Both base excision repair and O6-methylguanine-DNA methyltransferase protect against methylation-induced colon carcinogenesis - Wikidata - awgldk - TriplyDB

Both base excision repair and O6-methylguanine-DNA methyltransferase protect against methylation-induced colon carcinogenesis

Both base excision repair and O6-methylguanine-DNA methyltransferase protect against methylation-induced colon carcinogenesis

http://www.wikidata.org/entity/Q34132791

about

Physiology of the read-write genome DNA glycosylases: in DNA repair and beyond Base excision repair and cancer Repair of endogenous DNA base lesions modulate lifespan in mice O6-methylguanine-DNA methyltransferase in the defense against N-nitroso compounds and colorectal cancer.Base excision repair capacity in informing healthspan.Mass spectrometry based approach to study the kinetics of O6-alkylguanine DNA alkyltransferase-mediated repair of O6-pyridyloxobutyl-2'-deoxyguanosine adducts in DNA.DNA repair is indispensable for survival after acute inflammation.Balancing repair and tolerance of DNA damage caused by alkylating agents Dendrophthoe pentandra (L.) Miq extract effectively inhibits inflammation, proliferation and induces p53 expression on colitis-associated colon cancer.Multifaceted roles of alkyltransferase and related proteins in DNA repair, DNA damage, resistance to chemotherapy, and research tools.Small-molecule inhibitors of DNA damage-repair pathways: an approach to overcome tumor resistance to alkylating anticancer drugs.MGMT testing--the challenges for biomarker-based glioma treatment.Protection by Salvia extracts against oxidative and alkylation damage to DNA in human HCT15 and CO115 cells.DNA repair by MGMT, but not AAG, causes a threshold in alkylation-induced colorectal carcinogenesis.The MUTYH base excision repair gene protects against inflammation-associated colorectal carcinogenesis The Mbd4 DNA glycosylase protects mice from inflammation-driven colon cancer and tissue injury.Colon carcinogenesis in wild type and immune compromised mice after treatment with azoxymethane, and azoxymethane with dextran sodium sulfate.Does increase in DNA repair allow "tolerance-to-insult" in chemical carcinogenesis? Skin tumor experiments with MGMT-overexpressing mice.Persistence of DNA adducts, hypermutation and acquisition of cellular resistance to alkylating agents in glioblastoma.

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Both base excision repair and O6-methylguanine-DNA methyltransferase protect against methylation-induced colon carcinogenesis

http://www.wikidata.org/entity/Q34132791

description

2010 nî lūn-bûn

@nan

2010 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի օգոստոսին հրատարակված գիտական հոդված

@hy

2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

Both base excision repair and ...... n-induced colon carcinogenesis

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Both base excision repair and ...... n-induced colon carcinogenesis

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Both base excision repair and ...... n-induced colon carcinogenesis

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type

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Both base excision repair and ...... n-induced colon carcinogenesis

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Both base excision repair and ...... n-induced colon carcinogenesis

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Both base excision repair and ...... n-induced colon carcinogenesis

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Both base excision repair and ...... n-induced colon carcinogenesis

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Both base excision repair and ...... n-induced colon carcinogenesis

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Both base excision repair and ...... n-induced colon carcinogenesis

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Both base excision repair and ...... n-induced colon carcinogenesis

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Bernd Kaina

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Georg Nagel

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Leona D Samson

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Leonid Eshkind

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Markus F Neurath

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Inactivation of the mouse Msh2 gene results in mismatch repair deficiency, methylation tolerance, hyperrecombination, and predisposition to cancer

Separation of killing and tumorigenic effects of an alkylating agent in mice defective in two of the DNA repair genes

Re-evaluating the role of dacarbazine in metastatic melanoma: what have we learned in 30 years?

Processed meat and colorectal cancer: a review of epidemiologic and experimental evidence.

DNA adduct formation from tobacco-specific N-nitrosamines.

Total N-nitroso compounds and their precursors in hot dogs and in the gastrointestinal tract and feces of rats and mice: possible etiologic agents for colon cancer.

Meat consumption and colorectal cancer: a review of epidemiologic evidence.

The adaptive imbalance in base excision-repair enzymes generates microsatellite instability in chronic inflammation.

Base excision repair in nuclear and mitochondrial DNA.

Haem, not protein or inorganic iron, is responsible for endogenous intestinal N-nitrosation arising from red meat.

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