Tissues of MSH2-deficient mice demonstrate hypermutability on exposure to a DNA methylating agent.
about
MLH3: a DNA mismatch repair gene associated with mammalian microsatellite instabilityDiffering patterns of genetic instability in mice deficient in the mismatch repair genes Pms2, Mlh1, Msh2, Msh3 and Msh6Accumulation of premutagenic DNA lesions in mice defective in removal of oxidative base damageIncreased hypermutation at G and C nucleotides in immunoglobulin variable genes from mice deficient in the MSH2 mismatch repair proteinMsh-2 suppresses in vivo mutation in a gene dose and lesion dependent mannerMsh2 status modulates both apoptosis and mutation frequency in the murine small intestineElevated mutant frequencies and predominance of G:C to A:T transition mutations in Msh6(-/-) small intestinal epitheliumAltered spectra of hypermutation in DNA repair-deficient mice.Detecting low penetrance genes in cancer: the way ahead.Mbd4 inactivation increases Cright-arrowT transition mutations and promotes gastrointestinal tumor formation.Tumor characteristics as an analytic tool for classifying genetic variants of uncertain clinical significance.O6-methylguanine-DNA methyltransferase in the defense against N-nitroso compounds and colorectal cancer.The oxidized deoxynucleoside triphosphate pool is a significant contributor to genetic instability in mismatch repair-deficient cellsMicrosatellite instability in Drosophila spellchecker1 (MutS homolog) mutants.Fusion tyrosine kinase NPM-ALK Deregulates MSH2 and suppresses DNA mismatch repair function novel insights into a potent oncoproteinElevated levels of the pro-carcinogenic adduct, O(6)-methylguanine, in normal DNA from the cancer prone regions of the large bowel.Minor Changes in Expression of the Mismatch Repair Protein MSH2 Exert a Major Impact on Glioblastoma Response to Temozolomide.Tumors of DNA mismatch repair-deficient hosts exhibit dramatic increases in genomic instability.Balancing repair and tolerance of DNA damage caused by alkylating agentsDNA repair in murine embryonic stem cells and differentiated cellsThe pathobiology of the oncogenic tyrosine kinase NPM-ALK: a brief update.Methylation tolerance in mismatch repair proficient cells with low MSH2 protein level.Multiple mutations are common at mouse Aprt in genotoxin-exposed mismatch repair deficient cells.Msh2 DNA mismatch repair gene deficiency and the food-borne mutagen 2-amino-1-methy1-6-phenolimidazo [4,5-b] pyridine (PhIP) synergistically affect mutagenesis in mouse colon.The ability to engage enterocyte apoptosis does not predict long-term crypt survival in p53 and Msh2 deficient mice.Mutational-reporter transgenes rescued from mice lacking either Mgmt, or both Mgmt and Msh6 suggest that O6-alkylguanine-induced miscoding does not contribute to the spontaneous mutational spectrum.
P2860
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P2860
Tissues of MSH2-deficient mice demonstrate hypermutability on exposure to a DNA methylating agent.
description
1998 nî lūn-bûn
@nan
1998年の論文
@ja
1998年論文
@yue
1998年論文
@zh-hant
1998年論文
@zh-hk
1998年論文
@zh-mo
1998年論文
@zh-tw
1998年论文
@wuu
1998年论文
@zh
1998年论文
@zh-cn
name
Tissues of MSH2-deficient mice ...... re to a DNA methylating agent.
@ast
Tissues of MSH2-deficient mice ...... re to a DNA methylating agent.
@en
type
label
Tissues of MSH2-deficient mice ...... re to a DNA methylating agent.
@ast
Tissues of MSH2-deficient mice ...... re to a DNA methylating agent.
@en
prefLabel
Tissues of MSH2-deficient mice ...... re to a DNA methylating agent.
@ast
Tissues of MSH2-deficient mice ...... re to a DNA methylating agent.
@en
P2093
P2860
P356
P1476
Tissues of MSH2-deficient mice ...... ure to a DNA methylating agent
@en
P2093
A H Reitmair
S E Andrew
P2860
P304
P356
10.1073/PNAS.95.3.1126
P407
P577
1998-02-01T00:00:00Z