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1 latter tumors showed hallmarks of defects in DNA mismatch repair.
2 e-can shorten or lengthen due to a defect in DNA mismatch repair.
3 endometrial and other cancers with defective DNA mismatch repair.
4 mp in the different steps of methyl-directed DNA mismatch repair.
5 Small looped mispairs are corrected by DNA mismatch repair.
6 cancer (HNPCC) is associated with defects in DNA mismatch repair.
7 trains with mutations in genes implicated in DNA mismatch repair.
8 tability (MSI), which results from deficient DNA mismatch repair.
9 lteration frequency is entirely dependent on DNA mismatch repair.
10 the context-dependence of the efficiency of DNA mismatch repair.
11 , suggesting a role for Dam in H. influenzae DNA mismatch repair.
12 pha heterodimer that is normally involved in DNA mismatch repair.
13 has been implicated in the excision step of DNA mismatch repair.
14 ding cells with adequate metabolites for the DNA mismatch repair.
15 ease activity of MutL and it is critical for DNA mismatch repair.
16 in defective in Pol epsilon proofreading and DNA mismatch repair.
17 ms2, is the major MutL activity in mammalian DNA mismatch repair.
18 ladder, and head and neck tumors with intact DNA mismatch repair.
19 extracts deficient in BLM were competent for DNA mismatch repair.
20 egregation of chromosomes or inactivation of DNA mismatch repair.
21 e sequences in the genome caused by impaired DNA mismatch repair.
22 2 pathway regulating DNA damage response and DNA mismatch repair.
23 initiation of chromosome replication or for DNA mismatch repair.
24 resolving recombination intermediates and in DNA mismatch repair.
25 sover resolution and the initiation steps of DNA mismatch repair(12,13) and evoke a novel model for c
26 o DNA-damaging agents and decreases cellular DNA mismatch repair activities by downregulation of MSH2
29 region of Msh6 are important for eukaryotic DNA mismatch repair and cellular response to alkylation
30 reased tumor burden correlates with impaired DNA mismatch repair and decreased expression of Mlh1 and
31 ypes, as defined by signatures for defective DNA mismatch repair and DNA polymerase epsilon proofread
32 adation, leading to substantial reduction in DNA mismatch repair and increased resistance to thiopuri
33 reaction in DNA homologous recombination and DNA mismatch repair and is also heavily utilized in DNA-
36 HNPCC patients have inherited defects in DNA mismatch repair and the microsatellite instability (
38 rD are identified and linked with defects in DNA mismatch repair and with the ability to cope with co
39 netic profile with type I showing defects in DNA-mismatch repair and mutations in PTEN, K-ras, and be
40 cancers, especially in tumors proficient in DNA mismatch repair, and thus represents a novel marker
41 included attachment, metabolism, transport, DNA mismatch repair, and transcriptional regulation, and
42 apeutics for cancer, because deficiencies in DNA mismatch repair are implicated in cancers, and cells
43 y, tumor cells with MSI (caused by defective DNA mismatch repair) are more resistant to 5-FU in cultu
44 antigen (PCNA) is thought to play a role in DNA mismatch repair at the DNA synthesis step as well as
45 ast MutL homologs Mlh1 and Pms1 required for DNA mismatch repair both possess independent, intrinsic
48 t is widespread in bacteria and functions in DNA mismatch repair, chromosome segregation, and virulen
49 consistent with the hypothesis of Mlh1-Mlh3 DNA mismatch repair complex acting as the major endonucl
54 ucleotide repeats (EMAST) is the most common DNA mismatch repair defect in colorectal cancers, observ
57 nce supporting the significant importance of DNA mismatch repair deficiencies and the efficacy of the
58 sed neoantigens in hypermutated cancers with DNA mismatch repair deficiency (dMMR) are proposed as th
60 compared prevalence of proximal location and DNA mismatch repair deficiency (dMMR) in CRC tumors, rel
63 d family histories and testing of tumors for DNA mismatch repair deficiency and/or microsatellite ins
64 ancers from 1,144 patients were assessed for DNA mismatch repair deficiency by two methods: MSI testi
65 nsive and up-to-date summary for the role of DNA mismatch repair deficiency in cancer, and its import
67 A feature in patients with constitutional DNA-mismatch repair deficiency is agenesis of the corpus
69 ced computed tomography (CE-CT) can identify DNA mismatch repair deficient (MMR-D) and/or tumor mutat
70 tic mechanism of malignant transformation in DNA mismatch repair deficient, microsatellite-unstable c
73 rosatellite instability (MSI-H) or defective DNA mismatch repair (dMMR) have improved survival and re
78 own (EXO1 - exonuclease 1) to be involved in DNA mismatch repair emerged as candidate susceptibility
79 ther show that overexpression of catalase or DNA mismatch repair enzyme, MutS, and antioxidant pretre
90 status of the tumor suppressor gene p16, the DNA mismatch repair gene hMLH1, and four CpG islands (MI
94 differential mutational burden downstream of DNA mismatch repair gene mutations and composite gene ex
97 uent identification of germline mutations in DNA mismatch repair genes (n = 47) or biallelic MUTYH mu
98 ants in base-excision (P = 2.4 x 10(-4)) and DNA mismatch repair genes (P = 6.1 x 10(-4)) consistent
99 ed hereditary breast and ovarian cancer, and DNA mismatch repair genes for suspected Lynch syndrome.
100 arate study, a decreased expression level of DNA mismatch repair genes involved in SHM in older indiv
102 ted for MSI, and promoter methylation of the DNA mismatch repair genes MLH1, MSH2, MLH3, MSH6, PMS2,
103 We tested these predictions by deleting the DNA mismatch repair genes MSH2 or MLH1 and analyzing the
105 nstability (MSI) and promoter methylation of DNA mismatch repair genes, is common in individual gland
106 ional repair genes, RAD51 and BRCA1, and the DNA mismatch repair genes, MLH1 and MSH2, are decreased
107 adenomatous polyposis coli gene (Apc) and/or DNA mismatch repair genes, we have analyzed the genetic
113 to colorectal cancer caused by mutations in DNA mismatch repair genes; colorectal cancer risk is hig
114 (HNPCC) is caused by inherited mutations in DNA mismatch-repair genes, most commonly MLH1 or MSH2.
116 ution of tumor stroma obscured signatures of DNA mismatch repair identified in cell lines with a hype
120 s review summarizes the current knowledge of DNA mismatch repair involvement in triplet repeat expans
131 explained by preferential recruitment of the DNA mismatch repair machinery to a protein modification
135 is colon cancer (HNPCC), is due to deficient DNA mismatch repair (MMR) and is defined with mono- and
136 plore this hypothesis we analyzed ERC within DNA mismatch repair (MMR) and meiosis proteins over phyl
138 ompromised by its dependence for activity on DNA mismatch repair (MMR) and the repair of the chemosen
140 ity to Fen1, and because Exo1 is involved in DNA mismatch repair (MMR) by interaction with Msh2 and M
141 erodimeric human MSH2-MSH6 protein initiates DNA mismatch repair (MMR) by recognizing mismatched base
143 Ls in vitro, and that cells deficient in the DNA mismatch repair (MMR) complex MutSbeta were sensitiv
148 s implicated multiple pathways in eukaryotic DNA mismatch repair (MMR) downstream of mispair recognit
149 cute myeloid leukaemia (t-AML) suggests that DNA mismatch repair (MMR) dysfunction may be an initiati
155 his effect, we report that expression of the DNA mismatch repair (MMR) gene Mlh1 is specifically redu
157 ratory indicated that expression of the MLH1 DNA mismatch repair (MMR) gene was necessary to restore
158 Lynch syndrome is caused by variants in DNA mismatch repair (MMR) genes and associated with an i
161 NPCC results from germ-line mutations in the DNA mismatch repair (MMR) genes hMSH2 and hMLH1 with rar
162 tic or epigenetic inactivation of one of the DNA mismatch repair (MMR) genes in tumor precursor cells
164 uals with heterozygous germline mutations in DNA mismatch repair (MMR) genes or hereditary nonpolypos
166 sed by germ-line mutations in one of several DNA mismatch repair (MMR) genes, most commonly in hMSH2
176 y a novel role for H3K36me3 that facilitates DNA mismatch repair (MMR) in cells by targeting the MMR
177 NA methyltransferase 1 (Dnmt1) deficiency on DNA mismatch repair (MMR) in mouse embryonic stem (ES) c
181 ity characterized by aneuploidy or defective DNA mismatch repair (MMR) indicated by microsatellite in
189 llite instability (MSI) secondary to loss of DNA mismatch repair (MMR) is present in adenomas and col
197 n screening approach, we discovered that the DNA mismatch repair (MMR) pathway is essential for club
199 Not all DNA repair pathways, including the DNA mismatch repair (MMR) pathway, have been well charac
201 Although it is clear that postreplicative DNA mismatch repair (MMR) plays a critical role in maint
202 dicated that the protein factors involved in DNA mismatch repair (MMR) possess meiotic functions beyo
207 rest and apoptosis in a manner requiring the DNA mismatch repair (MMR) proteins MutSalpha and MutLalp
211 , bcl-2, p53, proliferation marker Ki-67 and DNA mismatch repair (MMR) status in patients with Dukes'
217 Normally, this process is prevented by a DNA mismatch repair (MMR) system that maintains sequence
218 We examined whether the component of the DNA mismatch repair (MMR) system that normally recognize
219 tellites mutate more frequently in defective DNA mismatch repair (MMR) than shorter microsatellites.
222 stigate an unpredicted involvement of K-H in DNA mismatch repair (MMR) where K-H depletion led to con
225 eened this library for cells with defects in DNA mismatch repair (MMR), a system that detects and rep
226 exonuclease 1 (Exo1), which participates in DNA mismatch repair (MMR), have decreased CSR and change
227 Although known to be partly dependent on DNA mismatch repair (MMR), the cytotoxicity of 6-TG rema
229 ansformation process is greatly inhibited by DNA mismatch repair (MMR), the pattern of incorporation
230 rapeutic approaches for cancers deficient in DNA mismatch repair (MMR), we have carried out parallel
233 Dysfunction of cell-cycle checkpoints in DNA mismatch repair (MMR)-deficient cells in response to
234 investigate the effects of mutated K-ras on DNA mismatch repair (MMR)-deficient intestinal tumour fo
235 Such deletions occur one base at a time in DNA mismatch repair (MMR)-deficient yeast suggesting lar
236 ions, which occur frequently in hypermutated DNA mismatch repair (MMR)-proficient tumors and appear t
248 in A (RPA) is involved in multiple stages of DNA mismatch repair (MMR); however, the modulation of it
252 athways, including homologous recombination, DNA mismatch repair, nucleotide excision repair, and tra
254 anine identified all expected members of the DNA mismatch repair pathway, whereas another for the DNA
256 They included: (1) The genes involved in "DNA mismatch repair" pathway were up-regulated in HPV-po
258 f mutagenic DNA 8-oxoG and demonstrated that DNA mismatch repair prevented oxidation-related frameshi
260 the use of transient regulation of cellular DNA mismatch repair processes to enhance traits (e.g., a
261 ls have similar mechanistic efficacy against DNA mismatch repair-proficient tumor cells that lack exp
263 s (UvrD, RecG, RecQ), truncated forms of the DNA mismatch repair protein (MutS) and a primosomal comp
264 ons could also reliably identify tumors with DNA mismatch repair protein deficiency (MMR-D) on the ba
265 osatellite instability from reduction of the DNA mismatch repair protein MLH1, are unaffected by CENP
272 oth Chfr and Mlh1 (the gene that encodes the DNA mismatch-repair protein Mlh1) displayed dramatically
273 al approach, based on detection of foci of a DNA mismatch-repair protein, MLH1, on synaptonemal compl
274 y focuses on the long-range communication in DNA mismatch repair proteins MutS and its homologs where
275 rs that prevent carcinogenesis (such as p53, DNA mismatch repair proteins, and DNA base excision-repa
279 Pms1 may be relevant to its participation in DNA mismatch repair, recombination and cellular response
280 , MBD4 serves as a potent DNA glycosylase in DNA mismatch repair specifically targeting mCpG/TpG mism
281 s were compared with pathological variables, DNA mismatch repair status, and patient survival using C
283 tion by frameshift reversion is modulated by DNA mismatch-repair status and occurs in individual cell
284 fic manner by inactivation of PMS1-dependent DNA mismatch repair, suggesting that the mutator effects
286 instability (MSI) are caused by a defective DNA mismatch repair system that leads to the accumulatio
287 igh mutability is due to a saturation of the DNA mismatch repair system, leading to hypermutability a
288 o understand the evolutionary process of the DNA mismatch repair system, we conducted systematic phyl
289 cognised and repaired by the proteins of the DNA mismatch repair system, which identify the mismatch
292 more frequently in isolates with defects in DNA mismatch repair that confer an elevated mutation rat
294 Combining RNR deregulation with defects in DNA mismatch repair, the cellular mutation correction sy
295 or Dam methylase: directing post-replicative DNA mismatch repair to the correct strand, guiding the t
296 ion of this result is that the efficiency of DNA mismatch repair varies in different regions of the g
297 ound that the most common cause of defective DNA mismatch repair was low levels of the variant Msh2 p
298 ) hypermutated group that includes defective DNA mismatch repair with microsatellite instability and
299 Treatment of colon tumor cells deficient in DNA mismatch repair with the death-receptor ligand apo2
300 the transcription factor HIF-1alpha impairs DNA mismatch repair, yet the role of HIF-1alpha isoform,