ライフサイエンスコーパス: NHEJ

1 NHEJ has the potential to be highly mutagenic because it

2 NHEJ relies on Ku to thread onto DNA termini and thereby

3 NHEJ relies on polynucleotide kinase/phosphatase (PNKP),

4 ergo (reduced) CSR through an alternative(A)-NHEJ pathway, which introduces microhomologies in S-S ju

5 amage response and inappropriate repair by A-NHEJ.

6 ewly replicated telomeres from engaging in A-NHEJ mediated fusions that would otherwise promote genom

7 ic alternative non-homologous end joining (A-NHEJ) pathway.

8 t residues, limit the efficiency of accurate NHEJ by Polmu in vitro and in vivo.

9 lease accessibility, and recruits additional NHEJ factors, including Nej1 and Lif1.

10 f alternative nonhomologous end-joining (Alt-NHEJ) events, including chromosomal translocations.

11 t alternative nonhomologous end joining (alt-NHEJ), which did not generate fragile telomeres.

12 ection prior to repair by c-NHEJ and not alt-NHEJ.

13 merase delta (Pol delta) as promoters of Alt-NHEJ that results in more extensive intrachromosomal mut

14 port a model in which Pol delta promotes Alt-NHEJ in human cells at DSBs, including translocations.

15 This resistance is independent of alternate-NHEJ and is instead achieved by re-activation of HR.

16 t only has a slight influence on alternative NHEJ.

17 o intercept the more error-prone alternative NHEJ repair pathway by recruiting Ku and associated NHEJ

18 ed NBS1(S432) with TRF2 promotes alternative-NHEJ repair of telomeres lacking POT1-TPP1.

19 its differentiated mechanism of action as an NHEJ inhibitor, AZD7648 complements the current armament

20 The atomic structure of an NHEJ junction with a Pol X construct that mimics Pol mu

21 results for reporting HDR (R2 = 0.9722) and NHEJ (R2 = 0.919) events.

22 rin and the mechanisms of ATM activation and NHEJ at telomeres, before discussing the following quest

23 ordinate 2-way crosstalk between the BER and NHEJ pathways.

24 The BRCA and NHEJ pathways are required for the repair of CX-5461 and

25 lting from CRISPR/Cas9-mediated cleavage and NHEJ-mediated DSB repair of 6872 synthetic target sequen

26 at DSB sites to stably interact with DDR and NHEJ factors, specifically acting as a scaffold for the

27 on of homology-directed repair-dependent and NHEJ-dependent genome-editing tools comprises a powerful

28 ysis allows longitudinal tracking of HDR and NHEJ activities in cells, and enables detection of DSB r

29 ultaneously and longitudinally track HDR and NHEJ dynamics that is sufficiently versatile for elucida

30 pathways in the G2 phases where both HR and NHEJ can operate is not clearly understood.

31 approach, specifically for targeting HR and NHEJ deficient cancers and other tumours deficient for D

32 unctional switch in selecting between HR and NHEJ pathways.

33 tic lethal relationship between DEK loss and NHEJ inhibition.

34 g inhibition of XRCC4 polyubiquitination and NHEJ.

35 ade by decreasing the NAD(+) /NADH ratio and NHEJ-repair in vitro and in diabetes mouse models.

36 largely based on 5' to 3' DNA resection, and NHEJ proceeds only if resection has not been initiated.

37 pair pathway by recruiting Ku and associated NHEJ factors.

38 first discuss repair pathway choice between NHEJ and other DSB repair pathways.

39 ch uses a more entwined relationship between NHEJ and HR, incorporating protein co-localisation and R

40 BRCA1, leading to pathway selection between NHEJ and homologous recombination.

41 as9-DN1S fusion proteins significantly block NHEJ events specifically at Cas9 cut sites and improve H

42 ed in hyper-resection, which attenuated both NHEJ and HR and severely compromised DSB repair resultin

43 0% of alleles were repaired by HDR and 7% by NHEJ.

44 ay the foundation for curing hemophilia A by NHEJ knock-in of BDDF8 at Alb introns after AAV-mediated

45 p53 ablation and irrevocably deregulated by NHEJ inactivation.

46 a mechanism for iterative repair of DSBs by NHEJ.

47 Preventing DSB ligation by NHEJ, or enhancing homologous recombination by BRCA1-A c

48 nce between MEK5 signaling and DNA repair by NHEJ in conferring resistance to genotoxic stress in adv

49 or addition, explaining why DSBs repaired by NHEJ are rarely restored to their original DNA sequence.

50 Two-way crosstalk between BER and c-NHEJ repair pathway is mediated by Pol-beta and Ku70.

51 site, undergo resection prior to repair by c-NHEJ and not alt-NHEJ.

52 oes not commence, then repair can ensue by c-NHEJ, but when executed, Artemis is essential to complet

53 complex substitutes in vitro for the core c-NHEJ factor, XLF.

54 Core C-NHEJ factors, such as XRCC4, are required for joining DS

55 n chromosome 12 reveals that XLF-dependent C-NHEJ promotes deletion rearrangements in human cells and

56 Resection-dependent c-NHEJ represents an inducible process during which Plk3 p

57 Resection-dependent c-NHEJ significantly contributes to the formation of delet

58 essential to complete resection-dependent c-NHEJ.

59 DNA-binding REV7-Shieldin complex to favor C-NHEJ repair.

60 g ATXN3's role in PNKP-mediated error-free C-NHEJ.

61 elected DSBs are shepherd by DNA-PKcs from c-NHEJ to resection-dependent pathways for processing unde

62 hermore, an ATM kinase inhibitor increased C-NHEJ-mediated rearrangements only in U2OS cells.

63 the canonical non-homologous end joining (C-NHEJ) factor XLF promotes these rearrangements.

64 ways [canonical nonhomologous end joining (C-NHEJ) or alternative end joining (ALT-EJ)], which cause

65 a the canonical nonhomologous end joining (c-NHEJ) pathway.

66 d the classical nonhomologous end-joining (C-NHEJ) proteins, including PNKP, along with nascent RNAs

67 Canonical non-homologous end joining (c-NHEJ) repairs DNA double-strand breaks (DSBs) in G1 cell

68 ns by classical nonhomologous end joining (C-NHEJ).

69 d by canonical non-homologous end joining (C-NHEJ).

70 ) and classical nonhomologous end joining (C-NHEJ).

71 pecific differences in the contribution of C-NHEJ and ATM kinase inhibition influence these rearrange

72 ncovered that the relative contribution of C-NHEJ appears lower in U2OS than in HEK293 and A549 cells

73 inase may affect the relative influence of C-NHEJ vs. ALT-EJ on rearrangement formation.

74 deletion mutations, which is a hallmark of C-NHEJ.

75 rangement junctions that show hallmarks of C-NHEJ.

76 ably, hyper-resection is absent from other c-NHEJ mutants.

77 s of the canonical branch of NHEJ pathway (c-NHEJ).

78 Finally, several C-NHEJ factors are required for the increase in rearrangem

79 at is critical for an interaction with the C-NHEJ factor X-ray repair cross-complementing 4 (XRCC4),

80 We suggest that the contribution of the C-NHEJ pathway to the formation of a 0.4-Mbp deletion rear

81 ion in an experimental condition, in which C-NHEJ is the predominant EJ repair event (i.e., expressio

82 physical juxtaposition of DNA ends is called NHEJ synapsis.

83 at the individual DSB created by CRISPR/Cas9-NHEJ, MMEJ, and HDR-and show its applicability in evalua

84 h the Ku and inhibit in vitro NHEJ, cellular NHEJ, and potentiate the cellular activity of radiomimet

85 Consistent with prior reports, cis NHEJ was more efficient than trans NHEJ.

86 BER efficiency but also enhances the classic NHEJ repair.

87 Classical-NHEJ-mediated repair of telomeres lacking TRF2 requires

88 report that RECQL4 promotes and coordinates NHEJ and HR in different cell cycle phases.

89 lysis identified USP14 interaction with core NHEJ proteins, including Ku70, which was validated by co

90 sing the recruitment of 53BP1, and decreases NHEJ, rendering cells more sensitive to DSBs.

91 ver ZBTB24 as a regulator of PARP1-dependent NHEJ and class-switch recombination, providing a molecul

92 tingly, however, we implicate TDP2-dependent NHEJ in the formation of a rare subclass of translocatio

93 which arise from rare failures at different NHEJ steps.

94 Ku70/Ku80 (Ku) and Ku complexes that direct NHEJ.

95 Finally, we discuss NHEJ-related human diseases, including inherited disorde

96 HEJ), as well as between proximal and distal NHEJ repair.

97 During NHEJ DNA ends are held together by a multi-protein synap

98 ce of a decreased template dependency during NHEJ, which renders the error-rate of the mutants higher

99 address complementary DSB substrates during NHEJ in a manner indistinguishable from single-strand br

100 mplementary functions of PAXX and XLF during NHEJ.

101 a domain of Polmu for accurate and efficient NHEJ, but also its contribution to the error-prone behav

102 replaces a DNA repair protein for efficient NHEJ with implications for development of resistance to

103 show that pol mu alone can mediate efficient NHEJ synapsis of 3' overhangs that have at least 1 nt mi

104 lethal-mosaicism that dominantly eliminates NHEJ-induced mutations and favors inheritance of functio

105 nous Mcl-1 depletion reduced HR and enhanced NHEJ, Mcl-1 overexpression resulted in a net increase in

106 ells harboring the nej1-V338A mutant exhibit NHEJ-mediated repair deficiencies and hyper-resection 0.

107 e in eukaryotic cells and functions to favor NHEJ over HDR by suppressing end resection, which is the

108 NAD+ as an alternative adenylation donor for NHEJ repair and maintaining genomic stability.

109 bilization of the initial synaptic event for NHEJ.

110 Our results suggest a new mechanism for NHEJ utilizing a DNA-PK dimer to bring broken DNA ends t

111 ing the Ku inward to expose the overhang for NHEJ synapsis.

112 aried, a minimal tail length is required for NHEJ.

113 at DNA breaks, thereby promoting error-free NHEJ.

114 r t-loops in protecting chromosome ends from NHEJ and ATM activation, but that other mechanisms are i

115 While HDR can only occur in S/G2, NHEJ can happen in all cell cycle phases (except mitosis

116 hile avoiding the unwanted effects of global NHEJ inhibition.

117 Using CDDR, we found HF-NHEJ to be strictly dependent on DNA Ligase IV, XRCC4 an

118 kinase ATM, on the other hand, stimulated HF-NHEJ and suppressed HDR.

119 t used DSBs repair pathway in the cells, how NHEJ factors are sequentially recruited to damaged chrom

120 ineffective the DSBs repair via the impaired NHEJ may contribute to ATII cell death in emphysema.

121 es accumulation of genomic DSBs by impairing NHEJ repair, and thereby, sensitizing neurons to DSB str

122 Depletion of PP1 impairs NHEJ in both Xenopus egg extracts and human cells.

123 dence demonstrating the observed decrease in NHEJ is insufficient to impact immunoglobulin class swit

124 sarily consistent with an isolated defect in NHEJ.

125 t autophagy-deficient cells are defective in NHEJ, as indicated by decreased IR-induced foci (IRIF) f

126 Defects in NHEJ result in sensitivity to ionizing radiation and los

127 e DNA repair protein Ku is the first step in NHEJ, followed by the iterative binding of nucleases, DN

128 entral synaptic role of Ku, X4L4, and XLF in NHEJ for all eukaryotes.

129 prolongs MDC1 focus retention and increases NHEJ and radioresistance.

130 decrease DNA end resection, which increases NHEJ and chromosomal abnormalities, ultimately causing m

131 ore, knockdown of UBE2S expression inhibited NHEJ-mediated DSB repair and rendered glioblastoma cells

132 e11-Rad50-Nbs1 (MRN) complexes, with initial NHEJ proteins must be modeled to accurately depict repai

133 resolve DSBs are Non-Homologous End Joining (NHEJ) and Homologous Recombination (HR).

134 repair pathways, non-homologous end joining (NHEJ) and homologous recombination (HR).

135 ected repair and non-homologous end joining (NHEJ) are the two major DSB repair pathways that are hig

136 bination (HR) and nonhomologous end joining (NHEJ) at the same chromosomal site, we report that the e

137 ge signaling and non-homologous end joining (NHEJ) at unprotected telomeres.

138 I find that all non-homologous end joining (NHEJ) defective cells (whether deficient in components o

139 actor (XLF) is a non-homologous end joining (NHEJ) DNA double strand break repair protein.

140 y DNA ends during nonhomologous end joining (NHEJ) for the repair of double-strand breaks (DSBs) caus

141 T domain impairs non-homologous end joining (NHEJ) in cell.

142 assay shows that nonhomologous end joining (NHEJ) is compromised in cells with ablated MEK5 protein

143 Although non-homologous end joining (NHEJ) is the most used DSBs repair pathway in the cells,

144 Non-homologous end joining (NHEJ) is the predominant pathway that repairs DNA double

145 Non-homologous DNA end joining (NHEJ) is the predominant repair mechanism of any type of

146 ed by either the non-homologous end joining (NHEJ) or homologous recombination (HR) pathway.

147 epair either via non-homologous end joining (NHEJ) or, in the presence of a template, homology-direct

148 the error-prone non-homologous end joining (NHEJ) pathway.

149 mpairment of the non-homologous end joining (NHEJ) repair pathway and DNA damage in alveolar type II

150 ical role in the non-homologous end joining (NHEJ) repair pathway and the DNA damage response (DDR).

151 teins involved in nonhomologous end joining (NHEJ) repair restrict amplification of viral DNA.

152 While non-homologous end joining (NHEJ) repair results in various mutations, microhomology

153 h are involved in nonhomologous end joining (NHEJ) repair, enhance amplification of viral DNA.

154 e attenuation of non-homologous end joining (NHEJ) repair, the role of DEK in DNA repair remains inco

155 t activation and non-homologous end joining (NHEJ) repair.

156 Non-homologous end joining (NHEJ) repairs DNA double strand breaks in non-cycling eu

157 bination (HR) and nonhomologous end joining (NHEJ) through the investigation of the deSUMOylase SENP2

158 ole in mediating non-homologous end joining (NHEJ), a major repair pathway for DNA double-strand brea

159 During non-homologous DNA end joining (NHEJ), bringing two broken dsDNA ends into proximity is

160 tral component of nonhomologous end joining (NHEJ), repairing DNA double-strand breaks that would oth

161 repair (HDR) and non-homologous end joining (NHEJ), respectively.

162 predominantly by non-homologous end joining (NHEJ), which directly ligates DNA ends.

163 ning (MMEJ)-, and nonhomologous end joining (NHEJ)-based strategies for the knock-in of markers, figu

164 component of the nonhomologous end joining (NHEJ)-mediated DNA double-strand break (DSB) repair path

165 of WT TDP-43 in non-homologous end joining (NHEJ)-mediated DSB repair, where it acts as a scaffold f

166 s mainly through non-homologous end joining (NHEJ)-mediated knock-in.

167 hibits HR and not nonhomologous end joining (NHEJ).

168 ith HDR, such as non-homologous end joining (NHEJ).

169 rocess of precise nonhomologous end joining (NHEJ).

170 nation (HDR) and non-homologous end joining (NHEJ).

171 ntly repaired by non-homologous end joining (NHEJ).

172 break repair and non-homologous end joining (NHEJ).

173 it (DNA-PKcs) and nonhomologous end joining (NHEJ).

174 break repair by non-homologous end joining (NHEJ).

175 n the process of non-homologous end joining (NHEJ).

176 ntly repaired by non-homologous end joining (NHEJ).

177 repair (HDR) or non-homologous end joining (NHEJ).

178 ty to facilitate non-homologous end joining (NHEJ). We characterized LINP1 structure and flexibility

179 presses canonical nonhomologous end-joining (NHEJ) and promotes error-prone MMEJ, providing a mechani

180 ting Ku-dependent nonhomologous end-joining (NHEJ) at the expense of homologous recombination.

181 y TDP2-dependent non-homologous end-joining (NHEJ) but whether this promotes or suppresses translocat

182 RADD facilitates non-homologous end-joining (NHEJ) by recruiting NHEJ repair factors 53BP1 and Ku70/8

183 omponents of the non-homologous end-joining (NHEJ) complex and participated in the NHEJ-mediated DNA

184 ion of the XRCC4 non-homologous end-joining (NHEJ) DNA repair gene and p53 efficiently induces brain

185 ption induced by non-homologous end-joining (NHEJ) DNA repair offers a potential treatment option for

186 ting error-prone non-homologous end-joining (NHEJ) DNA repair pathway.

187 component of the non-homologous end-joining (NHEJ) DSB repair pathway.

188 patients affects nonhomologous end-joining (NHEJ) during immunoglobulin class-switch recombination a

189 recombination and nonhomologous end-joining (NHEJ) genes.

190 In humans, nonhomologous DNA end-joining (NHEJ) is the major pathway by which DNA double-strand br

191 Non-homologous end-joining (NHEJ) is the most prominent DNA double strand break (DSB

192 Nonhomologous DNA end-joining (NHEJ) is the predominant double-strand break (DSB) repai

193 coexpression the nonhomologous end-joining (NHEJ) machinery from the closely related archaeon, Metha

194 omponents of the non-homologous end-joining (NHEJ) machinery or of the BRCA1-A complex specifically c

195 e products of the nonhomologous end-joining (NHEJ) pathway and require Top1cc removal from DNA ends.

196 The nonhomologous end-joining (NHEJ) pathway is the primary repair pathway for DNA doub

197 The non homologous end-joining (NHEJ) pathway of double-strand break (DSB) repair often

198 ions (INDELs) by non-homologous end-joining (NHEJ) pathway underlies the mechanistic basis of CRISPR-

199 SB repair via the nonhomologous end-joining (NHEJ) pathway, by filling small sequence gaps in broken

200 nents for the nonhomologous DNA end-joining (NHEJ) pathway.

201 pation of various nonhomologous end-joining (NHEJ) pathways.

202 nation (HR) or by nonhomologous end-joining (NHEJ) pathways.

203 Non-homologous end-joining (NHEJ) plays an important role in double-strand break (DS

204 a core protein of nonhomologous end-joining (NHEJ) repair pathway, can directly interact with DNA pol

205 bination (HR) and nonhomologous end-joining (NHEJ) repair pathways but exclusively for heterochromati

206 bination (HR) and nonhomologous end-joining (NHEJ) repair pathways, with defective localization of Br

207 R) and decreased non-homologous end-joining (NHEJ) repair, suggesting that Wwox contributes to DNA DS

208 combination (HR), nonhomologous end-joining (NHEJ), and microhomology-mediated end-joining (MMEJ).

209 and error-prone non-homologous end-joining (NHEJ), as well as between proximal and distal NHEJ repai

210 (TDP2)-dependent non-homologous end-joining (NHEJ), but whether this process suppresses or promotes T

211 ination (HR) and non-homologous end-joining (NHEJ)-mediated repair.

212 nd DSB repair by non-homologous end-joining (NHEJ).

213 tes to facilitate nonhomologous end-joining (NHEJ).

214 hrough repair by non-homologous end-joining (NHEJ).

215 hways, including non-homologous end-joining (NHEJ).

216 epair via MMEJ or nonhomologous end-joining (NHEJ).

217 Moreover, chromatin recruitment of key NHEJ proteins, including, Ku70, Ku80, DNA-PKcs and XLF w

218 In addition to the key NHEJ synapsis proteins, Ku, X4L4, and XLF, it has been s

219 hich shares structural similarity with known NHEJ factors-XRCC4 and XLF.

220 tion of DNA-PKcs after DNA damage to mediate NHEJ.

221 ect was entirely dependent on 53BP1-mediated NHEJ.

222 re required for Mcl-1 to inhibit Ku-mediated NHEJ.

223 mbination, as effected by Ku70/Ku86-mediated NHEJ.

224 chromatin and shifts DSB repair to mutagenic NHEJ, revealing a backup function of 53BP1 when cNHEJ fa

225 tor, 26 PPIs in DDR pathways (BER, MMR, NER, NHEJ, HR, TLS, and ICL repair) are specifically discusse

226 PAXX is the newest NHEJ factor, which shares structural similarity with kno

227 we report that the efficiency of HR but not NHEJ negatively correlates with nucleosome density.

228 While we predictably observed NHEJ to be the predominant pathway for DSB repair in our

229 nt for L4 and is critical for the ability of NHEJ factors to promote stable pairing of ends.

230 lock, AKT inhibition rescued the activity of NHEJ-DDR proteins in autophagy- and PTEN-deficient cells

231 USP14 inhibition rescued the activity of NHEJ-DDR proteins in autophagy-deficient cells.

232 tic regeneration in vivo via augmentation of NHEJ.

233 Exploiting the bias of NHEJ outcomes towards microhomology mediated events, we

234 and XLF, members of the canonical branch of NHEJ pathway (c-NHEJ).

235 that RECQL4 modulates the pathway choice of NHEJ and HR in a cell cycle-dependent manner.

236 Repair is mediated by a core complex of NHEJ factors that includes a ligase (DNA Ligase IV; L4)

237 een paired sgRNA targets and the efficacy of NHEJ and HDR in repairing the chromosome when excising a

238 at explain genetic and molecular features of NHEJ and V(D)J recombination within cells.

239 ors can alter the efficiency and fidelity of NHEJ.

240 Our results indicate the impairement of NHEJ, as detected by low XLF expression.

241 Inactivation of NHEJ supresses the sensitivity of exo1- cells to PARPi,

242 with Ku-DBi's, consistent with inhibition of NHEJ and activation of homologous recombination to facil

243 Furthermore, drug inhibition of NHEJ in combination with chemo- and radiotherapy has pro

244 of certain cancers, suggesting that loss of NHEJ may be selected in some malignancies and that the d

245 grate recent insights into the mechanisms of NHEJ synapsis with updates on other steps of NHEJ, such

246 tudies have shown that the error patterns of NHEJ are strongly biased by sequence context, but these

247 el negative PTEN/Akt-dependent regulation of NHEJ by USP14.

248 we show that CYREN (cell cycle regulator of NHEJ) is a cell-cycle-specific inhibitor of cNHEJ.

249 e a late ZNF281-dependent regulatory step of NHEJ complex assembly at DNA lesions and suggest additio

250 The most critical step of NHEJ is synapsis, or the juxtaposition of the two DNA en

251 flexibility known to exist at other steps of NHEJ is now also apparent for the NHEJ synapsis step.

252 NHEJ synapsis with updates on other steps of NHEJ, such as DNA end processing and ligation.

253 TdT participates in a specialized version of NHEJ, V(D)J recombination.

254 noncanonical base pairs (3'-rA or 3'-rC) on NHEJ repair intermediates compromise the end joining by

255 leading to DNA repair by gene conversion or NHEJ.

256 ' overhangs without the involvement of other NHEJ proteins.

257 ession resulted in a net increase in HR over NHEJ.

258 l in the non-homologous end-joining pathway (NHEJ) used to detect and repair DNA double-strand breaks

259 t that PAXX is dispensable for physiological NHEJ in otherwise wild-type mice.

260 However, concomitant loss of the pro-NHEJ factors 53BP1, RIF1, REV7-Shieldin (SHLD1-3) or CST

261 RECQL4 interacts with Ku70 to promote NHEJ in G1 when overall cyclin-dependent kinase (CDK) ac

262 lso recruited to DNA damage sites to promote NHEJ.

263 iated clearance from DSBs, thereby promoting NHEJ.

264 nsertion, significantly reducing error-prone NHEJ events at the nuclease cleavage site, while avoidin

265 Using frog egg extracts that recapitulate NHEJ, we show that end processing requires the formation

266 -homologous end-joining (NHEJ) by recruiting NHEJ repair factors 53BP1 and Ku70/80 complex, whereas T

267 based precise genome editing, while reducing NHEJ locally, only at CRISPR-Cas9-induced DSBs.

268 s not directly involved in DNA break repair (NHEJ).

269 of FBXW7 to DNA damage sites for subsequent NHEJ repair.

270 OX, in which Brca1-Wwox interaction supports NHEJ as the dominant DSB repair pathway in Wwox-sufficie

271 hway choice-promoting HDR, while suppressing NHEJ and TLS.

272 These observations demonstrate that NHEJ contributes to p53-mediated glioblastoma suppressio

273 ple sites on introns 11 and 13 and find that NHEJ-mediated insertion of BDDF8 restores hemostasis.

274 l cut site in various genomic loci such that NHEJ in trans led to expression of a LEU2 reporter gene.

275 The NHEJ-dependent mutations included deletions ranging from

276 modulate the bridging of broken ends by the NHEJ core complex.

277 ermini that are critical for ligation by the NHEJ DNA ligase, LigIV.

278 r steps of NHEJ is now also apparent for the NHEJ synapsis step.

279 ining (NHEJ) complex and participated in the NHEJ-mediated DNA repair process.

280 Here, we directly observe the NHEJ synapsis by pol mu using a single molecule FRET (sm

281 mini and thereby improve the affinity of the NHEJ enzymatic components consisting of polymerases (Pol

282 ticipating in the ordered recruitment of the NHEJ repair factor XRCC4 at damage sites.

283 tion of ZNF281 impairs the efficiency of the NHEJ repair pathway and decreases cell viability upon DN

284 s HDR by suppressing the localization of the NHEJ-promoting factor 53BP1 to DSBs.

285 PNKP and LigIV require the NHEJ scaffolding protein, XRCC4.

286 exibility and analyzed interactions with the NHEJ factor Ku70/Ku80 (Ku) and Ku complexes that direct

287 t 3' overhangs, favoring the view that these NHEJ proteins are sequentially rather than concurrently

288 Thus, NHEJ is a single pathway with multiple enzymes at its di

289 he genome but has low efficiency compared to NHEJ, which is lowered even further when trying to creat

290 Similarly, Pol-beta knockdown impairs total-NHEJ capacity but only has a slight influence on alterna

291 (DSBs), allowing some to be subject to toxic NHEJ.

292 n to correlate with repair efficiency, trans NHEJ frequency remained essentially constant regardless

293 orts, cis NHEJ was more efficient than trans NHEJ.

294 surement of relative activity of MMEJ versus NHEJ.

295 rter gene, demonstrating gene disruption via NHEJ in vivo.

296 fferent, Top1-associated DSBs are joined via NHEJ, which results in deletion of the intervening seque

297 promoting error-prone DNA damage repair via NHEJ and suppressing apoptosis of damaged cells, our res

298 ly interact with the Ku and inhibit in vitro NHEJ, cellular NHEJ, and potentiate the cellular activit

299 ckout cells were sensitive to apoptosis with NHEJ inhibition.

300 egulate PNKP recruitment and activity within NHEJ.