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1 e sequences in the genome caused by impaired DNA mismatch repair.
2 endometrial and other cancers with defective DNA mismatch repair.
3 mp in the different steps of methyl-directed DNA mismatch repair.
4 Small looped mispairs are corrected by DNA mismatch repair.
5 cancer (HNPCC) is associated with defects in DNA mismatch repair.
6 trains with mutations in genes implicated in DNA mismatch repair.
7 lteration frequency is entirely dependent on DNA mismatch repair.
8 the context-dependence of the efficiency of DNA mismatch repair.
9 , suggesting a role for Dam in H. influenzae DNA mismatch repair.
10 pha heterodimer that is normally involved in DNA mismatch repair.
11 has been implicated in the excision step of DNA mismatch repair.
12 ding cells with adequate metabolites for the DNA mismatch repair.
13 in defective in Pol epsilon proofreading and DNA mismatch repair.
14 2 pathway regulating DNA damage response and DNA mismatch repair.
15 ms2, is the major MutL activity in mammalian DNA mismatch repair.
16 ladder, and head and neck tumors with intact DNA mismatch repair.
17 extracts deficient in BLM were competent for DNA mismatch repair.
18 egregation of chromosomes or inactivation of DNA mismatch repair.
19 rodimer of hMLH1 and hPMS2, is essential for DNA mismatch repair.
20 r cytosine methylation participates in human DNA mismatch repair.
21 h are characteristic of tumours defective in DNA mismatch repair.
22 ncer is associated with inherited defects in DNA mismatch repair.
23 th required to activate downstream events in DNA mismatch repair.
24 initiation of chromosome replication or for DNA mismatch repair.
25 resolving recombination intermediates and in DNA mismatch repair.
26 latter tumors showed hallmarks of defects in DNA mismatch repair.
27 e-can shorten or lengthen due to a defect in DNA mismatch repair.
28 o DNA-damaging agents and decreases cellular DNA mismatch repair activities by downregulation of MSH2
31 region of Msh6 are important for eukaryotic DNA mismatch repair and cellular response to alkylation
32 ypes, as defined by signatures for defective DNA mismatch repair and DNA polymerase epsilon proofread
33 adation, leading to substantial reduction in DNA mismatch repair and increased resistance to thiopuri
34 reaction in DNA homologous recombination and DNA mismatch repair and is also heavily utilized in DNA-
37 erevisiae Mlh1-Pms1 heterodimer required for DNA mismatch repair and other cellular processes is a DN
38 milar in the two cell types, indicating that DNA mismatch repair and other cellular processes respons
39 HNPCC patients have inherited defects in DNA mismatch repair and the microsatellite instability (
41 rD are identified and linked with defects in DNA mismatch repair and with the ability to cope with co
42 netic profile with type I showing defects in DNA-mismatch repair and mutations in PTEN, K-ras, and be
43 cancers, especially in tumors proficient in DNA mismatch repair, and thus represents a novel marker
44 included attachment, metabolism, transport, DNA mismatch repair, and transcriptional regulation, and
45 apeutics for cancer, because deficiencies in DNA mismatch repair are implicated in cancers, and cells
46 y, tumor cells with MSI (caused by defective DNA mismatch repair) are more resistant to 5-FU in cultu
47 antigen (PCNA) is thought to play a role in DNA mismatch repair at the DNA synthesis step as well as
48 ast MutL homologs Mlh1 and Pms1 required for DNA mismatch repair both possess independent, intrinsic
54 t is widespread in bacteria and functions in DNA mismatch repair, chromosome segregation, and virulen
55 consistent with the hypothesis of Mlh1-Mlh3 DNA mismatch repair complex acting as the major endonucl
59 ucleotide repeats (EMAST) is the most common DNA mismatch repair defect in colorectal cancers, observ
63 compared prevalence of proximal location and DNA mismatch repair deficiency (dMMR) in CRC tumors, rel
66 d family histories and testing of tumors for DNA mismatch repair deficiency and/or microsatellite ins
67 ancers from 1,144 patients were assessed for DNA mismatch repair deficiency by two methods: MSI testi
69 diploid yeast strains differing only in the DNA mismatch-repair deficiency used to elevate the mutat
70 A feature in patients with constitutional DNA-mismatch repair deficiency is agenesis of the corpus
72 tic mechanism of malignant transformation in DNA mismatch repair deficient, microsatellite-unstable c
75 rosatellite instability (MSI-H) or defective DNA mismatch repair (dMMR) have improved survival and re
79 own (EXO1 - exonuclease 1) to be involved in DNA mismatch repair emerged as candidate susceptibility
80 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
95 uent identification of germline mutations in DNA mismatch repair genes (n = 47) or biallelic MUTYH mu
96 ants in base-excision (P = 2.4 x 10(-4)) and DNA mismatch repair genes (P = 6.1 x 10(-4)) consistent
97 ed hereditary breast and ovarian cancer, and DNA mismatch repair genes for suspected Lynch syndrome.
99 ted for MSI, and promoter methylation of the DNA mismatch repair genes MLH1, MSH2, MLH3, MSH6, PMS2,
100 We tested these predictions by deleting the DNA mismatch repair genes MSH2 or MLH1 and analyzing the
102 nstability (MSI) and promoter methylation of DNA mismatch repair genes, is common in individual gland
103 ional repair genes, RAD51 and BRCA1, and the DNA mismatch repair genes, MLH1 and MSH2, are decreased
105 adenomatous polyposis coli gene (Apc) and/or DNA mismatch repair genes, we have analyzed the genetic
109 to colorectal cancer caused by mutations in DNA mismatch repair genes; colorectal cancer risk is hig
110 (HNPCC) is caused by inherited mutations in DNA mismatch-repair genes, most commonly MLH1 or MSH2.
112 ution of tumor stroma obscured signatures of DNA mismatch repair identified in cell lines with a hype
116 s review summarizes the current knowledge of DNA mismatch repair involvement in triplet repeat expans
128 explained by preferential recruitment of the DNA mismatch repair machinery to a protein modification
132 is colon cancer (HNPCC), is due to deficient DNA mismatch repair (MMR) and is defined with mono- and
133 plore this hypothesis we analyzed ERC within DNA mismatch repair (MMR) and meiosis proteins over phyl
135 ompromised by its dependence for activity on DNA mismatch repair (MMR) and the repair of the chemosen
136 urn mispairs with thymine, triggering futile DNA mismatch repair (MMR) and ultimately cell death.
138 ity to Fen1, and because Exo1 is involved in DNA mismatch repair (MMR) by interaction with Msh2 and M
139 erodimeric human MSH2-MSH6 protein initiates DNA mismatch repair (MMR) by recognizing mismatched base
140 accharomyces cerevisiae strains deficient in DNA mismatch repair (MMR) can be used to determine de no
142 Ls in vitro, and that cells deficient in the DNA mismatch repair (MMR) complex MutSbeta were sensitiv
146 s implicated multiple pathways in eukaryotic DNA mismatch repair (MMR) downstream of mispair recognit
147 cute myeloid leukaemia (t-AML) suggests that DNA mismatch repair (MMR) dysfunction may be an initiati
150 analysis showed that Sgs1p is redundant with DNA mismatch repair (MMR) for suppressing GCRs and for s
154 his effect, we report that expression of the DNA mismatch repair (MMR) gene Mlh1 is specifically redu
156 Non-Polyposis Colorectal Cancer (HNPCC) and DNA mismatch repair (MMR) gene product hMSH2, both in vi
157 ratory indicated that expression of the MLH1 DNA mismatch repair (MMR) gene was necessary to restore
160 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 al, and gastric cancers harboring defects in DNA mismatch repair (MMR) genes We used the microsatelli
167 sed by germ-line mutations in one of several DNA mismatch repair (MMR) genes, most commonly in hMSH2
178 y a novel role for H3K36me3 that facilitates DNA mismatch repair (MMR) in cells by targeting the MMR
179 NA methyltransferase 1 (Dnmt1) deficiency on DNA mismatch repair (MMR) in mouse embryonic stem (ES) c
183 ity characterized by aneuploidy or defective DNA mismatch repair (MMR) indicated by microsatellite in
191 llite instability (MSI) secondary to loss of DNA mismatch repair (MMR) is present in adenomas and col
200 Not all DNA repair pathways, including the DNA mismatch repair (MMR) pathway, have been well charac
202 Although it is clear that postreplicative DNA mismatch repair (MMR) plays a critical role in maint
203 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'
218 Normally, this process is prevented by a DNA mismatch repair (MMR) system that maintains sequence
219 We examined whether the component of the DNA mismatch repair (MMR) system that normally recognize
220 tellites mutate more frequently in defective DNA mismatch repair (MMR) than shorter microsatellites.
223 stigate an unpredicted involvement of K-H in DNA mismatch repair (MMR) where K-H depletion led to con
226 eened this library for cells with defects in DNA mismatch repair (MMR), a system that detects and rep
227 disease caused by defects in the process of DNA mismatch repair (MMR), and mutations in the hMLH1 or
228 exonuclease 1 (Exo1), which participates in DNA mismatch repair (MMR), have decreased CSR and change
229 Although known to be partly dependent on DNA mismatch repair (MMR), the cytotoxicity of 6-TG rema
230 ansformation process is greatly inhibited by DNA mismatch repair (MMR), the pattern of incorporation
231 rapeutic approaches for cancers deficient in DNA mismatch repair (MMR), we have carried out parallel
234 Dysfunction of cell-cycle checkpoints in DNA mismatch repair (MMR)-deficient cells in response to
235 investigate the effects of mutated K-ras on DNA mismatch repair (MMR)-deficient intestinal tumour fo
236 Such deletions occur one base at a time in DNA mismatch repair (MMR)-deficient yeast suggesting lar
237 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
249 of somatic and germline mutations related to DNA mismatch-repair (MMR) genes can clarify the prevalen
253 athways, including homologous recombination, DNA mismatch repair, nucleotide excision repair, and tra
257 anine identified all expected members of the DNA mismatch repair pathway, whereas another for the DNA
259 They included: (1) The genes involved in "DNA mismatch repair" pathway were up-regulated in HPV-po
261 f mutagenic DNA 8-oxoG and demonstrated that DNA mismatch repair prevented oxidation-related frameshi
263 the use of transient regulation of cellular DNA mismatch repair processes to enhance traits (e.g., a
264 ls have similar mechanistic efficacy against DNA mismatch repair-proficient tumor cells that lack exp
265 s (UvrD, RecG, RecQ), truncated forms of the DNA mismatch repair protein (MutS) and a primosomal comp
266 ons could also reliably identify tumors with DNA mismatch repair protein deficiency (MMR-D) on the ba
267 osatellite instability from reduction of the DNA mismatch repair protein MLH1, are unaffected by CENP
273 oth Chfr and Mlh1 (the gene that encodes the DNA mismatch-repair protein Mlh1) displayed dramatically
274 al approach, based on detection of foci of a DNA mismatch-repair protein, MLH1, on synaptonemal compl
275 y focuses on the long-range communication in DNA mismatch repair proteins MutS and its homologs where
276 rs that prevent carcinogenesis (such as p53, DNA mismatch repair proteins, and DNA base excision-repa
280 Pms1 may be relevant to its participation in DNA mismatch repair, recombination and cellular response
281 , MBD4 serves as a potent DNA glycosylase in DNA mismatch repair specifically targeting mCpG/TpG mism
282 s were compared with pathological variables, DNA mismatch repair status, and patient survival using C
284 tion by frameshift reversion is modulated by DNA mismatch-repair status and occurs in individual cell
285 fic manner by inactivation of PMS1-dependent DNA mismatch repair, suggesting that the mutator effects
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
293 Combining RNR deregulation with defects in DNA mismatch repair, the cellular mutation correction sy
294 or Dam methylase: directing post-replicative DNA mismatch repair to the correct strand, guiding the t
295 ion of this result is that the efficiency of DNA mismatch repair varies in different regions of the g
296 ATPase activity plays a proofreading role in DNA mismatch repair, verification of mismatch recognitio
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,
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