ベンツピレンジオールエポキシド
WordNet
- any of a class of alcohols having 2 hydroxyl groups in each molecule (同)glycol, dihydric_alcohol
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English Journal
- Variants of mouse DNA polymerase κ reveal a mechanism of efficient and accurate translesion synthesis past a benzo[a]pyrene dG adduct.
- Liu Y1, Yang Y, Tang TS, Zhang H, Wang Z, Friedberg E, Yang W, Guo C.Author information 1Laboratory of Cancer Genomics and Individualized Medicine, Beijing Institute of Genomics and State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China.AbstractDNA polymerase κ (Polκ) is the only known Y-family DNA polymerase that bypasses the 10S (+)-trans-anti-benzo[a]pyrene diol epoxide (BPDE)-N(2)-deoxyguanine adducts efficiently and accurately. The unique features of Polκ, a large structure gap between the catalytic core and little finger domain and a 90-residue addition at the N terminus known as the N-clasp, may give rise to its special translesion capability. We designed and constructed two mouse Polκ variants, which have reduced gap size on both sides [Polκ Gap Mutant (PGM) 1] or one side flanking the template base (PGM2). These Polκ variants are nearly as efficient as WT in normal DNA synthesis, albeit with reduced accuracy. However, PGM1 is strongly blocked by the 10S (+)-trans-anti-BPDE-N(2)-dG lesion. Steady-state kinetic measurements reveal a significant reduction in efficiency of dCTP incorporation opposite the lesion by PGM1 and a moderate reduction by PGM2. Consistently, Polκ-deficient cells stably complemented with PGM1 GFP-Polκ remained hypersensitive to BPDE treatment, and complementation with WT or PGM2 GFP-Polκ restored BPDE resistance. Furthermore, deletion of the first 51 residues of the N-clasp in mouse Polκ (mPolκ(52-516)) leads to reduced polymerization activity, and the mutant PGM2(52-516) but not PGM1(52-516) can partially compensate the N-terminal deletion and restore the catalytic activity on normal DNA. However, neither WT nor PGM2 mPolκ(52-516) retains BPDE bypass activity. We conclude that the structural gap physically accommodates the bulky aromatic adduct and the N-clasp is essential for the structural integrity and flexibility of Polκ during translesion synthesis.
- Proceedings of the National Academy of Sciences of the United States of America.Proc Natl Acad Sci U S A.2014 Feb 4;111(5):1789-94. doi: 10.1073/pnas.1324168111. Epub 2014 Jan 21.
- DNA polymerase κ (Polκ) is the only known Y-family DNA polymerase that bypasses the 10S (+)-trans-anti-benzo[a]pyrene diol epoxide (BPDE)-N(2)-deoxyguanine adducts efficiently and accurately. The unique features of Polκ, a large structure gap between the catalytic core and little finger domain an
- PMID 24449898
- Interaction of benzo[a]pyrene with other risk factors in hepatocellular carcinoma: a case-control study in Xiamen, China.
- Su Y1, Zhao B2, Guo F1, Bin Z3, Yang Y1, Liu S1, Han Y1, Niu J4, Ke X5, Wang N6, Geng X7, Jin C7, Dai Y8, Lin Y8.Author information 1State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, School of Public Health, Xiamen University, Fujian, China.2State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, School of Public Health, Xiamen University, Fujian, China. Electronic address: benhuazhao@sina.com.3Organ Transplantation Institute of Xiamen University, Fujian, China.4Xiamen Center for Disease Control and Prevention, Fujian, China.5Institute of Child Health, University College London, London, UK.6Department of Hematology, First Affiliated Hospital of Xiamen University, Fujian, China.7Xiamen Hospital of Traditional Chinese Medicine, Fujian, China.8Digestive System Department of the 174th Hospital of People's Liberation Army, Xiamen, Fujian, China.AbstractPURPOSE: Large epidemiologic studies about the relationship between benzo[a]pyrene (B[a]P) and hepatocellular carcinoma (HCC) have been limited. B[a]P diol epoxide (BPDE) is a highly reactive metabolite of B[a]P that binds covalently to form DNA adducts. We evaluated the interaction between B[a]P exposure with other risk factors in HCC, in a case-control study of 345 HCC and 961 healthy controls.
- Annals of epidemiology.Ann Epidemiol.2014 Feb;24(2):98-103. doi: 10.1016/j.annepidem.2013.10.019. Epub 2013 Nov 9.
- PURPOSE: Large epidemiologic studies about the relationship between benzo[a]pyrene (B[a]P) and hepatocellular carcinoma (HCC) have been limited. B[a]P diol epoxide (BPDE) is a highly reactive metabolite of B[a]P that binds covalently to form DNA adducts. We evaluated the interaction between B[a]P ex
- PMID 24480391
- Rutin inhibits B[a]PDE-induced cyclooxygenase-2 expression by targeting EGFR kinase activity.
- Choi S1, Lim TG, Hwang MK, Kim YA, Kim J, Kang NJ, Jang TS, Park JS, Yeom MH, Lee KW.Author information 1Department of Bioscience and Biotechnology, Konkuk University, Seoul 143-701, Republic of Korea.AbstractRutin is a well-known flavonoid that exists in various natural sources. Accumulative studies have represented the biological effects of rutin, such as anti-oxidative and anti-inflammatory effects. However, the underlying mechanisms of rutin and its direct targets are not understood. We investigated whether rutin reduced B[a]PDE-induced-COX-2 expression. The transactivation of AP-1 and NF-κB were inhibited by rutin. Rutin also attenuated B[a]PDE-induced Raf/MEK/ERK and Akt activation, but had no effect on the phosphorylation of EGFR. An in vitro kinase assay revealed rutin suppressed EGFR kinase activity. We also confirmed direct binding between rutin and EGFR, and found that the binding was regressed by ATP. The EGFR inhibitor also inhibited the B[a]PDE-induced MEK/ERK and Akt signaling pathways and subsequently, suppressed COX-2 expression and promoter activity, in addition to suppressing the transactivation of AP-1 and NF-κB. In EGFR(-/-)mouse embryonic fibroblast cells, B[a]PDE-induced COX-2 expression was also diminished. Collectively, rutin inhibits B[a]PDE-induced COX-2 expression by suppressing the Raf/MEK/ERK and Akt signaling pathways. EGFR appeared to be the direct target of rutin.
- Biochemical pharmacology.Biochem Pharmacol.2013 Nov 15;86(10):1468-75. doi: 10.1016/j.bcp.2013.08.066. Epub 2013 Sep 7.
- Rutin is a well-known flavonoid that exists in various natural sources. Accumulative studies have represented the biological effects of rutin, such as anti-oxidative and anti-inflammatory effects. However, the underlying mechanisms of rutin and its direct targets are not understood. We investigated
- PMID 24021351
Related Links
- Benzopyrene diol epoxide synonyms, Benzopyrene diol epoxide antonyms. Information about Benzopyrene diol epoxide in the free online English dictionary and encyclopedia. Benzopyrene diol epoxide - definition of Benzopyrene ...
- Information about Benzopyrene diol epoxide in Free online English dictionary. What is Benzopyrene diol epoxide? Meaning of Benzopyrene diol epoxide medical term. What does Benzopyrene diol epoxide mean? http://medical ...
★リンクテーブル★
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- 英
- benzpyrene diol epoxide BPDE
- 同
- ベンゾピレンジオールエポキシド benzoapyrene diol epoxide benzopyrene diol epoxide
- 関
- 7,8-ジヒドロ-7,8-ジヒドロキシベンゾピレン-9,10-オキシド
- 体内代謝で生成する発癌性物質