ライフサイエンスコーパス: mismatch repair

1 activity of MutL and it is critical for DNA mismatch repair.

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

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

4 iming, nucleosome occupancy or deficiency in mismatch repair.

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

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

7 to inflammation, ErbB signalling pathway and mismatch repair.

8 mutations are found in tumors with defective mismatch repair.

9 thway regulating DNA damage response and DNA mismatch repair.

10 diffusion mechanics along the DNA to direct mismatch repair.

11 cer diagnostic for detecting deficiencies in mismatch repair.

12 two components: polymerase proofreading and mismatch repair.

13 charomyces cerevisiae that are deficient for mismatch repair.

14 of MutL in organisms lacking methyl-directed mismatch repair.

15 MLH1 show a mutation signature of deficient mismatch repair.

16 lity (MSI), which results from deficient DNA mismatch repair.

17 ic hypermutability that arises from impaired mismatch repair(1-4).

18 r resolution and the initiation steps of DNA mismatch repair(12,13) and evoke a novel model for cross

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

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

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

22 repeat expansion without impeding canonical mismatch repair activity.

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

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

25 ed tumor burden correlates with impaired DNA mismatch repair and decreased expression of Mlh1 and Msh

26 ed negatively with homologous recombination, mismatch repair and G2M checkpoint genes.

27 s are low-fidelity replication, insufficient mismatch repair and increased double-strand breaks.

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

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

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

31 otide excision repair, base excision repair, mismatch repair, and DNA double-strand break repair.

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

33 1-PMS1 in yeast) functions in early steps of mismatch repair as a latent endonuclease that requires a

34 9 in the PETACC-8 phase III randomized trial.Mismatch repair, BRAF V600E, and KRAS exon 2 mutational

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

36 ith consideration in HOXB13, BRCA1, ATM, and mismatch repair carriers.

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

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

39 pair complex, Rad10-Rad1(ERCC1-XPF), and the mismatch repair complex, Msh2-Msh3, are required for Z-D

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

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

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

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

44 minase activity (COSMIC signature 2) and DNA mismatch repair (COSMIC signature 6).

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

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

47 tly contribute to genetic instability in DNA mismatch repair-defective human tumors.

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

49 supporting the significant importance of DNA mismatch repair deficiencies and the efficacy of the ant

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

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

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

53 neoantigens in hypermutated cancers with DNA mismatch repair deficiency (dMMR) are proposed as the ma

54 DNA mismatch repair deficiency (dMMR) hallmarks consensus mo

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

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

57 should be offered somatic tumor testing for mismatch repair deficiency (dMMR).

58 Tumors with mismatch repair deficiency (MMR-d) are characterized by

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

60 Microsatellite instability (MSI) and/or mismatch repair deficiency (MMR-D) testing has tradition

61 static non-small-cell lung cancer (NSCLC) or mismatch repair deficiency (MMRD) carcinoma treated with

62 omologous recombination deficiency (HRD) and mismatch repair deficiency (MMRD).

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

64 e and up-to-date summary for the role of DNA mismatch repair deficiency in cancer, and its importance

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

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

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

68 Mismatch repair deficiency was identified in 1% of tumor

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

70 testing for microsatellite instability high/mismatch repair deficiency, BRCA mutations, and TRK alte

71 10%) had tumors with histologic evidence for mismatch repair deficiency.

72 Two tumors had hypermutation consistent with mismatch repair deficiency.

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

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

75 Microsatellite instability (MSI) and mismatch-repair deficiency (dMMR) in colorectal tumors a

76 mline mutations, representing constitutional mismatch-repair deficiency.

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

78 esting for microsatellite instability and/or mismatch repair-deficiency (MSI/IHC) and clinical predic

79 Additionally, mismatch-repair-deficiency was analyzed by checking the

80 Mismatch repair deficient (dMMR) gastro-oesophageal aden

81 computed tomography (CE-CT) can identify DNA mismatch repair deficient (MMR-D) and/or tumor mutationa

82 tissue-agnostic approval of pembrolizumab in mismatch repair deficient (MMRD) solid tumors, important

83 and 1 expression, microsatellite-high and/or mismatch repair deficient (MSI-H/MMR-D) status, and soma

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

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

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

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

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

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

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

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

92 patients with sporadic, RAS/BRAF wild-type, mismatch repair-deficient colorectal cancer tumors with

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

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

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

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

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

98 ers also had inadequate outcomes: ~4.7% were mismatch-repair-deficient (another targetable defect, no

99 agnosis for 76.1% and 60.8% of patients with mismatch-repair-deficient (MMRd) CRC and EC without and

100 ndreds of randomly selected clones from both mismatch-repair-deficient and -proficient populations.

101 ts to explain the fitness difference between mismatch-repair-deficient and -proficient strains.

102 omputation of the mean clone fitness for the mismatch-repair-deficient strain permits an estimation o

103 ort-term competitive fitness deficit for the mismatch-repair-deficient strain.

104 Although PD-1 inhibitors for mismatch-repair-deficient tumours and NTRK inhibitors fo

105 e for phosphorylation of AID at serine 38 in mismatch repair-dependent CSR and affinity maturation.

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

107 Tumors with defective mismatch repair (dMMR) are responsive to immunotherapy b

108 Deficient DNA mismatch repair (dMMR) induces a hypermutator phenotype

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

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

111 of-function missense variants in the key DNA mismatch repair factor MSH2.

112 Recent genetic evidence indicates that the mismatch repair factor MutSbeta (Msh2-Msh3 complex) and

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

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

115 ARP) inhibitor or platinum chemotherapy, and mismatch repair gene defects and microsatellite instabil

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

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

118 ely in tumors with low expression of the DNA mismatch repair gene MLH1.

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

120 The mismatch repair gene MSH3 has been implicated as a genet

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

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

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

124 erential mutational burden downstream of DNA mismatch repair gene mutations and composite gene expres

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

126 Expression of the mismatch repair gene MutL homolog 1 (MLH1) is silenced i

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

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

129 ple, lung samples with low expression of the mismatch-repair gene MLH1 show a mutation signature of d

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

131 was analyzed for mutations in LS-associated mismatch repair genes ( MLH1, MSH2, MSH6, PMS2, EPCAM).

132 adults with pathogenic germline variants in mismatch repair genes (60% women; mean age, 47 +/- 14 ye

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

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

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

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

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

138 e study, a decreased expression level of DNA mismatch repair genes involved in SHM in older individua

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

140 mutations involving BRCA1, BRCA2, PRSS1, and mismatch repair genes predispose patients to PDAC.

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

142 disease treatment included BRCA2, BRCA1, and mismatch repair genes, with broader testing, such as ATM

143 ic variant in the BRCA1/2, PTEN, TP53 or DNA mismatch repair genes.

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

145 somatic hypermethylation or mutations in the mismatch repair genes.

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

147 nts with pathogenic germline variants in DNA mismatch repair genes.

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

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

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

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

152 including microsatellite instability and DNA mismatch repair immunohistochemistry results.

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

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

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

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

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

158 DNA mismatch repair is a conserved antimutagenic pathway tha

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

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

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

162 A shared paradigm of mismatch repair (MMR) across biology depicts extensive e

163 ceptor (EGFR)/BRAF inhibition down-regulates mismatch repair (MMR) and homologous recombination DNA-r

164 otypes on lifespan using yeast defective for mismatch repair (MMR) and/or leading strand (Polepsilon)

165 lamp that acts as a central co-ordinator for mismatch repair (MMR) as well as DNA replication.

166 functions of the yeast MutLalpha (Mlh1-Pms1) mismatch repair (MMR) complex.

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

168 DNA mismatch repair (MMR) corrects errors that occur during

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

170 Mismatch repair (MMR) deficiencies are a hallmark of var

171 aberrations, most notably BRCA1/2 mutations, mismatch repair (MMR) deficiencies or NTRK1-3 fusions, h

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

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

174 Mismatch repair (MMR) deficiency was determined by micro

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

176 amined, expansion is dependent on functional mismatch repair (MMR) factors, including MutLgamma, a he

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

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

179 Lynch syndrome is caused by variants in DNA mismatch repair (MMR) genes and associated with an incre

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

181 constitutional defects in DNA polymerase and mismatch repair (MMR) genes, and a more common post-trea

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

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

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

185 Mismatch repair (MMR) is a conserved mechanism exploited

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

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

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

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

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

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

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

193 reening approach, we discovered that the DNA mismatch repair (MMR) pathway is essential for club cell

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

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

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

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

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

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

200 nthetic lethal phenotype requires functional mismatch repair (MMR) proteins and p53.

201 ical (IHC) loss of expression of one or more mismatch repair (MMR) proteins and/or documented mutatio

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

203 We observed a higher expression of DNA mismatch repair (MMR) proteins in EGFRvIII+ cells and pa

204 Immunohistochemistry for p53 and mismatch repair (MMR) proteins, and DNA sequencing for P

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

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

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

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

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

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

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

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

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

214 The post-replicative mismatch repair (MMR) system has anti-recombination acti

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

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

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

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

219 Furthermore, TC-NER interacts with mismatch repair (MMR) under physiological conditions to

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

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

222 ficiencies in DNA repair pathways, including mismatch repair (MMR), have been linked to higher tumor

223 Mismatch repair (MMR), IHC, and promoter hypermethylatio

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

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

226 MSI, caused by defective mismatch repair (MMR), occurs frequently in colorectal,

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

228 DNA mismatch repair (MMR), the guardian of the genome, comme

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

230 itor nivolumab previously showed activity in mismatch repair (MMR)-deficient colon cancer.

231 Mismatch repair (MMR)-deficient colorectal cancer cells

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

233 essing POLE tumor variants, with and without mismatch repair (MMR).

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

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

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

237 in strains lacking Poldelta proofreading or mismatch repair (MMR).

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

239 encoded by these genes are required for DNA mismatch repair (MMR).

240 ough inherited pathogenic variants affecting mismatch-repair (MMR) genes.

241 We further demonstrate that signature mismatch-repair (MMR) mutations activate enhancers using

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

243 egative regulator mutations, TET2 mutations, mismatch repair mutations and high tumour mutational bur

244 ce of antibiotic resistance in comparison to mismatch-repair (mutS) mutators, and leads to new resist

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

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

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

248 tential therapeutic approaches targeting the mismatch repair pathway.

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

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

251 roles of the base excision repair (BER) and mismatch repair pathways, respectively, in CSR.

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

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

254 ut the role of immune checkpoint blockade in mismatch repair-proficient (MMRP) and -deficient endomet

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

256 5.0 months, respectively, in the cohort with mismatch repair-proficient colorectal cancer (hazard rat

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

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 tal cancer (CRC) resistant to immunotherapy, mismatch-repair-proficient or microsatellite instability

261 Inactivation of DNA mismatch repair propels colorectal cancer (CRC) tumorige

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

263 bust lymphocytic infiltrate, such as loss of mismatch repair protein expression or expression of Epst

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

265 which can be detected by MutS homolog (MSH) mismatch repair protein heterodimers.

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

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

268 The mismatch repair protein MutL has an internal clamp-bindi

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

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

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

272 MutL homolog 1 (MLH1) is a key DNA mismatch repair protein, which plays an important role i

273 POLE and mismatch repair protein-encoding genes were mutated at l

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

275 orectal tumors that had normal expression of mismatch repair proteins (validation cohort).

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

277 xposure, we found a strong repression of the mismatch repair proteins MSH2, MSH6, and EXO1 as well as

278 r programmed cell death ligand 1 (PD-L1) and mismatch repair proteins MutL homolog 1 (MLH1), MutS hom

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

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

281 5, BAT26, NR-21, NR-22 and NR-27 and loss of mismatch repair proteins using four different markers (M

282 DNA methylation of mitochondrial fusion and mismatch repair proteins, Mfn2 and Mlh1 respectively, wa

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

284 ication and to inactivation of genes such as mismatch-repair-related genes.

285 gender, age, tumor location, tumor grade, or mismatch repair status in any cancer stage.

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

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

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

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

290 tS homolog 2 (MSH2), MSH6, and PMS1 homolog, mismatch repair system component 2 (PMS2) was performed.

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

292 tability (MSI) are caused by a defective DNA mismatch repair system that leads to the accumulation of

293 cancers through inactivation of the cellular mismatch repair system.

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

295 e frequently in isolates with defects in DNA mismatch repair that confer an elevated mutation rate.

296 We find thirteen mismatch repair variants of uncertain significance that

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

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

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

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