 and USP11, co-purify with human PRC1-type complexes

46 Rather, OTUD4 is a scaffold for USP7 and USP9X, two deubiquitinases that act directly on

47 ated ubiquitin-specific protease; also named USP7) and blocked the access of p53 to the same region o

48 we identified ubiquitin specific protease-7 (USP7) and USP10 that bind NHE3.

49 itin-specific protease (HAUSP, also known as USP7), and that the integrity of this molecular framewor

50 ying novel candidate BL genes such as SIN3A, USP7, and CHD8, we demonstrate that EBV-positive tumors

51 R) signaling, the TRAF domains (TDs) of MUL, USP7, and SPOP are located near the NH(2) termini or cen

52 aining TDs homologous to those found in MUL, USP7, and SPOP throughout eukaryotes, including yeast, p

53 ICP0, that ICP0 mediated the degradation of USP7, and that amino acid substitutions in ICP0 that abo

54 urodifferentiation, our results suggest that USP7- and ncPRC1.1-associated neurodevelopmental disorde

55 MUL and USP7 are capable of binding in vitro via their TDs to al

56 re, we identify the de-ubiquitylating enzyme USP7 as a critical regulator of Rad18 protein levels.

57 GN3 and identify the deubiquitylating enzyme USP7 as a key regulator of NGN3 stability.

58 We identified the deubiquitinase USP7 as a MYCN-associated synthetic vulnerability.

59 Taken together, these observations identify USP7 as a novel component of the cellular DDR involved i

60 Here we identify USP7 as a novel interacting protein of the oligonucleoti

61 Here, we identify USP7 as a potent negative regulator of Wnt/beta-catenin

62 Together, these results identify USP7 as a promising therapeutic target for the treatment

63 excessive degradation of Axin and identifies USP7 as a target for sensitizing cells to Wnt/beta-caten

64 ses limit the use of catalytic inhibitors of USP7 as anti-inflammatory agents.

65 eubiquitinase Ubiquitin Specific Protease-7 (USP7) as a regulator of NF-kappaB transcriptional activi

66 enzyme (DUB), ubiquitin-specific protease 7 (USP7), as a novel regulator of Poleta stability.

67 tification of a ubiquitin-specific protease, USP7, as a regulatory switch in a protein quality-contro

68 nalysis, and tandem affinity purification of USP7-associated proteins, we compiled a list of 20 high-

69 We demonstrate that USP7 associates with Rad18 directly via a consensus USP7

70 , KDM6A, SMARCA4, ASXL2, CREBBP, EZH2, MLL2, USP7, ASXL1, NSD2, SETD2, SMC1A and ZMYM3.

71 We show that USP7 attenuates UbE2E1-mediated ubiquitination, an effec

72 work of proteins, including the CCT complex, USP7, Aurora kinase, Nedd4, and Trim24, that bind mutant

73 n a noncovalent ligand of USP7, we developed USP7-based DUBTACs that stabilized the DeltaF508-CFTR mu

74 mal and distal isotopic labels and measuring USP7 binding by nuclear magnetic resonance.

75 in the cell, consistent with their lack of a USP7 binding domain.

76 UbE2E1 in vitro and in vivo through the ASTS USP7 binding motif within its N-terminal extension in an

77 sion in an identical manner with other known USP7 binding proteins.

78 including ICP0 mutants that are defective in USP7 binding.

79 n that was abolished if either the ORF33- or USP7-binding domain in ORF45 was deleted.

80 erminal 19 amino acids (aa) of ORF45 and the USP7-binding domain to the reported consensus motif in t

81 sociates with Rad18 directly via a consensus USP7-binding motif and can disassemble Rad18-dependent p

82 its C-terminal UBL1-2 domains and mapped the USP7-binding site for ICP0.

83 F3 was found to be suppressed by vIRF-4 in a USP7-binding-associated manner in infected cells, but no

84 ubiquitination of vIRF-4 via K48-linkage and USP7-binding-associated suppression of vIRF-4 ubiquitina

85 USP7 binds directly to the supervillin N terminus and ca

86 served colocalization of ORF45 with ORF33 or USP7 both under transfected conditions and in KSHV-infec

87 Overexpression of wild-type USP7 but not its catalytically-defective mutants deubiqu

88 Expression of wildtype USP7, but not its catalytically defective mutant, result

89 Overexpression of wild-type USP7, but not its catalytically inactive or interaction-

90 trate that transiently compromising cellular USP7 by siRNA and chemical inhibition leads to accumulat

91 ting the therapeutic potential of inhibiting USP7 by this approach.

92 Although structures of the USP7 C terminus bound to its substrates could provide vi

93 The USP7 C-terminal region (C-USP7) contains five ubiquitin-

94 The multi-substrate nature of USP7, combined with the modest potency and selectivity o

95 The USP7 C-terminal region (C-USP7) contains five ubiquitin-like domains (UBL1-5) that

96 found that the amino acids (757)LDEL(760) in USP7 critically contribute to the interaction with the p

97 ubiquitinated forms of XPC, whereas complete USP7 deficiency leads to rapid ubiquitin-mediated XPC de

98 Moreover, USP7 deficiency severely impairs the repair of cyclobuta

99 olved in UV light-induced XPC degradation in USP7-deficient cells.

100 improved solubility while maintaining their USP7 degradation capability.

101 USP7-depleted cells also fail to elongate nascent daught

102 lusion of these studies is that depletion of USP7 destabilized ICP0, that ICP0 mediated the degradati

103 Loss of USP7 destabilizes Rad18 and compromises UV-induced PCNA

104 USP7 deubiquitinase activity is required for the stabili

105 attenuate ubiquitin binding and thus inhibit USP7 deubiquitinase activity.

106 Conversely, USP7 (deubiquitinase ubiquitin-specific peptidase 7) opp

107 USP7 deubiquitinates the E3 ubiquitin ligase NEDD4L, whi

108 Ubiquitin-specific protease 7 (USP7) deubiquitinates p53 and Hdm2 and regulates their s

109 Here, we show that the USP7 deubiquitinating enzyme is an integral component of

110 USP7 deubiquitination of NF-kappaB leads to increased tr

111 ort that the Ser18-containing isoform of the USP7 deubiquitylation enzyme (USP7S) controls Mule stabi

112 We have also found that USP7 directly binds ICP0 via its C-terminal UBL1-2 domai

113 tly focused on the mechanisms underlying how USP7 directly controls p53 stability, we recently showed

114 USP7 directly interacts with Axin through its TRAF domai

115 Thus, USP7 directly serves as a specific DUB for Poleta.

116 d demonstrate that bipartite binding to both USP7 domains is required for efficient Pol iota deubiqui

117 Furthermore, pharmacological inhibition of USP7 during endocrine specification in human iPSC models

118 Importantly, USP7 efficiently deubiquitinates XPC-ubiquitin conjugate

119 The USP7-encoding gene was also transcriptionally regulated

120 pigmentosum variant) cells, suggesting that USP7 facilitates UV-induced PCNA monoubiquitination by s

121 Furthermore, we find that Usp7 forms a complex with GMP-synthetase (GMPS) to promo

122 USP7 forms a complex with UbE2E1 in vitro and in vivo th

123 pendent relocalization of a portion of ORF33/USP7 from the nucleus to the cytoplasm.

124 USP7 has been proposed as a therapeutic target in severa

125 gnificance of the interaction of vIRF-4 with USP7 has remained undetermined.

126 causative gene in Mulibrey Nanism syndrome; USP7 (HAUSP), an ubiquitin protease; and SPOP, a POZ dom

127 y, we show that the mammalian counterpart of Usp7, HAUSP, positively regulates Hh signaling by modula

128 Knockdown of the p53 deubiquitinating enzyme USP7/HAUSP also reverses the supervillin phenotype, bloc

129 iquitinating enzymes USP5/isopeptidase T and USP7/HAUSP and the ubiquitin ligases ARF-BP1/HUWE1 and p

130 The deubiquitylation enzyme USP7/HAUSP plays a major role in regulating genome stabi

131 sence of over 100 human DUBs, only OTUB1 and USP7 have been utilized in the development of DUBTAC.

132 ating the enzyme's activity, the dynamics of USP7 have not been explored.

133 ith deubiquitinating enzymes (DUBs) USP2 and USP7, highlighting the use of our new method for efficie

134 ed by a deubiquitination enzyme and identify Usp7/HUASP as a critical regulator of Hh signaling and p

135 function of vIRF-4 and its interaction with USP7 identified a role of each in innate-immune suppress

136 Genetic knockout of USP7 improved the antileukemic efficacy of glucocorticoi

137 However, the broad regulatory roles of USP7 in cell death pathways, chromatin, and DNA damage r

138 We have shown that depletion of the USP7 in HFF-1 cells negatively affects the efficiency of

139 quitinating enzyme, and establish a role for USP7 in human neurodevelopmental disease.

140 o heterozygous loss-of-function mutations of USP7 in individuals with a neurodevelopmental disorder,

141 NA interference (RNAi)-mediated knockdown of USP7 in neuroblastoma cancer cell lines, or genetic abla

142 er, our findings reveal a modulatory role of USP7 in PCNA ubiquitination-mediated stress-tolerance pa

143 our findings uncovered an important role of USP7 in regulating NER via deubiquitinating XPC and by p

144 ma cancer cell lines, or genetic ablation of Usp7 in the mouse brain, destabilizes N-Myc, which leads

145 he ubiquitin-specific processing protease 7 (USP7) in paediatric leukaemia, which result in decreased

146 eubiquitylase ubiquitin-specific protease 7 (USP7) in the regulation of the p53-dependent DNA damage

147 Knockout of USP7 increased the steady-state level of Poleta and slow

148 rlay analyses, we found here that inhibiting USP7 increases NF-kB ubiquitination and degradation, pre

149 st this hypothesis, we studied the effect of USP7 inhibition in chronic lymphocytic leukemia (CLL) wh

150 Consequently, USP7 inhibition induces significant tumor-cell killing i

151 Moreover, USP7 inhibition sensitized p53-defective, chemotherapy-r

152 lar effects of XL177A reveals that selective USP7 inhibition suppresses cancer cell growth predominan

153 tional status as a biomarker for response to USP7 inhibition.

154 dy therefore supports clinical evaluation of USP7 inhibitor, alone or in combination, as a potential

155 y potent, selective, and orally bioavailable USP7 inhibitor.

156 mutant cancer cell lines, demonstrating that USP7 inhibitors can suppress tumor growth through multip

157 at interest exists, therefore, in developing USP7 inhibitors for clinical evaluation.

158 Perspective focuses on the current status of USP7 inhibitors from various organizations active in dev

159 gn, we describe the development of selective USP7 inhibitors GNE-6640 and GNE-6776.

160 g design strategy, a new class of reversible USP7 inhibitors has been identified that is highly poten

161 Although a range of USP7 inhibitors have been developed over the last decade

162 to lead to successful clinical outcomes for USP7 inhibitors in cancer treatment.

163 recapitulated in HPV-negative disease using USP7 inhibitors in clinical development.

164 potency and selectivity of early generation USP7 inhibitors, has presented a challenge in defining p

165 ibitors, either alone or in combination with USP7 inhibitors.

166 th a unique N-terminal extension, is a novel USP7-interacting protein.

167 vIRF-2, and activities of vIRF-2 and vIRF-2-USP7 interaction in HHV-8 latent and lytic biology.IMPOR

168 show, through genetic ablation of the vIRF-4-USP7 interaction in infected cells, that vIRF-4 associat

169 negatively by USP7 and positively by vIRF-2-USP7 interaction, the latter competing for USP7-TRAF ass

170 PEL cell viability, likely independently of USP7 interaction, while lytic replication was inhibited

171 inhibited by vIRF-2, in part or in whole via USP7 interaction.

172 ulates antiviral signaling via disruption of USP7 interactions with innate immune signaling proteins

173 with USP7, via a means distinguishable from USP7 interactions with other vIRFs and other proteins, t

174 interact with ubiquitin-specific protease 7 (USP7); interactions of vIRF-1 and vIRF-3 with USP7 promo

175 Here we show that USP7 interacts with and deubiquitinates Tip60 both in vi

176 We also showed that USP7 interacts with vIRF1 in U2OS cells.

177 USP7 is a deubiquitinase implicated in destabilizing the

178 USP7 is a promising target for cancer therapy as its inh

179 USP7 is a protein deubiquitinase with an essential role

180 The deubiquitinase USP7 is a regulator of key cellular pathways, modulates

181 gulation of uH2AK119 to USP7 and showed that USP7 is also a key regulator for monoubiquitination at H

182 te that the deubiquitination of NF-kappaB by USP7 is critical for target gene transcription.

183 Additionally, USP7 is critical in maintaining the steady state levels

184 A clue as to why USP7 is degraded emerged from the observation that, notw

185 of USP7 leads to reduction of ICP0 and that USP7 is degraded in an ICP0-dependent manner.

186 pitation (ChIP) experiments demonstrate that USP7 is found at SCML2 and BMI1 target genes.

187 USP7 is involved in the cellular stress response by regu

188 infected cells, that vIRF-4 association with USP7 is necessary for optimal expression of vIRF-4 and n

189 In addition, human USP7 is targeted by several viruses of the Herpesviridae

190 We demonstrate that USP7 is upregulated in CLL cells, and its loss or inhibi

191 Ubiquitin specific peptidase 7 (USP7) is a deubiquitinating enzyme (DUB) that removes ub

192 Ubiquitin-specific protease 7 (USP7) is a deubiquitinating enzyme found in all eukaryot

193 Human ubiquitin-specific protease 7 (USP7) is a deubiquitinating enzyme that prevents protein

194 Ubiquitin specific protease 7 (USP7) is a known deubiquitinating enzyme for tumor suppr

195 Ubiquitin-specific protease 7 (USP7) is a prominent deubiquitinating enzyme, with an ex

196 itions; whereas when after arsenic exposure, USP7 itself can be ubiquitinated at K476, thereafter pro

197 mportant role in controlling other proteins, USP7 itself has not been recognized as a target for regu

198 a centrosomes, which is similar phenotype to USP7-knockdown cells.

199 Second, inhibition of USP7 leads to a reduction in the level of ubiquitinated

200 We show here that, indeed, depletion of USP7 leads to reduction of ICP0 and that USP7 is degrade

201 USP7 localized predominantly to the nucleus, in a TD-dep

202 Collectively, these findings suggest that USP7 may act to modulate abundance of Nrf1 protein to in

203 In addition to this, USP7 may also play a role in chromatin remodelling by di

204 This suggests that targeting USP7 may have therapeutic potential even in tumors with

205 n increases the Tip60 stability by promoting USP7-mediated deubiquitination of Tip60.

206 e association of USP7 and p53 and attenuates USP7-mediated p53 deubiquitination.

207 Here, we provide new evidence that USP7 modulated chromatin remodelling is important for ba

208 trols p53 stability, we recently showed that USP7 modulates the stability of the DNA damage responsiv

209 Analysis of various MUL and USP7 mutants by transient transfection assays indicated

210 ts USP7, utilizing a PSTS motif matching the USP7 N-terminal domain-binding A/PxxS consensus, but uni

211 These are located on the USP7 N-terminal TRAF-like (TRAF) domain and the first an

212 ssays demonstrated that vIRF1 interacts with USP7-NTD via its EGPS motif.

213 cated that the vIRF1 peptide interacted with USP7-NTD with a Kd of 2.0 mum.

214 ed chemical perturbations after titration of USP7-NTD with vIRF1 (44)SPGEGPSGTG(53) peptide.

215 nteracts with the N-terminal domain of USP7 (USP7-NTD).

216 e of binding as that of the EBNA1 peptide to USP7-NTD.

217 The crystal structure of the USP7-NTD.vIRF1 peptide complex revealed an identical mod

218 However, overexpression of USP7 or substitution in ICP0 of a single amino acid to a

219 Knockdown of USP7 or USP10 resulted in increased NHE3 ubiquitination

220 We were able to identify UbVs that bound USP7 or USP10 with high affinity and inhibited deubiquit

221 trieval of NHE3 was promoted by depletion of USP7 or USP10, with increased association of NHE3 with R

222 Ablation of either USP7 or USP11 in primary human fibroblasts results in de

223 Moreover, we show that loss of OTUD4, USP7, or USP9X in tumor cells makes them significantly m

224 gans model of SOD1-linked ALS identified the USP7 ortholog as a suppressor of proteotoxicity in the n

225 The actions of USP7 orthologs on misfolded proteins were found to be co

226 nus, that is not mimicked by USP2A, USP4, or USP7, other members of the deubiquitination catalytic fa

227 cellular assays and extremely selective for USP7 over other deubiquitinases.

228 Also, USP7 physically binds Poleta in vitro and in vivo.

229 We show that USP7 physically interacts with XPC in vitro and in vivo.

230 ubiquitin Lys48 side chain, suggesting that USP7 preferentially interacts with and cleaves ubiquitin

231 SP7); interactions of vIRF-1 and vIRF-3 with USP7 promote PEL cell viability and regulate productive

232 Furthermore, ectopic expression of USP7 promoted the UV-induced proliferating cell nuclear

233 Moreover, USP7-promoted PHF8 stabilization conferred cellular resi

234 We showed that USP7 promotes breast carcinogenesis by stabilizing PHF8

235 Specifically, we demonstrated that USP7 promotes deubiquitination and stabilization of PHF8

236 Inhibition of USP7 protected against proteotoxicity in mammalian neuro

237 oup, Ubp15 from yeast and its human ortholog USP7, rapidly remove mono- and diubiquitin from substrat

238 data identify a new molecular determinant of USP7 recognition, TRAF3/6-specific targeting by the deub

239 RAF3 and TRAF6, and that vIRF-2 targeting of USP7 regulates HHV-8 productive replication.

240 Here we report that USP7 regulates nucleotide excision repair (NER) via deub

241 Inhibition of USP7 regulates osteoblast differentiation and adipocyte

242 USP7 regulates Poleta stability through both indirect an

243 Here, we provide evidence that USP7 regulates the activity of Polycomb repressive compl

244 USP7 regulates the posttranslational status of RING1B an

245 for example, ubiquitin-specific protease-7 (USP7) regulates stability of the p53 tumour suppressor a

246 Here, we report that USP7 regulation plays a central role in DNA damage signa

247 Besides providing a detailed map of the USP7 regulome during neurodifferentiation, our results s

248 Besides defining the USP7 regulome, our results reveal that H2AK119ub1 dosage

249 Pharmacological inhibition of USP7 resensitized chemoresistant MYCN-overexpressing PDX

250 2A Lys-119 as both knockdown and deletion of USP7 results in decreased levels of uH2AK119.

251 inhibition of ubiquitin-specific protease 7 (USP7) results in the degradation of the oncogenic E3 lig

252 e interactor, ubiquitin-specific protease 7 (Usp7), results in impairment of somatic cell differentia

253 ic ablation or pharmacological inhibition of USP7 robustly increases Wnt/beta-catenin signaling in mu

254 ficient but not complete CRISPR knock-out of USP7 showed accelerated cell growth and validated transc

255 stitutions in ICP0 that abolished binding to USP7 significantly impaired the ability of HSV-1 to repl

256 We show that transient USP7 siRNA knockdown did not change the levels or activi

257 d understanding the molecular mechanism of C-USP7 specificity toward its substrates and may provide t

258 Thus, not only does USP7 stabilize PRC1 components, its catalytic activity i

259 ed ubiquitin-specific protease (Hausp, a.k.a Usp7), stabilizing Cry1 and shifting circadian clock tim

260 these data establish a new bipartite mode of USP7 substrate binding.

261 provide vital information for understanding USP7 substrate specificity, no such data has been availa

262 at DNA polymerase iota (Pol iota) is a novel USP7 substrate that interacts with both TRAF and UBL1-2.

263 rget engagement in cells, FT671 destabilizes USP7 substrates including MDM2, increases levels of p53,

264 Characterized USP7 substrates primarily interact with one of two major

265 ns, we compiled a list of 20 high-confidence USP7 substrates that includes known and novel USP7 subst

266 domains (UBL1-5) that interact with several USP7 substrates.

267 SP7 substrates that includes known and novel USP7 substrates.

268 Consistent with USP7 target engagement in cells, FT671 destabilizes USP7

269 ent populations that would benefit most from USP7-targeted drugs.

270 nfected PEL-cell pro-viability phenotypes of USP7 targeting have been identified for vIRFs 1-3, the s

271 We identify amino acids in TPP1 and USP7 that are critical for their interaction and multipl

272 Ubiquitin specific protease 7 (USP7), the most widely studied among the nearly 100 deub

273 sis included the ubiquitin-specific protease USP7, the transcriptional repressor TRIM27, DNA repair p

274 Rad23A, Rad23B, and Ddi2; the deubiquitylase Usp7, the ubiquitin ligase Parkin, the cochaperone Bag6,

275 the binding of a ubiquitin-specific protease Usp7 to Ci, which positively regulates Hh signaling acti

276 Our study mechanistically links USP7 to epigenetic regulation and DNA repair.

277 deregulation of the deubiquitinating enzyme USP7 to inhibit p53-mediated antiviral responses.

278 factor Elongin BC and the H2B deubiquitinase USP7 to modulate transcriptional processes in mESCs simi

279 of SCML2 and its associated deubiquitylase, USP7, to the sex chromosomes during pachynema.

280 2-USP7 interaction, the latter competing for USP7-TRAF association.

281 In this work we have demonstrated that the USP7 ubiquitin-like domains can be studied in isolation

282 al ORF33 and the 130-kDa protein is cellular USP7 (ubiquitin-specific protease 7).

283 end, we identified an NF-kB-binding site in USP7, ubiquitin-like domain 2, that selectively mediates

284 In contrast to Ubp15 and USP7, Ubp12 readily cleaves the ends of long chains, reg

285 that interacts with the N-terminal domain of USP7 (USP7-NTD).

286 ls, is accomplished by a specific isoform of USP7 (USP7S), which is phosphorylated at serine 18 by th

287 Here, we report that vIRF-2 also targets USP7, utilizing a PSTS motif matching the USP7 N-termina

288 e, we report that vIRF-2 also interacts with USP7, via a means distinguishable from USP7 interactions

289 level of the claspin deubiquitinating enzyme USP7 was detected.

290 USP7 was overexpressed in breast carcinomas, and the lev

291 Based on a noncovalent ligand of USP7, we developed USP7-based DUBTACs that stabilized th

292 tic centre of the auto-inhibited apo form of USP7, which differs from other USP deubiquitinases.

293 1 is an inhibitor of deubiquitylating enzyme USP7, which induces apoptosis in MM cells resistant to c

294 the vIRFs is ubiquitin-specific protease 7 (USP7); while replication-modulatory and latently infecte

295 that two compounds, FT671 and FT827, inhibit USP7 with high affinity and specificity in vitro and wit

296 2, that selectively mediates interactions of USP7 with NF-kB subunits but is dispensable for interact

297 dulates the localization of USP7 and bridges USP7 with PRC1.4, allowing for the stabilization of BMI1

298 pment of XL177A, which irreversibly inhibits USP7 with sub-nM potency and selectivity across the huma

299 Inhibiting USP7 with the small-molecule inhibitor P22077 attenuates

300 tribution of the ubiquitin-specific protease USP7 within the cell, consistent with their lack of a US