کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2833483 | 1163873 | 2007 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Cigarette tar phenols impede T cell cycle progression by inhibiting cyclin-dependent kinases
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کلمات کلیدی
CDKPBMCCATSTIMStimulatedHuman - انسانCell differentiation - تمایز سلولیCell proliferation - تکثیر سلولیperipheral blood mononuclear cells - سلول های تک هسته ای خون محیطیT cells - سلول های تیCell activation - فعال سازی سلولPhenol - فنل Phen - فینHydroquinone - هیدروکینونCatechol - کاتچولcyclin-dependent kinases - کیناز وابسته به سیکلین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شناسی مولکولی
پیش نمایش صفحه اول مقاله
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چکیده انگلیسی
Cigarette smoking causes profound suppression of pulmonary T cell responses, which is associated with increased susceptibility to respiratory tract infections and decreased tumor surveillance. We previously demonstrated that the phenolic compounds in cigarette tar inhibit blastogenesis and interfere with human T cell cycle progression. To identify the mechanism by which cell cycle arrest occurs, we examined the effects of these compounds on cyclin-dependent kinases (Cdk) that control the G0/G1 transition. We found that hydroquinone inhibited induction of Cdk4 and Cdk6 kinase activities by >80%, while catechol and phenol were markedly less potent. HQ did not affect mitogenic induction of the Cdk6 protein, but inhibited expression of cyclin D3 by >90% resulting in a dramatic reduction in proper Cdk6/Cyclin D3 complex formation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Immunology - Volume 44, Issue 4, January 2007, Pages 488-493
Journal: Molecular Immunology - Volume 44, Issue 4, January 2007, Pages 488-493
نویسندگان
Ashley A. Frazer-Abel, Jesica M. McCue, Sabine Lazis, Mary Portas, Cherie Lambert, Brian M. Freed,