ライフサイエンスコーパス: mismatch repair

1 a ATPase, and MutLalpha function in in vitro mismatch repair.

2 mutations are found in tumors with defective mismatch repair.

3 thway regulating DNA damage response and DNA mismatch repair.

4 diffusion mechanics along the DNA to direct mismatch repair.

5 cer diagnostic for detecting deficiencies in mismatch repair.

6 two components: polymerase proofreading and mismatch repair.

7 ions, including directing the orientation of mismatch repair.

8 of Exo1 is required for its participation in mismatch repair.

9 tiation of chromosome replication or for DNA mismatch repair.

10 ersion, possibly associated with error-prone mismatch repair.

11 lving recombination intermediates and in DNA mismatch repair.

12 er tumors showed hallmarks of defects in DNA mismatch repair.

13 in vitro and in vivo, while also eliminating mismatch repair.

14 ded DNA gaps and/or involve Mlh1-independent mismatch repair.

15 iming, nucleosome occupancy or deficiency in mismatch repair.

16 quences in the genome caused by impaired DNA mismatch repair.

17 ll lines that are proficient or deficient in mismatch repair.

18 to inflammation, ErbB signalling pathway and mismatch repair.

19 e (nucleotide selectivity and proofreading), mismatch repair, a balanced supply of nucleotides, and t

20 A-damaging agents and decreases cellular DNA mismatch repair activities by downregulation of MSH2.

21 n Escherichia coli, but completely abrogates mismatch repair activity in Bacillus subtilis.

22 on, knockdown of MSH2 decreases the cellular mismatch repair activity.

23 cer (CRC) has been linked to deficiencies in mismatch repair and adenomatous polyposis coli (APC) pro

24 l cell functions, including gene expression, mismatch repair and chromosome replication.

25 We visualized Escherichia coli (Ec) ensemble mismatch repair and confirmed that EcMutS mismatch recog

26 , as defined by signatures for defective DNA mismatch repair and DNA polymerase epsilon proofreading

27 tion in DNA homologous recombination and DNA mismatch repair and is also heavily utilized in DNA-base

28 (MSH) and MutL (MLH/PMS) homologues initiate mismatch repair and, in higher eukaryotes, act as DNA da

29 es: age related, double-strand break repair, mismatch repair, and 1 with unknown etiology (signature

30 resulting conversion tracts are affected by mismatch repair - are not well understood.

31 1-PMS1 in yeast) functions in early steps of mismatch repair as a latent endonuclease that requires a

32 lowing pathways: nucleotide excision repair, mismatch repair, base excision repair, nonhomologous end

33 9 in the PETACC-8 phase III randomized trial.Mismatch repair, BRAF V600E, and KRAS exon 2 mutational

34 uvant setting will have to take into account mismatch repair, BRAF, and KRAS status for stratificatio

35 widespread in bacteria and functions in DNA mismatch repair, chromosome segregation, and virulence r

36 sistent with the hypothesis of Mlh1-Mlh3 DNA mismatch repair complex acting as the major endonuclease

37 g to investigate how Msh2-Msh3, a eukaryotic mismatch repair complex, navigates on crowded DNA.

38 Imaging of nucleosomes and DNA mismatch repair complexes demonstrates that DREEM can re

39 characterized by a nonsense mutation in the mismatch repair component MSH2.

40 The genomes of cancers deficient in mismatch repair contain exceptionally high numbers of so

41 otide repeats (EMAST) is the most common DNA mismatch repair defect in colorectal cancers, observed i

42 nstrate that a mutator phenotype caused by a mismatch repair defect is prevalent in C. glabrata clini

43 an innovative therapeutic regime for certain mismatch-repair-defective cancers that are refractory to

44 ry nonpolyposis colorectal carcinoma with no mismatch repair defects.

45 h a large number of somatic mutations due to mismatch-repair defects may be susceptible to immune che

46 Biallelic mismatch repair deficiency (bMMRD) is a highly penetrant

47 priate management of patients with biallelic mismatch repair deficiency (BMMRD) syndrome, also called

48 nomes from children with inherited biallelic mismatch repair deficiency (bMMRD).

49 DNA mismatch repair deficiency (dMMR) hallmarks consensus mo

50 ared prevalence of proximal location and DNA mismatch repair deficiency (dMMR) in CRC tumors, relativ

51 Microsatellite instability (MSI) caused by mismatch repair deficiency (dMMR) is detected in a small

52 al cancers, and were mutually exclusive with mismatch repair deficiency (MMR-D) in the 6277 cases for

53 al processes associated with APOBEC enzymes, mismatch repair deficiency and homologous recombinationa

54 mily histories and testing of tumors for DNA mismatch repair deficiency and/or microsatellite instabi

55 he interaction between microbiota, diet, and mismatch repair deficiency in CRC induction.

56 feature in patients with constitutional DNA-mismatch repair deficiency is agenesis of the corpus cal

57 Therefore, assessing the general impact of mismatch repair deficiency on the likelihood of mutation

58 from mutation carriers demonstrating the DNA mismatch repair deficiency phenotype.

59 (BMMRD) syndrome, also called constitutional mismatch repair deficiency syndrome.

60 Mismatch repair deficiency was identified in 1% of tumor

61 eviously showed that colorectal cancers with mismatch repair deficiency were sensitive to immune chec

62 enomatous polyposis, two with constitutional mismatch repair deficiency, two with biallelic MUTYH mut

63 cal disorders in patients with inherited DNA-mismatch repair deficiency.

64 to more UNG-dependent deletions, enhanced by mismatch repair deficiency.

65 10%) had tumors with histologic evidence for mismatch repair deficiency.

66 Two tumors had hypermutation consistent with mismatch repair deficiency.

67 ressive metastatic carcinoma with or without mismatch-repair deficiency.

68 mline mutations, representing constitutional mismatch-repair deficiency.

69 e-hundred and thirty-two (11.2%) tumours are mismatch repair deficient per immunohistochemistry.

70 Metastatic DNA mismatch repair-deficient (dMMR)/microsatellite instabil

71 ulting distributions of conversion tracts in mismatch repair-deficient and mismatch repair-proficient

72 ir subsequent transformation to AML in a DNA mismatch repair-deficient background.

73 y of PD-1 blockade in patients with advanced mismatch repair-deficient cancers across 12 different tu

74 ect sensitivity and specificity in detecting mismatch repair-deficient cancers in two independent pop

75 he large proportion of mutant neoantigens in mismatch repair-deficient cancers make them sensitive to

76 icient colorectal cancers, and patients with mismatch repair-deficient cancers that were not colorect

77 responses similar to those of patients with mismatch repair-deficient colorectal cancer (immune-rela

78 survival were not reached in the cohort with mismatch repair-deficient colorectal cancer but were 2.2

79 and 78% (7 of 9 patients), respectively, for mismatch repair-deficient colorectal cancers and 0% (0 o

80 f body weight every 14 days in patients with mismatch repair-deficient colorectal cancers, patients w

81 ely models the mutation profiles observed in mismatch repair-deficient colorectal cancers.

82 s that accumulate in the nuclear genome of a mismatch repair-deficient diploid yeast strain with elev

83 Patients with mismatch repair-deficient noncolorectal cancer had respo

84 mean of 1782 somatic mutations per tumor in mismatch repair-deficient tumors, as compared with 73 in

85 have been modest, except in neoantigen-laden mismatch repair-deficient tumors.

86 Kan and colleagues utilized mismatch repair detection (MRD) technology to identify s

87 n dNTP pools in combination with inactivated mismatch repair dramatically increase mutation rates.

88 Further, error rates and DNA mismatch repair efficiency both vary by mismatch type, r

89 (EXO1 - exonuclease 1) to be involved in DNA mismatch repair emerged as candidate susceptibility gene

90 show that overexpression of catalase or DNA mismatch repair enzyme, MutS, and antioxidant pretreatme

91 The EcMutH endonuclease that targets mismatch repair excision only binds clamped EcMutL, incr

92 ive endonuclease activity encoded by the DNA mismatch repair factor Mlh1-Mlh3.

93 d by the uracil-DNA glycosylase (UNG) or the mismatch repair factor MSH2/MSH6, must process the deoxy

94 ezomib partially restored protein levels and mismatch repair function for low-level variants and reve

95 ted regulatory mechanism controlling the DNA mismatch repair function of MSH2.

96 erstood compared with other Lynch-associated mismatch repair gene (MMR) mutations.

97 ckpoint inhibitor-based regimen because of a mismatch repair gene anomaly are presented.

98 By targeting the DNA mismatch repair gene MLH1 CGI, we could generate a PSC m

99 n accumulation in organoids deficient in the mismatch repair gene MLH1 is driven by replication error

100 ypermethylation of many genes, including the mismatch repair gene MLH1.

101 Strains carrying alterations in mismatch repair gene MSH2 exhibit a higher propensity to

102 was detected for a variant rs1800932 in the mismatch repair gene MSH6 (P = 1.9 x 10(-9)), which was

103 ing endometrial cancer risk for women with a mismatch repair gene mutation (Lynch syndrome).

104 tive cohort study included 1128 women with a mismatch repair gene mutation identified from the Colon

105 ed, these findings suggest that women with a mismatch repair gene mutation may be counseled like the

106 For women with a mismatch repair gene mutation, some endogenous and exoge

107 ated, and that all hypermutated cancers have mismatch repair gene mutations and microsatellite instab

108 Moreover, recent research suggests that DNA mismatch repair gene mutations may facilitate acquisitio

109 g S. Enteritidis harboured a mutation in the mismatch repair gene mutS that accelerated the genomic m

110 ng S. Enteritidis harbored a mutation in the mismatch repair gene mutS that accelerated the genomic m

111 Seventeen EOC cases carried a mutation in a mismatch repair gene, including 10 MSH6 mutation carrier

112 -of-function (LoF) germline mutations in the mismatch-repair gene MSH3.

113 Mutations in mismatch repair genes (EXO1, MSH2, and MSH6) were associ

114 that is caused by pathogenic variants in the mismatch repair genes (MLH1, MSH2, MSH6, PMS2, EPCAM).

115 identification of germline mutations in DNA mismatch repair genes (n = 47) or biallelic MUTYH mutati

116 in base-excision (P = 2.4 x 10(-4)) and DNA mismatch repair genes (P = 6.1 x 10(-4)) consistent with

117 Defects in human mismatch repair genes cause Lynch syndrome or hereditary

118 ereditary breast and ovarian cancer, and DNA mismatch repair genes for suspected Lynch syndrome.

119 rre syndrome showed loss of staining for the mismatch repair genes MSH2 and MSH6.

120 xa is not commonly associated with a loss of mismatch repair genes or microsatellite instability.

121 somatic mutations in the DNA proofreading or mismatch repair genes POLE, MLH1, and MSH6 and the tumor

122 yndrome, caused by germline mutations in the mismatch repair genes, is associated with increased canc

123 rcinomas maintained strong staining of the 4 mismatch repair genes, while tumor from the patient with

124 ype that harboured inactivating mutations in mismatch repair genes.

125 cluding tumor suppressor, mitochondrial, and mismatch repair genes.

126 somatic hypermethylation or mutations in the mismatch repair genes.

127 (n = 98), and 8 (0.4%) had mutations in DNA mismatch repair genes.

128 and NBN MRN complex genes; the MLH1 and PMS2 mismatch repair genes; and NF1 were not associated with

129 BRCA2, ATM, PALB2, BRCA1, STK11, CDKN2A and mismatch-repair genes and low-penetrance loci are associ

130 ses harbored unique somatic mutations in MLH mismatch-repair genes.

131 Paradoxically, mutagenic action of mismatch repair has been implicated as a cause of triple

132 n of tumor stroma obscured signatures of DNA mismatch repair identified in cell lines with a hypermut

133 including microsatellite instability and DNA mismatch repair immunohistochemistry results.

134 tion errors are corrected by strand-directed mismatch repair in Escherichia coli and human cells.

135 ATRA-induced differentiation were related to mismatch repair in eukaryotes, DNA double-strand break r

136 tSbeta- and MutLalpha-endonuclease-dependent mismatch repair in nuclear extracts of human cells.

137 Here we show that the efficiency of mismatch repair in Saccharomyces cerevisiae is reduced b

138 er only weak mutator phenotypes, inactivates mismatch repair in the yeast cell.

139 ficity of Msh2-Msh3- and Msh2-Msh6-dependent mismatch repair in vivo.

140 t PMS1 motif ((723)QKLIIP) reduce or abolish mismatch repair in vivo.

141 ned with defects in Poldelta proofreading or mismatch repair, indicating that pathways correcting DNA

142 view summarizes the current knowledge of DNA mismatch repair involvement in triplet repeat expansion,

143 DNA mismatch repair is a conserved antimutagenic pathway tha

144 postreplication errors and initiation of the mismatch repair is carried out by two MutS homologs: Mut

145 ls in whom biallelic germline deficiency for mismatch repair is compounded by somatic loss of functio

146 DNA mismatch repair is initiated by either the Msh2-Msh6 or

147 The process of DNA mismatch repair is initiated when MutS recognizes mismat

148 as concluded that Exo1 function in mammalian mismatch repair is restricted to a structural role, a co

149 e of UNG activity, deleterious processing by mismatch repair leads to telomere loss and defective cel

150 ained by preferential recruitment of the DNA mismatch repair machinery to a protein modification that

151 Exonucleolytic proofreading and DNA mismatch repair (MMR) act in series to maintain high-fid

152 e this hypothesis we analyzed ERC within DNA mismatch repair (MMR) and meiosis proteins over phylogen

153 omised by its dependence for activity on DNA mismatch repair (MMR) and the repair of the chemosensiti

154 e and repair of newly synthesized DNA by the mismatch repair (MMR) apparatus.

155 in GBM cells, even a modest decrease in the mismatch repair (MMR) components MSH2 and MSH6 have prof

156 Using over 6000 indels accumulated in four mismatch repair (MMR) defective strains, and statistical

157 The clinicopathologic significance of mismatch repair (MMR) defects in endometrioid endometria

158 Mismatch repair (MMR) deficiency (MMRD) and microsatelli

159 ention efforts, including: tumor testing for mismatch repair (MMR) deficiency in Lynch syndrome estab

160 Mismatch repair (MMR) deficiency was determined by micro

161 tment for prognostic variables that included mismatch repair (MMR) deficiency, ColDx high-risk patien

162 plicated multiple pathways in eukaryotic DNA mismatch repair (MMR) downstream of mispair recognition

163 Decreased expression of mismatch repair (MMR) gene MSH2 in cells exposed to oxid

164 In addition, families with known mismatch repair (MMR) gene mutations that were recorded

165 for identification of patients with germline mismatch repair (MMR) gene mutations.

166 tients with bi-allelic germline mutations in mismatch repair (MMR) genes (MLH1, MSH2, MSH6, or PMS2)

167 is known about cancer risks and mutations in mismatch repair (MMR) genes in AAs with the most common

168 cause of a germline mutation in one of their mismatch repair (MMR) genes.

169 cer cell lines differing by mutations in DNA mismatch repair (MMR) genes.

170 drome is caused by germline mutations in the mismatch repair (MMR) genes.

171 ancer, is caused by inherited defects in DNA mismatch repair (MMR) genes.

172 fectively to study missense mutations in DNA mismatch repair (MMR) genes.

173 ying a pathogenic germline mutation in three mismatch repair (MMR) genes: MLH1, MSH2, and MSH6.

174 DNA mismatch repair (MMR) identifies and corrects errors mad

175 with microsatellite instability (MSI) and a mismatch repair (MMR) immunohistochemical deficit withou

176 novel role for H3K36me3 that facilitates DNA mismatch repair (MMR) in cells by targeting the MMR mach

177 Mismatch repair (MMR) is a conserved mechanism exploited

178 Mismatch repair (MMR) is a near ubiquitous pathway, esse

179 , without GATC methylation, methyl-dependent mismatch repair (MMR) is deleterious and, fueled by the

180 Mismatch repair (MMR) is one of the main systems maintai

181 DNA mismatch repair (MMR) is required for the maintenance of

182 A repair, for example, by the well-known DNA mismatch repair (MMR) mechanism.

183 A problem in understanding eukaryotic DNA mismatch repair (MMR) mechanisms is linking insights int

184 We aimed to describe a large cohort of mismatch repair (MMR) mutation carriers ascertained thro

185 In Escherichia coli, a DNA mismatch repair (MMR) pathway corrects errors that occur

186 h as FANCJ, BRCA1, and FANCD2, interact with mismatch repair (MMR) pathway factors, but the significa

187 The DNA mismatch repair (MMR) pathway recognizes and repairs err

188 t all DNA repair pathways, including the DNA mismatch repair (MMR) pathway, have been well characteri

189 Base excision repair (BER) and mismatch repair (MMR) pathways play an important role in

190 rocessed by uracil-DNA glycosylase (UNG) and mismatch repair (MMR) pathways to generate mutations at

191 eatment Group N0147 trial) were analyzed for mismatch repair (MMR) protein expression and mutations i

192 were assessed for MSI, MLH1 methylation, and mismatch repair (MMR) protein expression.

193 J localization, whereas interaction with the mismatch repair (MMR) protein MLH1 is essential.

194 We have previously demonstrated that the mismatch repair (MMR) protein MSH2 is required for expan

195 Loss of the DNA mismatch repair (MMR) protein MSH3 leads to the developm

196 Loss of MutS homolog 2 (MSH2), a mismatch repair (MMR) protein, abrogated early inflammat

197 MutS homolog 2 (MSH2) is an essential DNA mismatch repair (MMR) protein.

198 Mammalian and Saccharomyces cerevisiae mismatch repair (MMR) proteins catalyze two MMR reaction

199 ality.Immunohistochemical (IHC) staining for mismatch repair (MMR) proteins in SNs can be used to scr

200 ions in single alleles of genes encoding the mismatch repair (MMR) proteins MLH1, MSH2, MSH6, and PMS

201 nuclease activity and were recognized by the mismatch repair (MMR) proteins.

202 or more somatic mutations in genes encoding mismatch repair (MMR) proteins.

203 of an Mlh1-Pms1-independent 5' nick-directed mismatch repair (MMR) reaction using Saccharomyces cerev

204 Defects in DNA mismatch repair (MMR) result in elevated mutagenesis and

205 update presents 10-year OS and OS and DFS by mismatch repair (MMR) status and BRAF mutation.

206 To determine the association of DNA mismatch repair (MMR) status and somatic mutation in the

207 context, a combination of MGMT activity and mismatch repair (MMR) status of the tumor are important

208 w prognostic score (mGPS), and combined BRAF-mismatch repair (MMR) status.

209 However, DNA mismatch repair (MMR) suppresses the efficiency of gene

210 The DNA mismatch repair (MMR) system corrects DNA mismatches in

211 conformations acting in the Escherichia coli mismatch repair (MMR) system in solution.

212 The DNA mismatch repair (MMR) system plays a major role in promo

213 trains, these mismatches are repaired by the mismatch repair (MMR) system, producing a gene conversio

214 gative mutant protein of the methyl-directed mismatch repair (MMR) system, we achieved a transient su

215 extended into duplex DNA and excised by the mismatch repair (MMR) system.

216 iated base-excision repair and MSH2-mediated mismatch repair (MMR) to yield mutations and DNA strand

217 Tumors deficient or proficient in DNA mismatch repair (MMR) were identified based on detection

218 ate an unpredicted involvement of K-H in DNA mismatch repair (MMR) where K-H depletion led to concomi

219 air (BER), nucleotide excision repair (NER), mismatch repair (MMR), non-homologous end joining (NHEJ)

220 ransferase (MGMT) activity, small changes in mismatch repair (MMR), nucleotide excision repair (NER),

221 report that MLH1, a key protein involved in mismatch repair (MMR), suppresses telomeric sequence ins

222 lity homologous DNA recombination depends on mismatch repair (MMR), which antagonizes recombination b

223 ithout error, nature evolved postreplicative mismatch repair (MMR), which improves the fidelity of DN

224 tability (MSI) is the hallmark lesion of DNA mismatch repair (MMR)-deficient cancers.

225 nique cell-selective cytotoxicity, targeting mismatch repair (MMR)-deficient cells over MMR-proficien

226 Mismatch repair (MMR)-deficient colorectal cancer cells

227 tations make up the molecular fingerprint of mismatch repair (MMR)-deficient tumors and convey them w

228 , which occur frequently in hypermutated DNA mismatch repair (MMR)-proficient tumors and appear to be

229 and requires base excision repair (BER) and mismatch repair (MMR).

230 es that escape proofreading are corrected by mismatch repair (MMR).

231 (MLH/PMS) are the fundamental components of mismatch repair (MMR).

232 DNA replication is generally followed by DNA mismatch repair (MMR).

233 A-damaging agents while also contributing to mismatch repair (MMR).

234 selectivity, proofreading activity, and DNA mismatch repair (MMR).

235 yps, tumor microsatellite instability [MSI], mismatch repair [MMR] deficiency) is unknown.

236 risk (P = .001) after adjustment for stage, mismatch repair, nodes examined, grade, and treatment.

237 nt backgrounds and demonstrated that neither mismatch repair nor interstrand crosslink repair affects

238 icase II (UvrD) functions in methyl-directed mismatch repair, nucleotide excision repair, and homolog

239 ays, including homologous recombination, DNA mismatch repair, nucleotide excision repair, and transle

240 her that SIM of CAG repeats does not involve mismatch repair, nucleotide excision repair, or transcri

241 oviding a potential mechanism for triggering mismatch repair on nonreplicating DNA.

242 ontexts influence the preferential access of mismatch repair or uracil glycosylase (UNG) to AID-initi

243 ntify a novel role for FEN1 in a specialized mismatch repair pathway and a new cancer etiological mec

244 Further, we provide evidence that the mismatch repair pathway has a role in regulating beta-ca

245 e identified all expected members of the DNA mismatch repair pathway, whereas another for the DNA top

246 tential therapeutic approaches targeting the mismatch repair pathway.

247 hey included: (1) The genes involved in "DNA mismatch repair" pathway were up-regulated in HPV-positi

248 ion of developmental fate and cell cycle and mismatch repair pathways and altered activities of key u

249 downs showed that both the base excision and mismatch repair pathways are involved.

250 Although error correction by mismatch repair plays a key role in preventing microsate

251 a MutSalpha-dependent, MutLalpha-independent mismatch repair process we call Pol alpha-segment error

252 Compared with mismatch repair proficient (MMR-P) POLE wild-type tumour

253 Combining these improvements in a mismatch repair proficient strain reduced counter-select

254 ilies who met the Amsterdam criteria and had mismatch repair-proficient cancers with no previously as

255 5.0 months, respectively, in the cohort with mismatch repair-proficient colorectal cancer (hazard rat

256 -deficient colorectal cancers, patients with mismatch repair-proficient colorectal cancers, and patie

257 18 patients) and 11% (2 of 18 patients) for mismatch repair-proficient colorectal cancers.

258 sion tracts in mismatch repair-deficient and mismatch repair-proficient strains.

259 air-deficient tumors, as compared with 73 in mismatch repair-proficient tumors (P=0.007), and high so

260 These individuals had mismatch repair-proficient tumors and each carried nonse

261 could also reliably identify tumors with DNA mismatch repair protein deficiency (MMR-D) on the basis

262 ent current mechanistic hypotheses regarding mismatch repair protein function in mediating triplet re

263 tion and heterogeneous nuclear levels of the mismatch repair protein hMSH3.

264 ombine at sites marked by the binding of the mismatch repair protein MLH1.

265 hout a protruding nonhomologous 3' tail, the mismatch repair protein Msh2 does not discourage homeolo

266 nd one of its weak-binding partners, the DNA mismatch repair protein MutL.

267 equire the presence, not the absence, of the mismatch repair protein MutSbeta (Msh2-Msh3 heterodimer)

268 MSH2 is a key DNA mismatch repair protein, which plays an important role i

269 MutS protein homolog 2 (MSH2) is a key DNA mismatch repair protein.

270 on also participate in interaction with MLH1 mismatch-repair protein, suggesting that the FANCJ activ

271 mistry was used to analyze the presence of 4 mismatch repair proteins (MLH1, MSH2, MSH6, and PMS2) in

272 o identify those with dMMR, based on loss of mismatch repair proteins MLH1, MSH2, MSH6, and/or PMS2.

273 Cells lacking mismatch repair proteins Msh6 and Mlh1 form chimeric rec

274 cuses on the long-range communication in DNA mismatch repair proteins MutS and its homologs where int

275 tection of biological macromolecules such as mismatch repair proteins through biotinylated DNA substr

276 other cytokines, caused hMSH3, but no other mismatch repair proteins, to move from the nucleus to th

277 MSH2 is required for DNA mismatch repair recognition in eukaryotes.

278 Here we show that the budding yeast mismatch repair related MutLbeta complex, Mlh1-Mlh2, spe

279 D4 serves as a potent DNA glycosylase in DNA mismatch repair specifically targeting mCpG/TpG mismatch

280 ossibly owing to a lack of stratification on mismatch repair status.

281 ltration in colorectal cancer, regardless of mismatch repair status.

282 This study showed that mismatch-repair status predicted clinical benefit of imm

283 Double-strand break repair and mismatch repair subtypes were associated with increased

284 ier for heterologous recombination, with the mismatch repair system providing a second level of proof

285 mutability is due to a saturation of the DNA mismatch repair system, leading to hypermutability and e

286 ised and repaired by the proteins of the DNA mismatch repair system, which identify the mismatch site

287 stranded DNA), much like the proteins of the mismatch repair system.

288 cancers through inactivation of the cellular mismatch repair system.

289 d a strain for transient inactivation of the mismatch repair system.

290 ized by the presence of a defect in the MMR (mismatch repair) system, the presence of the CpG island

291 present in DNA after replication may direct mismatch repair to the continuously replicated nascent l

292 lta and rad27Delta (replication), msh2Delta (mismatch repair), tsa1Delta (oxidative stress), mre11Del

293 We find thirteen mismatch repair variants of uncertain significance that

294 that the most common cause of defective DNA mismatch repair was low levels of the variant Msh2 prote

295 With every eighth base pair mismatched, repair was about 14% of that of completely h

296 With every sixth base pair mismatched, repair was still more than 5%.

297 and lagging-strand replication fidelity and mismatch repair, we accumulated 40,000 spontaneous mutat

298 the replication processivity clamp to impair mismatch repair, we find that MutS dynamically moves to

299 permutated group that includes defective DNA mismatch repair with microsatellite instability and POLE

300 exonuclease 1 (Exo1) in yeast and mammalian mismatch repair, with results suggesting that function o