Tobacco cigarette nicotine and its metabolite 4-(methylnitrosamino)-1-(3-pyridy1)-1-butanone (NNK) induced normal breast epithelial cells transformation through activation of the a9-nicotinic acetylcholine receptor-mediated signaling pathways

Ho Y. S.; Fattah F. -S. Abdul

首页> 外文期刊>Toxicology Letters: An International Journal Providing a Forum for Original and Pertinent Contributions in Toxicology Research >Tobacco cigarette nicotine and its metabolite 4-(methylnitrosamino)-1-(3-pyridy1)-1-butanone (NNK) induced normal breast epithelial cells transformation through activation of the a9-nicotinic acetylcholine receptor-mediated signaling pathways

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Tobacco cigarette nicotine and its metabolite 4-(methylnitrosamino)-1-(3-pyridy1)-1-butanone (NNK) induced normal breast epithelial cells transformation through activation of the a9-nicotinic acetylcholine receptor-mediated signaling pathways

机译：烟草香烟尼古丁及其代谢物4-（甲基亚氨基氨基）-1-（3-Pyridy1）-1-丁酮（NNK）通过激活A9烟碱乙酰胆碱受体介导的信号传导途径诱导正常乳腺上皮细胞转化

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来源
《Toxicology Letters: An International Journal Providing a Forum for Original and Pertinent Contributions in Toxicology Research》 |2018年第2018期|共1页
作者
Ho Y. S.; Fattah F. -S. Abdul;
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Taipei Med Univ Grad Inst Med Sci Taipei Taiwan;

Taipei Med Univ Grad Inst Med Sci Taipei Taiwan;

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正文语种 eng
中图分类毒物学（毒理学）;
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1. Tobacco cigarette nicotine and its metabolite 4-(methylnitrosamino)-1-(3-pyridy1)-1-butanone (NNK) induced normal breast epithelial cells transformation through activation of the a9-nicotinic acetylcholine receptor-mediated signaling pathways [J] . Ho Y. S., Fattah F. -S. Abdul Toxicology Letters: An International Journal Providing a Forum for Original and Pertinent Contributions in Toxicology Research . 2018,第期

机译：烟草香烟尼古丁及其代谢物4-（甲基亚氨基氨基）-1-（3-Pyridy1）-1-丁酮（NNK）通过激活A9烟碱乙酰胆碱受体介导的信号传导途径诱导正常乳腺上皮细胞转化
2. Long-term exposure to extremely low-dose of nicotine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) induce non-malignant breast epithelial cell transformation through activation of the a9-nicotinic acetylcholine receptor-mediated signaling pathway [J] . Fararjeh Abdul-Fattah Salah, Tu Shih-Hsin, Chen Li-Ching, Environmental toxicology . 2019,第1a2期

机译：长期暴露于极低剂量的尼古丁和4-（甲基亚硝胺基）-1-（3-吡啶基）-1-丁酮（NNK）通过激活a9-烟碱乙酰胆碱受体-诱导非恶性乳腺上皮细胞转化
3. Tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) induces cell proliferation in normal human bronchial epithelial cells through NFkappaB activation and cyclin D1 up-regulation. [J] . Ho YS, Chen CH, Wang YJ, Toxicology and Applied Pharmacology . 2005,第2期

机译：烟草特异性致癌物4-（甲基亚硝胺基）-1-（3-吡啶基）-1-丁酮（NNK）通过NFkappaB激活和细胞周期蛋白D1上调诱导正常人支气管上皮细胞中的细胞增殖。
4. Cationic polystyrene nanosphere induces autophagy through inhibition of the Akt/mTOR and activation of the AMPK signaling pathways in macrophage and epithelial cells [C] . Hui-Wen Chiu, Tian Xia, Jui-Chen Tsai, Annual NSTI nanotechnology conference and expo . 2013

机译：阳离子聚苯乙烯纳米球通过抑制Akt / mTOR和激活巨噬细胞和上皮细胞中的AMPK信号通路来诱导自噬
5. Stereo- and regioselectivity in the cytochrome P450-mediated metabolism of the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). [D] . Jalas, John Raymond. 2003

机译：烟草特异性亚硝胺4-（甲基亚硝胺基）-1-（3-吡啶基）-1-丁酮（NNK）在细胞色素P450介导的代谢中的立体选择性和区域选择性。
6. Cigarette toxin 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) induces experimental pancreatitis through α7 nicotinic acetylcholine receptors (nAChRs) in mice [O] . A. A. Alahmari, B. Sreekumar, V. Patel, 2012

机译：香烟毒素4-（甲基亚硝胺基）-1-（3-吡啶基）-1-丁酮（NNK）通过α7烟碱乙酰胆碱受体（nAChRs）诱导小鼠实验性胰腺炎
7. Stereoselective metabolism and tissue retention in rats of the individual enantiomers of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), metabolites of the tobacco-specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) [O] . C. L. Zimmerman 2004

机译：大鼠中4-（甲基亚硝基氨基）-1-（3-吡啶基）-1-丁醇（NNaL）的单个对映体的立体选择性代谢和组织保留，烟草特异性亚硝胺的代谢物，4-（甲基亚硝基氨基）-1-（ 3-吡啶基）-1-丁酮（NNK）

Tobacco cigarette nicotine and its metabolite 4-(methylnitrosamino)-1-(3-pyridy1)-1-butanone (NNK) induced normal breast epithelial cells transformation through activation of the a9-nicotinic acetylcholine receptor-mediated signaling pathways

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