ライフサイエンスコーパス: repair pathway

1 Fanconi anemia (FA) double-strand break DNA repair pathway.

2 ajor mammalian DNA double-strand break (DSB) repair pathway.

3 he potentially mutagenic double-strand break repair pathway.

4 ole in DNA repair in the nucleotide excision repair pathway.

5 ponents of the zebularine-induced DNA damage repair pathway.

6 herapeutic approaches targeting the mismatch repair pathway.

7 d 11 strains, each defective for a major DNA repair pathway.

8 ex that forms part of the Fanconi anemia DNA repair pathway.

9 ), and BRCA1 is an important factor for this repair pathway.

10 ing on the DNA double-strand break (DSB) and repair pathway.

11 p in preparing for DSB repair via the HR DNA repair pathway.

12 is a potential therapeutic target in the DNA repair pathway.

13 he molecular defect in FA is an impaired DNA repair pathway.

14 viding key insight into the conserved FA DNA repair pathway.

15 NHEJ), a major DNA double-strand break (DSB) repair pathway.

16 by increased expression of genes in the DNA repair pathway.

17 DNA damage is repaired by the base excision repair pathway.

18 en indirect, and usually limited to a single repair pathway.

19 osylase 1 (OGG1)-initiated DNA base excision repair pathway.

20 Our study provides insights into this repair pathway.

21 repair of DNA lesions via the base excision repair pathway.

22 totoxic but are removed by the base excision repair pathway.

23 machinery and the mitoNEET cluster transfer repair pathway.

24 as EHMT1) are critical components of the DNA repair pathway.

25 ral oncogenes were shown to disrupt this DSB repair pathway.

26 the error-free homologous recombination (HR) repair pathway.

27 coli lines, each deficient in a distinct DNA repair pathway.

28 of how PARP-2 is specialized toward specific repair pathways.

29 s a critical role in multiple eukaryotic DNA repair pathways.

30 ine/receptor pair in acute intestinal injury/repair pathways.

31 DCAF1) E3 to remove key enzymes in three DNA repair pathways.

32 ency is counteracted by multiple complex DNA repair pathways.

33 r their collective work on the different DNA repair pathways.

34 talling and checkpoint signaling to activate repair pathways.

35 DNA lesions and influencing their subsequent repair pathways.

36 ni anemia (FA), and homologous recombination repair pathways.

37 roles for Akt3, consisting primarily of DNA repair pathways.

38 istry for their seminal work in defining DNA repair pathways.

39 articipates in early steps of particular DNA repair pathways.

40 logous end joining (NHEJ), the two major DSB repair pathways.

41 endonucleases, is important for several DNA repair pathways.

42 been demonstrated for several organisms and repair pathways.

43 ated with the local activation of DNA-damage repair pathways.

44 ing competition with non-crossover promoting repair pathways.

45 members of the PI3-kinase and homologous DNA repair pathways.

46 at the UBP is not efficiently excised by DNA repair pathways.

47 strand break repair, and nucleotide excision repair pathways.

48 s consistent with each functioning in unique repair pathways.

49 endent PARPs and their specific roles in DNA repair pathways.

50 s and form protein complexes that act in DNA repair pathways.

51 ficantly altered immune reactivation and DNA repair pathways.

52 ted genes are enriched in cell cycle and DNA repair pathways.

53 y and cisplatin by regulating DNA damage and repair pathways.

54 changes to DNA by activation of various DNA repair pathways.

55 defects in the Fanconi anemia (FA)/BRCA DNA repair pathway, (2) defects in telomere maintenance, and

56 Conversely, inhibiting the base excision repair pathway accentuated NAD decline in response to GM

57 s homologous recombination (HR)-mediated DNA repair pathway activity of samples.

58 ter regulator of the double strand DNA break-repair pathway after genotoxic stress.

59 ovide a targeted approach to enhance mucosal repair pathways after colitis.

60 ication, pathogen-response and mitochondrial-repair pathways after inhibition of mitochondrial functi

61 n repair, as well as virtually all other DNA repair pathways, alleviated smc6 mutant's hypersensitivi

62 red DSB-clusters, compromises first-line DSB-repair pathways, allowing alt-EJ to function as rescuing

63 Mutations in CCND1 and DNA repair pathway alterations (TP53, ATM, ATR, and ZNFHX4 m

64 ovel role for FEN1 in a specialized mismatch repair pathway and a new cancer etiological mechanism.

65 tes the activation of the Fanconi anemia DNA repair pathway and facilitates replication traverse of D

66 conjugating enzyme of the Fanconi anemia DNA repair pathway and it is overexpressed in several cancer

67 uncovered association between the DNA damage repair pathway and pathological angiogenesis could open

68 al role in the nonhomologous end-joining DNA repair pathway and provides prosurvival signaling during

69 ein required for the nucleotide excision DNA repair pathway and represents a therapeutic target in on

70 provides a global analysis of an entire DNA repair pathway and reveals the mechanism of SMC5/6 reloc

71 velopmental fate and cell cycle and mismatch repair pathways and altered activities of key upstream r

72 ucleosome assembly without involving the DNA repair pathways and exerts its effect via suppression of

73 ition of G9a catalytic activity disrupts DNA repair pathways and increases sensitivity to ionizing ra

74 amage and apoptosis, induction of DNA damage repair pathways and ROS detoxification systems, cellular

75 L2 layer cells express genes involved in DNA repair pathways and telomere maintenance, and the L3 lay

76 association between DNA damage-response and repair pathways and the age at onset of disease.

77 CC2 is indispensable for nucleotide excision repair pathway, and its functional polymorphisms may be

78 c inhibitor kinase, regulates the DNA damage repair pathway, and therapeutic inhibition of WEE1 in co

79 embly checkpoint, numerous DNA recombination/repair pathways, and the initiation of autophagy.

80 een age at onset and genetic variants in DNA repair pathways, and we therefore tested whether the mod

81 PK) and the nonhomologous end joining (NHEJ) repair pathway are intrinsically antiviral and that ICP0

82 DNA repair pathways are aberrant in cancer, enabling tumor c

83 The results suggest that repair pathways are activated differently in alpha- comp

84 Multiple DNA double-strand break (DSB) repair pathways are active in S phase of the cell cycle;

85 Small-molecule inhibitors of DNA repair pathways are being intensively investigated as pr

86 Alterations in DNA repair pathways are common in tumors and can result in c

87 Efficient DNA repair pathways are crucial in these organelles to fix d

88 n by mtp53 suggests that DNA replication and repair pathways are major targets of mtp53 and highlight

89 lar mechanism and role relative to canonical repair pathways are poorly understood.

90 However, how these repair pathways are regulated and interconnected is stil

91 We show that PARP-mediated repair pathways are upregulated in prostate cancer follo

92 These results demonstrate that several DSB repair pathways are used during rereplication in the fol

93 ch are involved in multiple conventional DNA repair pathways, are frequently altered in cancer.

94 homeostasis network and nucleotide excision repair pathway, as a modifier of the toxicity of two dis

95 It typically does not compete with canonical repair pathways but, in NHEJ-deficient cells, is engaged

96 ciently repaired via the single-strand break repair pathway, but relatively little is known about the

97 (MRN) and Ku70-Ku80 (Ku) direct distinct DSB repair pathways, but the interplay between these complex

98 Vpr also interferes with the base-excision repair pathway by antagonizing the uracil DNA glycosylas

99 hat HIV-1 Vpr targets the Fanconi anemia DNA repair pathway by interacting with and activating an end

100 ycosylases, which initiate the base excision repair pathway by locating and excising aberrant nucleob

101 ercept the more error-prone alternative NHEJ repair pathway by recruiting Ku and associated NHEJ fact

102 eregulation of the cell cycle and DNA damage repair pathways by modulating transcription factors p53

103 thymidine kinase contributes to several DNA repair pathways by providing deoxythymidine triphosphate

104 gements (LST), and the status of several DNA repair pathways by transcriptome and genome analysis.

105 d by the classical nonhomologous end-joining repair pathway (c-NHEJ), regenerating the target site.

106 on the mycobacterial chromosome, that other repair pathways can compensate for the loss of NHEJ and

107 s illustrate that specific rereplication DSB repair pathways can have major effects on cellular physi

108 e mediated by either of two end-joining (EJ) repair pathways [canonical nonhomologous end joining (C-

109 (TNR) expansion, yet how these two different repair pathways cause the mutation is unknown.

110 l4 ligase activity, and has implications for repair pathway choice and resection regulation upon DSB

111 oreover, relative DSB order controls the DSB repair pathway choice and, ultimately, recombination out

112 t functions of CSB in regulating the DNA DSB repair pathway choice as well as G2/M checkpoint activat

113 With these inhibitors, we examined repair pathway choice at DSBs generated in G2 following

114 rolysis primes the MR function and regulates repair pathway choice in cells.

115 53BP1 is a key regulator of DSB repair pathway choice in eukaryotic cells and functions

116 histone H3K36 modification in regulating DSB repair pathway choice in fission yeast.

117 in S phase and providing a mechanism of DSB repair pathway choice in mammalian cells.

118 This detailed characterization of repair pathway choice in response to CRISPR-Cas9 enables

119 functions as a regulatory mechanism for DNA repair pathway choice in the context of cell cycle progr

120 ts, revealing an important role of DNA break repair pathway choice in the preservation of genome inte

121 rating that the V(D)J recombinase influences repair pathway choice in vivo.

122 hosphorylation status of NBS1 determines the repair pathway choice of dysfunctional telomeres.

123 horylation status of the NBS1(S432) dictates repair pathway choice of dysfunctional telomeres.

124 MT5-mediated arginine methylation during DSB repair pathway choice through its ability to regulate ac

125 udy uncovers a critical role for Ape1 in DNA repair pathway choice, and provides a mechanistic unders

126 tablishes CEP-1 as a critical determinant of repair pathway choice.

127 3BP1's regulation of DNA double-strand break repair pathway choice.

128 modelling during resection is underlying DSB repair pathway choice.

129 an H3K36 chromatin switch in regulating DSB repair pathway choice.

130 EXO1 by CDKs is a novel mechanism regulating repair pathway choice.

131 suggesting that Wwox contributes to DNA DSB repair pathway choice.

132 ory mechanism for ATM that also controls DNA repair pathway choice.

133 t a ubiquitylation cascade that controls DNA repair pathway choice.

134 critical determinant of double-strand break repair pathway choice.

135 by ACLY participates in the mechanism of DNA repair pathway choice.

136 nt with p97-driven Ku release also affecting repair pathway choice.

137 am of 53BP1 in coordinating pathological DSB repair pathway choices in BRCA1-deficient cells.

138 lication-dependent DNA interstrand crosslink repair pathway commonly referred to as the Fanconi anemi

139 ession is influenced by genomic position and repair pathway competition.

140 ted proficiency of the homology-directed DNA repair pathway constrain gene targeting in human HSCs.

141 hogenesis, we have identified that the wound repair pathway, controlled by the epidermal growth facto

142 in the DNA damage response and in HR, a DNA repair pathway critical for tumor suppression.

143 Therapeutic strategies targeting DNA repair pathway defects have been widely explored, but of

144 r genes in the DNA double-strand break (DSB) repair pathway disrupt binding of the encoded proteins,

145 eletion of TPA1 along with the base excision repair pathway DNA glycosylase MAG1 renders the tpa1Delt

146 ls towards error-prone instead of error-free repair pathways, dramatically increasing the frequency o

147 this system to test the roles of several DSB repair pathways during rereplication, using fork progres

148 nding of the nature of these lesions and the repair pathways engaged is critical to realizing the ful

149 ing from each Cas9 variant and the resulting repair pathway engagement.

150 ts a specialized DNA replication-coupled DPC repair pathway essential for DNA replication progression

151 Targeting the PARP DNA repair pathway extensively sensitized IDH1-mutated gliom

152 tify a member of the Fanconi anemia (FA) DNA repair pathway, FANCI, as a key effector of dormant orig

153 ter interfering and noninterfering crossover repair pathways (fancm and zip4) to demonstrate that rem

154 understanding the contribution of different repair pathways following the introduction of a targeted

155 define the specificity of the base excision repair pathway for discreet, detrimental modifications,

156 us end-joining (NHEJ) pathway is the primary repair pathway for DNA double strand breaks (DSBs) in hu

157 on-homologous end joining (NHEJ) is the main repair pathway for DNA double-strand breaks (DSBs) in ce

158 Nonhomologous end-joining (NHEJ) is a major repair pathway for DNA double-strand breaks (DSBs), invo

159 g non-homologous end joining (NHEJ), a major repair pathway for DNA double-strand breaks (DSBs).

160 epair (NER) is a conserved and versatile DNA repair pathway for many DNA-distorting lesions, includin

161 The key event in the choice of repair pathways for DNA double-strand breaks (DSBs) is t

162 pair processes, the requirement of known DNA repair pathways for integration is controversial.

163 Alternative repair pathways for Top1cc involve endonuclease cleavage

164 excision repair (BER) is one of several DNA repair pathways found in all three domains of life.

165 nt of embryos lacking the Fanconi anemia DNA repair pathway gene Fanca.

166 Mutations in other DSB repair pathway genes produce molecular phenocopies.

167 wed that COH29 reduces the expression of DNA repair pathway genes, suggesting that COH29 interferes w

168 rther, we provide evidence that the mismatch repair pathway has a role in regulating beta-catenin act

169 In eukaryotes, DNA repair pathways help to maintain genome integrity and ep

170 switch between DNA double-strand break (DSB) repair pathways, how SIRTs play a central role in the cr

171 processed by proteins from a variety of DNA repair pathways; however, a clear understanding of ICL r

172 alk between glutamine metabolism and the DNA repair pathway identified in this study highlights a pot

173 ion to gene expression in ovarian cancer DNA repair pathways illustrates how the model may be used to

174 ing (the predominant DNA double-strand break repair pathway in higher eukaryotes) and is stimulated b

175 most prominent DNA double strand break (DSB) repair pathway in mammalian cells.

176 ) is the major DNA double-strand break (DSB) repair pathway in mammals and resolves the DSBs generate

177 ization of components of a potential NAD(P)H repair pathway in plants comprising a stereospecific deh

178 sistent with activation of a GRHL3-regulated repair pathway in psoriasis, we found that GRHL3 is upre

179 nteraction supports NHEJ as the dominant DSB repair pathway in Wwox-sufficient cells.

180 (PCNA) plays a vital role in a number of DNA repair pathways in eukaryotes and archaea by acting as a

181 mage sensing, cell cycle progression and DNA repair pathways in eukaryotic cells.

182 e of the major DNA double-strand break (DSB) repair pathways in mammalian cells.

183 gain insight into the role of different DNA repair pathways in resolving nuclease-induced DNA breaks

184 (Cdh1) plays a critical role in choosing the repair pathways in S/G2 cells.

185 ces and types of DNA damage and the relevant repair pathways in the nervous system (summarized in Fig

186 s, the role of downstream AID-associated DNA repair pathways in the pathogenesis of lymphoma is unkno

187 tigations about the involvement of other DNA repair pathways in the removal of these lesions and for

188 d convergence between Wnt signalling and DNA repair pathways in tumorigenesis and tissue regeneration

189 aintenance and DNA double strand break (DSB) repair pathways including RAD51-mediated homologous reco

190 MRE11/RAD50/NBS1 (MRN) complex mediates DNA repair pathways, including double-strand breaks induced

191 d crosslinks requires action of multiple DNA repair pathways, including homologous recombination.

192 hance activities of members of different DNA repair pathways, including NEIL1 DNA glycosylase, which

193 etition from other double-strand break (DSB) repair pathways, including non-homologous end-joining (N

194 Not all DNA repair pathways, including the DNA mismatch repair (MMR)

195 uired for the non-homologous end joining DNA repair pathway, increases the efficiency of gene targeti

196 are repaired by the multi-step base excision repair pathway initiated by human alkyladenine glycosyla

197 se excision repair (BER) is an essential DNA repair pathway involved in the maintenance of genome sta

198 Other DNA repair pathways involving ATM and DNA-PKcs are unaffecte

199 bility to dysregulate the Fanconi anemia DNA repair pathway is an essential function of Vpr in vivo.

200 in vivo and a robust ribonucleotide excision repair pathway is critical to keeping incorporation leve

201 ysregulate members of the Fanconi anemia DNA repair pathway is essential for HIV/SIV replication in v

202 The Fanconi Anemia (FA) DNA repair pathway is essential for the recognition and repa

203 at the strand specificity of the accelerated repair pathway is independent of the requirement for a l

204 The Fanconi anemia DNA repair pathway is pivotal for the efficient repair of DN

205 repair of DSB, the choice of the appropriate repair pathway is pivotal.

206 The DNA base excision repair pathway is the main system involved in the remova

207 This error-prone repair pathway is triggered upon telomere de-protection

208 One of the major DSBs repair pathways is nonhomologous end joining for which K

209 otential crosstalk between metabolic and DNA repair pathways is poorly understood.

210 Errors in this DNA repair pathway lead to genomic instability and cancer pr

211 Our results identify a DNA repair pathway leading from MK2 and ATM to ATDC, suggest

212 inappropriate activity of these alternative repair pathways, leading to chromosome mis-segregation.

213 ce with a non-functional Fanconi anaemia DNA repair pathway, led to a complete collapse of the haemat

214 Multiple DNA repair pathways maintain genome stability and ensure tha

215 es, proteins of the homologous recombination repair pathway may be considered essential, since gemini

216 ells, suggesting that repression of the NHEJ repair pathway may be involved in COH29-induced DSBs in

217 strategies relying on the homology-directed repair pathway may repair genetic defects, whereas genet

218 plication in normally growing cells and that repair pathways may exist primarily to defend against ex

219 ated) nonhomologous end-joining, whereas DNA repair pathways mediated by poly(ADP)ribose polymerase 1

220 signature, higher neoantigen burden, and DNA repair pathway mutations; each factor was also associate

221 Despite the major importance of this repair pathway, MutS-MutL are absent in almost all Actin

222 Thomson Syndrome, promotes the two major DSB repair pathways, non-homologous end joining (NHEJ) and h

223 reas its involvement in the second major DSB repair pathway, nonhomologous end-joining (NHEJ), remain

224 The choice between two main DSB repair pathways, nonhomologous end-joining (NHEJ) and ho

225 ecting the balance between the two major DSB repair pathways-nonhomologous end-joining and homologous

226 genetic interaction of Ubp7 with DNA damage repair pathways of homologous recombination and nucleoti

227 xoguanine (8-oxoG) via the DNA base excision repair pathway (OGG1-BER).

228 Tumor cells compromised in DNA repair pathways or DNA damage checkpoints, cells reliant

229 ations arise either from inactivation of DNA repair pathways or in a repair-competent background due

230 as clearly a result of the base excision DNA repair pathway: oxidative Polbeta-DPC depended on the Ap

231 des presynaptic stimulation of the bacterial repair pathway perhaps by contributing to the RecA homol

232 The homologous recombination (HR) DNA repair pathway plays a major role in repairing DSBs indu

233 r previous findings that the recombinational repair pathway plays a minor role in M. genitalium.

234 ficiencies in certain key components of this repair pathway predominantly exhibiting growth deficits,

235 competition with the noncrossover-promoting repair pathways, prevents loss of heterozygosity.

236 DNA damage and repair pathway profiling revealed patient-level variatio

237 ion factors at DSBs, providing insights into repair pathway regulation.

238 The nucleotide excision repair pathway removes ultraviolet (UV) photoproducts fr

239 The major DNA repair pathway removing DNA lesions caused by exposure t

240 ing the nonhomologous end-joining (NHEJ) DNA repair pathway result in radiation-sensitive severe comb

241 to elucidate how loss of the 53BP1-dependent repair pathway results in PARPi resistance in BRCA1 pati

242 complex is directly involved in an excision repair pathway(s) that repairs DNA damage with ribonucle

243 that ruxolitinib-induced deficiencies in DSB repair pathways sensitized MPN cells to synthetic lethal

244 ation stress (DRS), making them dependent on repair pathways such as break-induced replication (BIR)

245 We propose that errors in DNA repair pathways, such as non-homologous end joining and

246 pho-H2AX and strong impairment of DNA damage repair pathways, suggesting a key role for TET proteins

247 ng therapeutic agents via utilization of DNA repair pathways, suggesting that DNA repair capacity (DR

248 cer predisposition to the Fanconi anemia DNA repair pathway, supporting the connection between genome

249 tify an undescribed function of WRN as a DSB repair pathway switch.

250 branch of the DNA damage nucleotide excision repair pathway, termed transcription-coupled repair (TCR

251 ogous end joining (NHEJ), an alternative DNA repair pathway that competes with homology-directed repa

252 ons in the homologous recombination (HR) DNA repair pathway that confer sensitivity to both drugs.

253 , we describe here a replication-coupled ICL repair pathway that does not require incisions or FANCI-

254 the ataxia telangiectasia mutated (ATM) DNA repair pathway that in normal cells acts to repair doubl

255 This occurred via a mutagenic DNA repair pathway that included DNA double-strand break rep

256 ng (NHEJ) is a major DNA double-strand break repair pathway that is conserved in eukaryotes.

257 nconi anemia/BRCA (FA/BRCA) pathway is a DNA repair pathway that is required for excision of DNA inte

258 plication (BIR) is a DNA double-strand break repair pathway that leads to genomic instabilities simil

259 ta underscore a unique replication-dependent repair pathway that leads to the mitochondrial common de

260 gous recombination (HR) is a template-driven repair pathway that mends DNA double-stranded breaks (DS

261 tion (HR) is a DNA double-strand break (DSB) repair pathway that protects the genome from chromosomal

262 entifies a GRHL3-regulated epidermal barrier repair pathway that suppresses disease initiation and he

263 ing (SSA) is a DNA double-strand break (DSB) repair pathway that uses homologous repeats to bridge DS

264 telomeres, underlining the complexity of DNA repair pathways that act at chromosome ends lacking prot

265 ed downregulation of genes within DNA damage repair pathways that are controlled by MOF, as correlate

266 By demonstrating specific metabolic and repair pathways that are differentially activated in liv

267 ous end joining (NHEJ) are the two major DSB repair pathways that are highly conserved from yeast to

268 e stability is carried out by a suite of DNA repair pathways that ensure the repair of damaged DNA an

269 clei and LST and specific alterations in DNA repair pathways that essentially monitor DSB repair defe

270 n-coupled DNA repair (TCR) are among the DNA repair pathways that evolved to maintain genome integrit

271 A breaks may engage one of several competing repair pathways that lead to distinct types of genomic a

272 age and is essential for invigorating tissue repair pathways that may help prevent tumorigenesis.

273 e poorly understood, as are the specific DNA repair pathways that protect these cells.

274 Specifically, we show that the base excision repair pathway, the main pathway utilized for the repair

275 ase involved in initiating the base excision repair pathway, the major cellular mechanism for repairi

276 s an adverse effect on the DNA base excision repair pathway, the major DNA repair system that deals w

277 ubset of EOC with alterations in another DNA repair pathway, the nucleotide excision repair (NER) pat

278 al components of the Fanconi anemia (FA) DNA repair pathway, the tumor suppressor proteins FANCI and

279 14s work redundantly in DNA repair and which repair pathways they participate in.

280 croRNAs (miRNAs) have been implicated in DNA repair pathways through transcriptional responses to DNA

281 is the predominant double-strand break (DSB) repair pathway throughout the cell cycle and accounts fo

282 DNA glycosylases found in the base excision repair pathway to excise the modification.

283 or doxorubicin, acting upstream of different repair pathways to block histone polyADP-ribosylation (P

284 property will make it difficult for the DNA repair pathways to detect this adduct.

285 cells (PSCs) are presumed to have robust DNA repair pathways to ensure genome stability.

286 hether Poltheta interacts with canonical DNA repair pathways to prevent genomic instability remains u

287 The cellular DNA repair pathway, translesion synthesis (TLS), is disrupte

288 s, we reasoned that rLOX-PP could target DNA repair pathways typically elevated in cancer.

289 with endogenous angiotensin-(1-7) promoting repair pathways via interaction with Mas and higher amou

290 The PARP1-associated DNA repair pathway was extensively compromised in mutant cel

291 st, those encoding antioxidants and cellular repair pathways were unchanged.

292 ded: (1) The genes involved in "DNA mismatch repair" pathway were up-regulated in HPV-positive tumors

293 changes in the regulation of six DNA damage repair pathways, were employed.

294 s a component of the Fanconi anemia (FA) DNA repair pathway, which is frequently found defective in h

295 generated following DNA-damage also activate repair pathways, which can help prevent tumor developmen

296 Of particular importance are the repair pathways, which respond to DNA double-strand brea

297 has been excised by the nucleotide excision repair pathway, while others participate in trans-lesion

298 these mutations in double-strand-break (DSB) repair pathways with earlier observations in correspondi

299 on (HR) and nonhomologous end-joining (NHEJ) repair pathways, with defective localization of Brca1 an

300 ed if inhibiting the ribonucleotide excision repair pathway would exacerbate the smc6 mutant in respo