ライフサイエンスコーパス: 53BP1

1 inase complex, as a novel binding partner of 53BP1.

2 , the PP4 regulatory subunit that recognizes 53BP1.

3 abilizes 53BP1 and thus positively regulates 53BP1.

4 ineered ubiquitin variants for inhibitors of 53BP1.

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

6 M on this rearrangement seems independent of 53BP1.

7 e significantly diminished in the absence of 53BP1.

8 trand break-induced protein complex centring 53BP1.

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

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

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

12 biquitin and nucleosome surfaces accessed by 53BP1.

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

14 aired recruitment of repair factors MDC1 and 53BP1.

15 ticipates in the interplay between BRCA1 and 53BP1.

16 ionizing radiation-induced DSBs but not with 53BP1.

17 identified RIF1 as the critical effector of 53BP1.

18 ining with antibodies against gamma-H2AX and 53BP1.

19 d phosphorylation sites in the N-terminus of 53BP1.

20 immunoglobulin class switching that rely on 53BP1.

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

22 DNA damage response (DDR) by phosphorylating 53BP1, a critical DDR mediator, to prevent its localizat

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

24 ntrols the DDR by inhibiting the function of 53BP1, a key factor for DNA double-strand break repair b

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

26 JNK links to 53BP1, a nuclear protein that negatively regulates DNA d

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

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

29 functional telomeres, which in turn promotes 53BP1 accumulation at damaged sites, therefore in a miRN

30 ell lines and breast carcinoma NuMA prevents 53BP1 accumulation at DNA breaks, and high NuMA expressi

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

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

33 53BP1 activity drives genome instability and lethality i

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

35 es RNF168-mediated ubiquitination as well as 53BP1 and BRCA1 ionizing radiation-induced foci formatio

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

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

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

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

40 ZPET hinders resection independently of 53BP1 and HELB.

41 romatin, visualized by fluorescently labeled 53BP1 and histone H2B, respectively.

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

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

44 Kap1, and 53BP1 phosphorylation, compromises 53BP1 and RIF1 co-recruitment to sites of DNA lesions, a

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

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

47 use super-resolution microscopy to show that 53BP1 and RIF1 form an autonomous functional module that

48 perresection are associated with loss of Ku, 53BP1 and RIF1 resection inhibitors from the break site.

49 rotect DNA ends against aberrant processing, 53BP1 and RIF1 safeguard epigenetic integrity at loci th

50 The alternating distribution of 53BP1 and RIF1 stabilizes several neighbouring TAD-sized

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

52 the influence of RNF8 on EJ is distinct from 53BP1 and the ALT-EJ factor, POLQ.

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

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

55 53BP1 and TIRR form a stable complex, which is required

56 multi-domain 'scaffold' proteins, including 53BP1 and TOPBP1, which recognise post-translational mod

57 y a phosphorylation-dependent interaction of 53BP1 and TOPBP1.

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

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

60 romote recruitment of p53-binding protein 1 (53BP1) and Mediator of DNA damage checkpoint 1 (MDC1) to

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

62 BRCA1 at DSBs, causing aberrant build-up of 53BP1, and allowing anti-resection activity to prevail i

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

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

65 mRNA for DNA damage response mediators ATM, 53BP1, and MDC1.

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

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

68 Current evidence indicates that 53BP1 assembles a cohort of DNA damage response (DDR) fa

69 s of CHD7-HDAC1/2-dependent cNHEJ reinforces 53BP1 assembly at the damaged chromatin and shifts DSB r

70 ions of BRCA1 and the p53-binding protein 1 (53BP1)-associated complex in DNA resection sheds light o

71 gulates the DDR by hampering the activity of 53BP1 at damaged chromosomes.

72 e accumulation of the pro-end joining factor 53BP1 at DSBs in S and G(2) cell cycle phases.

73 s revealed by accumulation of gammaH2A.X and 53BP1 at mitochondrial DNA foci.

74 This process is initiated by accumulation of 53BP1 at regions of compact chromatin that colocalize wi

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

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

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

78 Defects in the 53BP1 axis partially restore the ability of a BRCA1-defi

79 ires double strand break repair by promoting 53BP1 binding to double-strand breaks.

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

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

82 nimum and maximum resection lengths, whereas 53BP1, BRCA1 and EXO1 play surprisingly minimal roles.

83 radiotherapy as an acquired vulnerability of 53BP1;BRCA1-deficient cells in vitro and in vivo.

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

85 omatin modified by pUbT12 is inaccessible to 53BP1 but permissive to the homologous recombination (HR

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

87 ed a novel posttranslational modification of 53BP1 by ADP-ribosylation that is targeted by a PAR-bind

88 e a mechanism involving the sequestration of 53BP1 by NuMA in the absence of DNA damage.

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

90 Loss of 53BP1 caused hypersensitivity to licensing inhibition wh

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

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

93 dependent ubiquitin signaling and downstream 53BP1 chromatin recruitment.

94 opose that some of the fidelity functions of 53BP1 coevolved with class switch recombination (CSR) in

95 iminished formation of gammaH2AX foci and of 53BP1-containing telomere dysfunction-induced foci (TIFs

96 Human 53BP1 contains a UTX-binding site that diverges from its

97 53BP1 controls two downstream subpathways, one mediated

98 ishes recruitment of TOPBP1, ATR and CHK1 to 53BP1 damage foci, abrogating cell cycle arrest and perm

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

100 atalytic hydrolase activity was required for 53BP1 de-ADP-ribosylation, 53BP1 protein stability, and

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

102 The consequences of 53BP1 deficiency, such as diminished PARPi efficacy in B

103 alpha looping interactions are unaffected by 53BP1 deficiency.

104 onstrate that PALB2 DSB recruitment in BRCA1/53BP1-deficient cells is mediated by an interaction betw

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

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

107 the synthetic rescue of BRCA1 deficiency by 53BP1 deletion, and it predisposes BRCA1 heterozygous mi

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

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

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

111 LC8 as an important mediator of a subset of 53BP1-dependent DSB responses.

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

113 itment to sites of DNA lesions, and inhibits 53BP1-dependent fusion of dysfunctional telomeres.

114 ates at laser-induced DNA damage tracks in a 53BP1-dependent manner and requires the canonical H2AX-M

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

116 53BP1-dependent p53 modulation requires both auto-oligom

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

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

119 e underlying mechanism of kinetic control of 53BP1 dephosphorylation in mitosis.

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

121 Strikingly, reintroduction of BRCA1 or 53BP1 depletion restored HR and rescued the ability of c

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

123 the structural protein NuMA, which controls 53BP1 diffusion.

124 Here we show that UTX and 53BP1 directly interact and co-occupy promoters in human

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

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

127 We fused a dominant-negative mutant of 53BP1, DN1S, to Cas9 nucleases, and the resulting Cas9-D

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

129 ze (represented by the local accumulation of 53BP1), DSB density, and the local chromatin compaction.

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

131 RCA1 recruitment to DSBs by interacting with 53BP1 during repair.

132 DYNLL1) as an important 53BP1 effector.

133 y DNA double-strand breaks and recognized by 53BP1 enable focal accumulation of this multifunctional

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

135 the nucleosome acidic patch region, which in 53BP1-expressing cells is bound by 53BP1's ubiquitin-dir

136 ase activity are required for maintenance of 53BP1 expression and subsequent recruitment to DNA damag

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

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

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

140 Additionally, wild-type Cas9 induced fewer 53BP1 foci in TP53+/+ cells compared to TP53-/- cells an

141 eaks, indicated by ATM kinase activation and 53BP1 foci induction.

142 assay and observed a close similarity in the 53BP1 foci repair kinetics in the cells irradiated with

143 Unexpectedly, the number of 53BP1 foci that persisted in the mouse lens samples afte

144 Here, 53BP1 foci was used as a marker of DNA damage.

145 ch showed the expected reduction of residual 53BP1 foci with reducing dose-rate.

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

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

148 diation- and etoposide-induced gammaH2AX and 53BP1 foci, it markedly delays their resolution, indicat

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

150 uppressed RNF8/RNF168-dependent formation of 53BP1 foci, which plays important roles in DDR.

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 air kinetics using the p53 binding protein-1(53BP1) foci formation assay and observed a close similar

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

155 Recent studies have elevated 53BP1 from its modest status of (yet another) DNA damage

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

157 However, the upstream regulator(s) of 53BP1 function in DNA repair remain unknown.

158 he replicative state of the genome to oppose 53BP1 function, routing only DSBs within sister chromati

159 replication fork stability by counteracting 53BP1 function.

160 deterministic in DSB repair pathway choice, 53BP1 functions as a DSB escort that guards against ille

161 ataxia-telangiectasia mutated (ATM), phospho-53BP1, gammaH2AX and neuronal apoptosis.

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

163 We propose that 53BP1 has evolved to avoid mutagenic repair outcomes and

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

165 Here we show that depleting 53BP1 in BRCA1-null cells restores PALB2 accrual at rese

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

167 Protein phosphatase 4 (PP4) dephosphorylates 53BP1 in late mitosis to allow its recruitment to DNA le

168 nding partner and uncovers a unique role for 53BP1 in replication fork stability.

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

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

171 the recruitment of Rap80/BRCA1-A, Rad18, and 53BP1, in cellular resistance to ionizing radiation and

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

173 In response to DNA damage, ADP-ribosylated 53BP1 increased significantly, resulting in its ubiquiti

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

175 53BP1 interacts with the structural protein NuMA, which

176 molecular crowding of DDR proteins, such as 53BP1, into foci that exhibit liquid-liquid phase-separa

177 53BP1 is a chromatin-associated protein that regulates t

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 am role in RAD51 loading is dispensable when 53BP1 is absent.

182 53BP1 is an enigmatic DNA damage response factor that ga

183 Timely dephosphorylation of 53BP1 is critical for genome integrity, as premature rec

184 he presence of a feedback mechanism by which 53BP1 is regulated by a novel binding partner and uncove

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

186 TOPBP1 interaction with 53BP1 is structurally complimentary to its interaction w

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

188 iation and PARP inhibition, highlighting the 53BP1-LC8 module in counteracting BRCA1-dependent functi

189 hat NUDT16 plays a major role in controlling 53BP1 levels under both normal growth conditions and dur

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

191 ion of 53BP1 to regulate 53BP1 stability and 53BP1 localization at DSBs.

192 ates with 53BP1 to stabilize it and prevents 53BP1 localization to DNA damage sites by blocking 53BP1

193 NUDT16 catalytically inactive mutant blocked 53BP1 localization to double-strand breaks because (i) t

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

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

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

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

198 Additionally, recovery of 53BP1-mCherry was observed to be slowed at sites of DNA

199 nuclear diffusion of NLS-GFP and recovery of 53BP1-mCherry, a marker for DNA damage, in live MDA-MB-2

200 n, and this effect was entirely dependent on 53BP1-mediated NHEJ.

201 P53-binding protein 1 (53BP1) mediates DNA repair pathway choice and promotes c

202 surrounding nuclear environment and modulate 53BP1 mobility.

203 53BP1 movements are constrained throughout the nucleopla

204 Codepletion of POLD2 with 53BP1 nearly eliminates translocations.

205 inhibition caused DNA damage to manifest as 53BP1 nuclear bodies in daughter G(1) cells leading to G

206 trand breaks, and accumulate high numbers of 53BP1 nuclear bodies, a marker of genomic instability in

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

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

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

210 Increased 53BP1 occupancy at DNA lesions induced by enoxacin ultim

211 of these sites does not affect formation of 53BP1 or ATM foci following DNA damage, but abolishes re

212 se via several mechanisms, including loss of 53BP1 or its downstream co-factors.

213 Depletion of 53BP1 or RIF1 (but not shieldin) disrupts this arrangeme

214 Moreover, 53BP1 or USP28 deletion restored NPC proliferation and b

215 TP53-dependent but is not rescued by loss of 53BP1 or USP28.

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

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

218 unveil an additional level of regulation of 53BP1 outside repair foci.

219 9 (histone H3 lysine 9) hyperacetylation and 53BP1 (p53 binding protein 1) binding, indicative of tel

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

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

222 e TCGA database revealed lower expression of 53BP1 pathway genes in prostate cancer, suggesting that

223 ough BRCA1 reconstitution, HR restoration by 53BP1 pathway inactivation further increases radiosensit

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

225 uired drug resistance due to the loss of the 53BP1 pathway.

226 tivity attenuates ATM, Chk1, MDC1, Kap1, and 53BP1 phosphorylation, compromises 53BP1 and RIF1 co-rec

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

228 The tumor suppressor protein 53BP1 plays key roles in response to DNA double-strand b

229 ding E3 ubiquitin ligase, RNF146, leading to 53BP1 polyubiquitination and degradation.

230 agile telomeres and telomere loss as well as 53BP1-positive telomere dysfunction-induced foci (TIFs),

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

232 53BP1 promotes UTX chromatin binding, and in turn H3K27

233 was required for 53BP1 de-ADP-ribosylation, 53BP1 protein stability, and its function in cell surviv

234 Opposing end resection is the 53BP1 protein, which recruits the ssDNA-binding REV7-Shi

235 The DDC mediator 53BP1/Rad9 limits the nucleolytic processing (resection)

236 te that NUDT16 regulates 53BP1 stability and 53BP1 recruitment at double-strand breaks, providing yet

237 Inhibiting 53BP1 recruitment to damaged chromatin completely abolis

238 athway is operative but becomes critical for 53BP1 recruitment to DNA-damage sites and cell survival

239 Our results establish CDK5 as a regulator of 53BP1 recruitment.

240 anti-resection factor TP53-binding protein 1(53BP1) (refs.

241 ce: This study provides a novel mechanism of 53BP1 regulation by demonstrating that NUDT16 has hydrol

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

243 d breaks, providing yet another mechanism of 53BP1 regulation.Significance: This study provides a nov

244 53BP1 relocates to chromatin by recognizing RNF168-media

245 53BP1 relocation is terminated by ubiquitin ligases RNF1

246 imaging, we characterized multiple cycles of 53BP1 repair foci formation and dissolution, with the fi

247 The anti-recombinogenic functions of 53BP1 require phosphorylation-dependent interactions wit

248 Strikingly, concurrent loss of 53BP1 rescues not only BRCA1/Rad51 recruitment but also

249 Loss of 53BP1 rescues the HR defect in BRCA1-deficient cells by

250 inactivation of LC8 or its interaction with 53BP1 resulted in checkpoint defects.

251 ormation by pS2056-, pT2609-DNA-PKcs, pS1778-53BP1, RIF1 and a reporter assay activation.

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

253 er, concomitant loss of the pro-NHEJ factors 53BP1, RIF1, REV7-Shieldin (SHLD1-3) or CST-DNA polymera

254 e individually responsible for counteracting 53BP1-RIF1-Shieldin activity and promoting RAD51 loading

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

256 the loss of end-resection antagonists of the 53BP1/RIF1/REV7/Shieldin/CST pathway.

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

258 which in 53BP1-expressing cells is bound by 53BP1's ubiquitin-directed recruitment (UDR) domain.

259 hat mutation of the PTIP interaction site in 53BP1 (S25A) allows sufficient DNA2-dependent end resect

260 ced targeting of PALB2 to ssDNA in BRCA1(D11)53BP1(S25A) cells restores RNF168 recruitment, RAD51 nuc

261 As a result, BRCA1(Delta11)53BP1(S25A) mice exhibit hallmark features of HR insuffi

262 remove ADP-ribosylation of 53BP1 to regulate 53BP1 stability and 53BP1 localization at DSBs.

263 ummary, we demonstrate that NUDT16 regulates 53BP1 stability and 53BP1 recruitment at double-strand b

264 hydrolase NUDT16, a TIRR homolog, regulates 53BP1 stability.

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

266 How cells appropriately dephosphorylate 53BP1, thereby restoring DDR, is unclear.

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

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

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

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

271 1, ultimately preventing the localization of 53BP1 to damaged chromatin.

272 Cell death resulted from the recruitment of 53BP1 to DNA break sites and inhibition of DNA end resec

273 a recruitment module for the localization of 53BP1 to DNA break sites.

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

275 enome integrity, as premature recruitment of 53BP1 to DNA lesions impairs mitotic fidelity.

276 he localization of the NHEJ-promoting factor 53BP1 to DSBs.

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

278 e activities that remove ADP-ribosylation of 53BP1 to regulate 53BP1 stability and 53BP1 localization

279 recently reported that TIRR associates with 53BP1 to stabilize it and prevents 53BP1 localization to

280 ar lamina and leakage of the nuclear protein 53BP1 to the cytosol.

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

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

283 the localization of other factors, including 53BP1, to DSB sites.

284 ized by the recruitment of gammaH2AX-but not 53BP1-to telomeres.

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

286 oad, together with massive end protection by 53BP1, triggers competition between error-free HR and mu

287 localization to DNA damage sites by blocking 53BP1 Tudor domain binding to H4K20me2 sites.

288 increased after IR; (ii) the mutant enhanced 53BP1 Tudor domain binding to TIRR, and (iii) the mutant

289 (iii) the mutant impaired the interaction of 53BP1 Tudor domain with H4K20me2.

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

291 hes its recognition and dephosphorylation of 53BP1, ultimately preventing the localization of 53BP1 t

292 hter cells by activating a pathway involving 53BP1, USP28, and TP53, termed the mitotic surveillance

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

294 mouse homolog by 41%, and disruption of the 53BP1-UTX interaction abrogated human, but not mouse, ne

295 The 53BP1-UTX interaction is required to upregulate key neur

296 Overall, our data suggest that the 53BP1-UTX interaction supports the activation of key gen

297 tagenic NHEJ, revealing a backup function of 53BP1 when cNHEJ fails.

298 protection involving p53 binding protein 1 (53BP1), which results in fast and error-free microhomolo

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

300 rm of genome surveillance is orchestrated by 53BP1, whose accumulation at DSBs triggers sequential re