ライフサイエンスコーパス: 53BP1

1 factor that antagonizes end resection (Ku or 53BP1).

2 and colocalization with p53-binding protein (53BP1).

3 this can be observed in the absence of Rad9(53BP1).

4 taining tumor protein p53 binding protein 1 (53BP1).

5 gly inhibited by the checkpoint adaptor Rad9(53BP1).

6 the tumor suppressor p53-binding protein 1 (53BP1).

7 abilizes 53BP1 and thus positively regulates 53BP1.

8 e significantly diminished in the absence of 53BP1.

9 ecoming enlarged and localized internally to 53BP1.

10 trand break-induced protein complex centring 53BP1.

11 s and induces an imbalance between BRCA1 and 53BP1.

12 otherapy or chemotherapy through stabilizing 53BP1.

13 rotected by H2AX and its downstream effector 53BP1.

14 ntially in the absence of DNA repair protein 53BP1.

15 of ubiquitin chains, which promotes loss of 53BP1.

16 n the accumulation of the DNA-repair protein 53BP1.

17 contributor to the control of DSB repair by 53BP1.

18 amage, and thus TIRR is also an inhibitor of 53BP1.

19 ineered ubiquitin variants for inhibitors of 53BP1.

20 e protein F (CENPF), interacting proteins of 53BP1.

21 he histone methyl-lysine binding function of 53BP1.

22 g radiation-induced foci formation region of 53BP1.

23 biquitin and nucleosome surfaces accessed by 53BP1.

24 nism of the nonhomologous end-joining factor 53BP1.

25 aired recruitment of repair factors MDC1 and 53BP1.

26 M on this rearrangement seems independent of 53BP1.

27 ticipates in the interplay between BRCA1 and 53BP1.

28 ote end resection, which can be regulated by 53BP1, 53bp1 deletion does not rescue the HDR defects of

29 We report that deficiency of 53BP1, a DNA damage-response protein, caused age-depende

30 of importin beta-dependent nuclear import of 53BP1, a large NCT cargo.

31 The tumor suppressor protein 53BP1, a pivotal regulator of DNA double-strand break (D

32 and cause localized accumulations of ectopic 53BP1-a DNA repair protein.

33 for rapid TRF2 recruitment while suppressing 53BP1 accumulation at damage sites.

34 We show that USP28 and 53BP1 act to stabilize p53 after centrosome loss and dem

35 Central to all 53BP1 activities is its recruitment to double-strand bre

36 This is likely because RIF1, but not 53BP1, also regulates the foci formation and chromatin l

37 Moreover, loss of 53BP1 alters the translocatome by increasing rearrangeme

38 the formation of ionizing radiation-induced 53BP1 and BRCA1 but not RNF168 foci, suggesting that USP

39 affect the initial formation of pH2A.X foci, 53BP1 and BRCA1 complex recruitment were reduced upon LS

40 53BP1 and BRCA1 directly influence DSB repair pathway ch

41 egulates the dynamic assembly/disassembly of 53BP1 and BRCA1 foci.

42 Next, we examine roles for 53BP1 and BRCA1 in this process.

43 Depletion of both 53BP1 and BRCA1 increases repair needing microhomology u

44 s the accumulation of repair factors such as 53BP1 and BRCA1 on the chromatin flanking the break site

45 The DNA damage response proteins 53BP1 and BRCA1 regulate the balance between NHEJ and HR

46 its downstream functional partners, such as 53BP1 and BRCA1, thus affecting the normal DNA damage re

47 d is necessary for downstream recruitment of 53BP1 and BRCA1.

48 he recruitment of DNA damage repair proteins 53BP1 and BRCA1.

49 nd recruitment of downstream factors such as 53BP1 and breast cancer 1 (BRCA1).

50 f RIF1, and results in its dissociation from 53BP1 and DSBs thereby facilitating HR initiation.

51 PASMCs exhibit increased DNA damage markers (53BP1 and gamma-H2AX) and an overexpression of PARP-1 (i

52 This process occurs without affecting 53BP1 and gammaH2AX levels during CSR.

53 ing (NHEJ) by recruiting NHEJ repair factors 53BP1 and Ku70/80 complex, whereas TRADD is dispensable

54 ngiectasia mutated was activated but not its 53BP1 and MDC1 targets.

55 ted in newly formed nuclei by recruitment of 53BP1 and other proteins until repair takes place.

56 Thus, the barriers posed by 53BP1 and RAP80 are relieved by BRCA1 and POH1, respecti

57 We examine the changes in 53BP1 and RAP80 ionizing radiation induced foci (IRIF) i

58 -telangiectasia mutated (ATM) phosphorylates 53BP1 and recruits RAP1-interacting factor 1 (RIF1) to d

59 rt a model whereby MCL-1 depletion increases 53BP1 and RIF1 colocalization at DSBs, which inhibits BR

60 lation of ATR, and higher levels of residual 53BP1 and RIF1 foci, suggesting that DNA double-strand b

61 that the default for all DSBs is to recruit 53BP1 and RIF1.

62 ted) phosphorylation-dependent interactor of 53BP1 and show that absence of Rif1 results in 5'-3' DNA

63 widen the repertoire of cellular targets for 53BP1 and suggest a previously unidentified role for 53B

64 The chromatin-binding protein 53BP1 and the histone variant H2AX are required for effi

65 interactions with the anti-resection factor 53BP1 and the pro-resection factor BRCA1, suggesting tha

66 the increased resection afforded by loss of 53BP1 and the rescue of BRCA1-deficiency depend on CtIP

67 On the one hand, it stabilizes 53BP1 and thus positively regulates 53BP1.

68 53BP1 and TIRR form a stable complex, which is required

69 tinct damage site recruitment thresholds for 53BP1 and TRF2 correlating with the dose-dependent incre

70 RCC36 or ABRAXAS allows establishment of the 53BP1 and ubiquitin chain-devoid core.

71 olocalized foci formation of phospho-ATM and 53BP1 and up-regulated phospho-BRCA1 in cisplatin-treate

72 We identified 53BP1 and USP28 as essential components acting upstream

73 ts mitotic accuracy by slowing down mitosis, 53BP1 and USP28 function in parallel to select against d

74 ersistent DNA damage response (gammaH2AX and 53BP1) and the expression of senescence-associated marke

75 ation at DSBs, decreasing the recruitment of 53BP1, and decreases NHEJ, rendering cells more sensitiv

76 s via the N-terminal phospho-SQ/TQ domain of 53BP1, and DSBs generated by ionizing radiation or durin

77 trasts with the low-affinity binding mode of 53BP1, and it ensures 53BP1 displacement by RNF169 from

78 M, ATR, DNA-PK, Rad50, Mre11, p95/NBS1, p53, 53BP1, and p63.

79 ulation of the DNA-damage markers gammaH2AX, 53BP1, and RAD51.

80 M has a role in HDR independent of the BRCA1-53BP1 antagonism and that its HDR function can become cr

81 air substrates we show that these effects of 53BP1 are correlated with a promotion of microhomology-m

82 he pro-NHEJ and antirecombinase functions of 53BP1 are mediated in part by RIF1, the only known facto

83 ATR and 53BP1 are not detected at either TIPs or non-TIPs in mit

84 e find that the anti-resection activities of 53BP1 are rate-limiting for mutagenic NHEJ but not for p

85 ced accumulation of ubiquitin conjugates and 53BP1 at DSBs, suggesting considerable functional redund

86 We propose that phosphorylation of 53BP1 at S380 accelerates complex formation with USP7 an

87 man and mouse cells, blocked accumulation of 53BP1 at sites of DNA damage and improved gene targeting

88 the initial recruitment to and retention of 53BP1 at sites of DNA damage; however, the mechanism for

89 Phosphorylation of 53BP1 at the N terminus is involved in the replicative s

90 ibit the retention of p53 binding protein 1 (53BP1) at the site of DSBs.

91 ation capture sequencing (TC-Seq) of primary 53BP1(-/-) B cells revealed that their chromosomal rearr

92 inding of the L3MBTL1 repressor and promotes 53BP1 binding, while limiting end-resection of DSBs.

93 ion mechanism is distinct from that by which 53BP1 binds to ubiquitylated H2A-Lys15 highlighting the

94 ulated by ATM signaling through CtIP/MRN and 53BP1-bound Rif1, respectively.

95 damage sites and the downstream assembly of 53BP1, BRCA1, and RAD51.

96 RNF168 results in the hyper-accumulation of 53BP1/BRCA1 which accelerates DSB repair.

97 pression of wild-type or phosphomimic mutant 53BP1 but not by expression of a dephosphomimic mutant.

98 e strand breaks led to robust recruitment of 53BP1 but not TRF2.

99 binding with Plk1 increases the stability of 53BP1 by accelerating its interaction with the deubiquit

100 Moreover, 53BP1 can transduce prolonged mitosis to cell cycle arre

101 Deep sequencing of the genome of 53BP1(-/-) cancer cells and translocation capture sequen

102 Loss of 53BP1 caused hypersensitivity to licensing inhibition wh

103 However, doubly deficient BRCA1(-/-)53BP1(-/-) cells or tumors become resistant to PARPis.

104 Furthermore, 53BP1 chromatin occupancy at sites in the Igh locus is B

105 anner dependent on the H2AX-MDC1-RNF8-RNF168-53BP1 chromatin pathway, and seems to block HR and promo

106 ining how RNF168, RNF169, and RAD18 regulate 53BP1 chromatin recruitment and how specificity can be a

107 in TRF2 recruitment to damage sites with no 53BP1 clustering.

108 e identify UBC9 and RAD50 as suppressors and 53BP1, DDB1 and poly(ADP)ribose polymerase 3 (PARP3) as

109 ckpoint adaptor and resection inhibitor Crb2(53BP1), decreased Exo1 association and delayed resection

110 However, the combination of 53BP1 deficiency and AID deregulation results in B cell

111 When 53BP1 deficiency is combined with overexpression of acti

112 However, loss of RIF1 differs from that of 53BP1 deficiency, as it cannot fully rescue RAD51 foci f

113 alpha looping interactions are unaffected by 53BP1 deficiency.

114 pact of tumor protein P53-binding protein 1 (53BP1) deficiency in lymphoma and translocation.

115 ay, present in WT mice and hyperactivated in 53BP1-deficient mice, by which microbiota signal via Tol

116 s involved in the replicative stress-induced 53BP1 degradation.

117 resection, which can be regulated by 53BP1, 53bp1 deletion does not rescue the HDR defects of Atm mu

118 tion defects of Brca1 mutants are rescued by 53bp1 deletion, the absence of 53BP1 did not rescue the

119 BRCA1 antagonizes 53BP1 dependent DNA end-blocking activity during S phase

120 l looping out and deletion mechanism that is 53BP1 dependent.

121 Upon shelterin removal, telomeres underwent 53BP1-dependent clustering, potentially explaining at le

122 ation-associated events, yet dispensable for 53BP1-dependent DSB repair regulation.

123 The 53BP1-dependent end-joining pathway plays a critical rol

124 omologous recombination (HR) and antagonizes 53BP1-dependent non-homologous end joining in S/G2 phase

125 53BP1-dependent p53 modulation requires both auto-oligom

126 NA repair, we decided to further explore the 53BP1-dependent pathway.

127 past few years to elucidate how loss of the 53BP1-dependent repair pathway results in PARPi resistan

128 rchestrated by the TIP60 complex to regulate 53BP1-dependent repair through competitive bivalent bind

129 Second, 53BP1-dependent repression of CtIP at double-strand brea

130 In addition, 53BP1 depletion reduces the levels of p53 and centromere

131 These phenotypes induced by 53BP1 depletion were rescued by expression of wild-type

132 re rescued by 53bp1 deletion, the absence of 53BP1 did not rescue the meiotic failure seen in Brca1 m

133 finity binding mode of 53BP1, and it ensures 53BP1 displacement by RNF169 from NCP-ubme.

134 histone H4K16 acetylation, which facilities 53BP1 displacement from DSBs.

135 at requires its phosphorylation, but whether 53BP1 does so directly is not known.

136 escence staining for colocalizing gamma-H2AX/53BP1 DSB-marking foci.

137 explanation of why CSR is so reliant on the 53BP1 DSB-response factor.

138 e persistent DNA damage response (gammaH2AX, 53BP1) due to chronic inflammation.

139 1 function in promoting the repositioning of 53BP1 during HR.

140 lear levels of CTSL, vitamin D receptor, and 53BP1 emerged as a novel triple biomarker signature for

141 es a plausible explanation for the link with 53BP1 enforcement of deletional CSR.

142 However, the mechanism by which 53BP1 facilitates deletional CSR and inhibits inversiona

143 53BP1, first identified as a DNA damage checkpoint prote

144 re to DNA crosslinking agents, gammaH2AX and 53BP1 foci accumulation, and enhanced p53/p21 activation

145 repressed DNA damage repair (DDR), increased 53BP1 foci and enhanced radioresponsiveness.

146 observed a 2-fold increase in the volume of 53BP1 foci by 8 h, which is not seen in G1 cells.

147 ed DNA damage, as evidenced by gammaH2AX and 53BP1 foci formation, which was carried through into mit

148 mere aberrations, long-lasting gammaH2AX and 53BP1 foci, and augmented cell death upon oxidative telo

149 tid exchange, gross chromosomal aberrations, 53BP1 foci, and micronuclei.

150 ation of phospho-SER139-H2AX (gammaH2AX) and 53BP1 foci, two factors involved in the DNA damage respo

151 rradiation, and the protein colocalized with 53BP1 foci.

152 e assessed by immunofluorescence analysis of 53BP1 foci; DSB levels were determined by neutral comet

153 AX) and generation of p53 binding protein 1 (53BP1) foci in K562 cells within 1 h of exposure, which

154 specifically required for ATM signalling and 53BP1 focus formation induced by replication stress, not

155 Excluding 53BP1 from chromatin is required to attenuate the DNA da

156 facilitates TIP60-dependent mobilization of 53BP1 from DNA breaks, promoting HR.

157 However, overexpression of TIRR impedes 53BP1 function by blocking its localization to double-st

158 AD50), double-stranded break repair molecule 53BP1, G2 checkpoint regulators (CHK1 and CHK2), and ant

159 Although 53BP1 has been established well as a mediator in DNA dam

160 eak (DSB) quantification (based on gammaH2AX/53BP1 high-resolution immunofluorescence microscopy) tha

161 sk whether increased expression of RNF168 or 53BP1 impacts physiological versus mutagenic NHEJ.

162 Structural elucidation of 53BP1 in complex with a methylated K810 pRb peptide emph

163 ected crucial function of REV7 downstream of 53BP1 in coordinating pathological DSB repair pathway ch

164 tanding of the cell-cycle-dependent roles of 53BP1 in DSB repair.

165 Interestingly, promotion of MMEJ by 53BP1 in G1-phase cells is only observed in the presence

166 In contrast to this role for 53BP1 in HR in G2 phase, we show that it is dispensable

167 We report a novel architectural role for 53BP1 in Igh chromatin looping in mouse B cells.

168 The functions of 53BP1 in NHEJ processes are not well understood.

169 d suggest a previously unidentified role for 53BP1 in regulating pRb tumor suppressor activity.

170 Depletion of TIRR destabilizes 53BP1 in the nuclear-soluble fraction and alters the dou

171 lates the DNA damage checkpoint protein Crb2(53BP1) in mitosis, the full impact of this modification

172 sion of one variant, named i53 (inhibitor of 53BP1), in human and mouse cells, blocked accumulation o

173 ave investigated the downstream effectors of 53BP1, including replication timing regulatory factor 1

174 Depletion of 53BP1 induces mitotic defects such as chromosomal misseg

175 8 to promote H2A/H2AX monoubiquitination and 53BP1 IRIF, but not RNF168 self-accumulation into IRIF,

176 n BRCA1 depleted cells, and for promotion of 53BP1 IRIF.

177 53BP1 IRIFs were suppressed when p18CycE was generated i

178 53BP1 is a key regulator of DSB repair pathway choice in

179 We found that 53BP1 is a mitotic-binding partner of the kinases Plk1 a

180 Inhibition of 53BP1 is a robust method to increase efficiency of HDR-b

181 eterogeneity in the expression of RNF168 and 53BP1 is found in human tumors, our results suggest that

182 Here we show that 53BP1 is phosphorylated during mitosis on two residues,

183 The 53BP1 is preferentially bound to larger replicons, where

184 Previous studies have shown that 53BP1 is pro-non-homologous end-joining and anti-HR.

185 Thus, 53BP1 is required for three-dimensional organization of

186 P53-binding protein 1 (53BP1) is a multi-functional double-strand break repair

187 ed near uncapped telomeres because less Rad9(53BP1) is recruited near uncapped telomeres.

188 r SOSS1 blocks resection, while depletion of 53BP1, Ku or DNA-dependent protein kinase catalytic subu

189 Depletion of UbcH7 stabilizes 53BP1, leading to inhibition of DSB end resection.

190 53BP1/LINC/microtubule-dependent mobility is also eviden

191 t double-strand break (DSB) sites, impairing 53BP1 localization and enabling BRCA1 recruitment and DN

192 er hand, its association with 53BP1 prevents 53BP1 localization to sites of DNA damage, and thus TIRR

193 to regulate acetylation-dependent control of 53BP1 localization.

194 RCA1 is downregulated at transcripts levels, 53BP1 loss is caused by activation of cathepsin L-mediat

195 Wdr70 is dispensable for resection upon Crb2(53BP1) loss, or when the Set9 methyltransferase that cre

196 Similar to 53BP1, loss of TIRR restores PARPi resistance in BRCA1-d

197 es resolved by HCoDES suggests that H2AX and 53BP1 may have distinct activities in end protection.

198 Intriguingly, 53BP1 mediates p53 activation independently of its DNA r

199 st before mitotic entry induced formation of 53BP1 NBs in the next cell cycle, showing that TopBP1 ac

200 section by promoting the recruitment of Rad9(53BP1) near DSBs.

201 While 53BP1 negatively regulates DNA end processing, depletion

202 : instead it elevated the recruitment of the 53BP1 NHEJ factor to DSBs.

203 Persistent TopBP1 foci transition into 53BP1 nuclear bodies (NBs) in G1 and precise temporal de

204 replication, causing mitotic abnormalities, 53BP1 nuclear body formation in the ensuing G1 phase, an

205 Thus, we uncover a DNA under replication-53BP1 nuclear body formation-G1 arrest axis as an unanti

206 dges, and G1-specific p53-binding protein 1 (53BP1) nuclear bodies provide a mechanism for resolving

207 This 53BP1(oligo) allele was previously found to be unable to

208 A mutant lacking the oligomerization domain (53BP1(oligo)) was only modestly impaired in promoting NH

209 Since 53BP1 or its known downstream effectors, PTIP and RIF1 (

210 acquired olaparib resistance through loss of 53BP1 or REV7.

211 gly, deletion of Rad3(ATR), Rad26ATRIP, Crb2(53BP1) or Cdc25 overexpression leads to reduced HR and i

212 unction as DNA repair proteins (e.g., BRCA1, 53BP1) or nucleases (e.g., Cas9, FokI), are depleted wit

213 y did not affect the accumulation of RNF168, 53BP1, or RPA at DSBs.

214 age as scored by induction of gamma-H2AX and 53BP1 (p53 binding protein 1) nuclear foci, and this ind

215 r data provide a mechanistic explanation for 53BP1-p53 cooperation in controlling anti-tumorigenic ce

216 PR/Cas9 knockout screens to identify a USP28-53BP1-p53-p21 signaling axis at the core of the centroso

217 Surprisingly, the USP28-53BP1-p53-p21 signaling pathway is also required to arre

218 t the TIP60 complex regulates association of 53BP1 partly by competing for H4K20me2 and by regulating

219 ults suggest that deregulation of the RNF168/53BP1 pathway could alter the chemosensitivity of BRCA1

220 ons regarding the upstream regulation of the 53BP1 pathway remain unanswered.

221 emis is the major downstream effector of the 53BP1 pathway, which prevents end resection and promotes

222 r basis of the competition between BRCA1 and 53BP1 pathways remains elusive.

223 Our results identify key sites of 53BP1 phosphorylation during mitosis, identify the count

224 by RIF1, the only known factor that requires 53BP1 phosphorylation for its recruitment to double-stra

225 uch as IR-induced gamma-H2AX ubiquitination, 53BP1 phosphorylation, and subsequent resolution of the

226 anslocates to damage sites via ATM-dependent 53BP1 phosphorylation.

227 The protein 53BP1 plays a central regulatory role in DNA double-stra

228 cronucleus formation, and elevated levels of 53BP1-positive G1 nuclear bodies, suggesting that defect

229 On the other hand, its association with 53BP1 prevents 53BP1 localization to sites of DNA damage

230 53BP1 promotes CSR in part by mediating synapsis of dist

231 Here, we report that 53BP1 promotes DNA double-strand break (DSB) repair and

232 We conclude that 53BP1 promotes productive CSR and suppresses mutagenic D

233 The DNA damage response (DDR) protein 53BP1 protects DNA ends from excessive resection in G1,

234 he DNA repair protein p53 binding protein 1 (53BP1) protects the genome by limiting nucleolytic proce

235 omitant increased mutant BRCA1 and decreased 53BP1 protein expression occur in clinical samples of BR

236 ation of cathepsin L-mediated degradation of 53BP1 protein.

237 53BP1, RAP80 and ubiquitin chains are enlarged following

238 Chromatin-targeted RNF168 rescues 53BP1 recruitment involved in non-homologous end joining

239 tes histone H4 and indirectly promotes early 53BP1 recruitment to DNA damage sites.

240 Tumor suppressor p53-binding protein 1 (53BP1) regulates the repair of dysfunctional telomeres l

241 may play both positive and negative roles in 53BP1 regulation.

242 53BP1 relocates to chromatin by recognizing RNF168-media

243 53BP1 relocation is terminated by ubiquitin ligases RNF1

244 showed significantly delayed gamma-H2AX and 53BP1 repair-related foci regression.

245 BRCA1 promotes 53BP1 repositioning to the periphery of enlarged foci an

246 We report that these functions of 53BP1 required its N-terminal ATM/ATR target sites and i

247 Loss of 53BP1 rescues BRCA1 deficiency and is associated with BR

248 Second, although loss of 53BP1 rescues the embryonic lethality and HR defects in

249 Depletion of 53BP1 rescues the formation of BRCA1 damage foci in CSB-

250 n mechanism in which phosphorylation of Crb2(53BP1) residues Thr215 and Thr235 promotes phosphorylati

251 jority of human DUBs on RNF8/RNF168-mediated 53BP1 retention at DSB sites, we found that USP44 and US

252 lysis of G1 phase cells deficient in H2AX or 53BP1 reveals DNA ends that are frequently resected to f

253 the DNA-damage response (DDR) proteins MDC1, 53BP1, RIF1 and P53, plus the nuclear architecture prote

254 aged chromatin but promotes the formation of 53BP1-Rif1 damage foci in S and G2 cells.

255 ndent hyper-resection when the repression by 53BP1/Rif1 is alleviated.

256 owever, telomere resection in the absence of 53BP1/Rif1 is more extensive upon complete removal of sh

257 , involves Exo1 and BLM, and is inhibited by 53BP1/Rif1.

258 activities to be distinct and separable from 53BP1's regulation of DNA double-strand break repair pat

259 s that were transmitted to daughter cells in 53BP1-shielded nuclear bodies.

260 Notably, the late DDR protein, 53BP1 shows in live-cell imaging strikingly stronger rec

261 with a specific role in MMEJ we confirm that 53BP1 status does not affect c-NHEJ.

262 Here, we reveal that 53BP1 stimulates genome-wide p53-dependent gene transact

263 eater mobility of damaged chromatin requires 53BP1, SUN1/2 in the linker of the nucleoskeleton, and c

264 53BP1 supports sequence deletion during MMEJ consistent

265 Ectopic recruitment of 53BP1-T1609A/S1618A to mitotic DNA lesions was associate

266 K810 pRb peptide emphasized the role of the 53BP1 tandem tudor domain in recognition of the methylat

267 covery of a genetically encoded inhibitor of 53BP1 that increases the efficiency of HDR-dependent gen

268 ation sites in the N-terminal region of Crb2(53BP1) that mediate interaction with Rad4(TopBP1) and re

269 ified genes encoding the p53-binding protein 53BP1, the deubiquitinase USP28, and the ubiquitin ligas

270 Moreover, the 53BP1-TIRR complex dissociates after DNA damage, and thi

271 Collectively, our data identified a novel 53BP1-TIRR complex in DNA damage response.

272 nteracting factor 1 (RIF1) to dissociate the 53BP1-TIRR complex.

273 ge and recruiting repair factors such as GFP-53BP1 to a large region around the locus.

274 T1609 and S1618 to allow the recruitment of 53BP1 to chromatin in G1 phase.

275 depleted cells, and promotes recruitment of 53BP1 to DNA damage and H2AX monoubiquitination at K13/1

276 ndered in their ability to recruit BRCA1 and 53BP1 to DNA damage sites.

277 ts recruitment of the damage response factor 53BP1 to DNA double-strand breaks (DSBs), thereby influe

278 CT domain, the GAR domain, or the binding of 53BP1 to dynein.

279 we identify Rif1 as the main factor used by 53BP1 to impair 5' end resection.

280 Significantly, binding of 53BP1 to methyl K810 occurs on E2 promoter binding facto

281 uitinated histone H2A and impedes binding of 53BP1 to mitotic chromatin.

282 PBP1 interaction enhances the recruitment of 53BP1 to nuclear foci in the S phase, resulting in impai

283 During S phase, BRCA1 antagonizes 53BP1 to promote HR.

284 response by facilitating the recruitment of 53BP1 to sites of DNA damage.

285 h is required for the initial recruitment of 53BP1 to sites of DNA double-strand breaks and for its f

286 tates recruitment of other DDR factors (e.g. 53BP1) to DNA damage, and inhibits homologous recombinat

287 te the recruitment of p53-binding protein 1 (53BP1) to the sites of DNA double-strand breaks.

288 eckpoint 1 (Mdc1) and p53 binding protein 1 (53BP1), to sites of DNA damage.

289 eckpoint 1 (MDC1) and p53 binding protein 1 (53BP1), to sites of DSBs.

290 stone H4 recruits repair proteins, including 53BP1, to DNA double-strand breaks (DSB) and undergoes d

291 Hyperstabilization of the 53BP1-TOPBP1 interaction enhances the recruitment of 53B

292 The mechanisms responsible for decreased 53BP1 transcript and protein levels in tumors remain unk

293 ng with increased staining of gamma-H2AX and 53bp1 (Trp53bp1) in areas of acinar ductal metaplasia, s

294 s results in the downregulation of BRCA1 and 53BP1, two key factors in DNA DSB repair by homologous r

295 Furthermore, we demonstrate 53BP1-USP28 cooperation to be essential for normal p53-p

296 alysis of centrinone resistance identified a 53BP1-USP28 module as critical for communicating mitotic

297 2609 and S2056-DNA-PKcs and its target S1778-53BP1 were greatly decreased in p18CycE-expressing cells

298 RNF168 mediates K63-linked ubiquitylation of 53BP1 which is required for the initial recruitment of 5

299 ing of the non-homologous end joining factor 53BP1, which engages chromatin through simultaneous bind

300 53BP1, which influences DSB repair by NHEJ, colocalizes