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Hypoxia-inducible factor 1{alpha} is a new target of microphthalmia-associated transcription factor (MITF) in melanoma cells
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Buscà R Berra E Gaggioli C Khaled M Bille K Marchetti B Thyss R Fitsialos G Larribère L Bertolotto C Virolle T Barbry P Pouysségur J Ponzio G Ballotti R 《The Journal of cell biology》2005,170(1):49-59
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c-Met expression is regulated by Mitf in the melanocyte lineage 总被引:5,自引:0,他引:5
McGill GG Haq R Nishimura EK Fisher DE 《The Journal of biological chemistry》2006,281(15):10365-10373
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Bcl2 regulation by the melanocyte master regulator Mitf modulates lineage survival and melanoma cell viability 总被引:25,自引:0,他引:25
McGill GG Horstmann M Widlund HR Du J Motyckova G Nishimura EK Lin YL Ramaswamy S Avery W Ding HF Jordan SA Jackson IJ Korsmeyer SJ Golub TR Fisher DE 《Cell》2002,109(6):707-718
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Huber WE Price ER Widlund HR Du J Davis IJ Wegner M Fisher DE 《The Journal of biological chemistry》2003,278(46):45224-45230
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Sanchez Mas J Martijnez-Esparza M Bastida CM Solano F Penafiel R Garcija-Borron JC 《Biochimica et biophysica acta》2002,1542(1-3):57-65
Ornithine decarboxylase (ODC) is the rate-limiting enzyme in the biosynthesis of polyamines, a family of cationic compounds required for optimal cell proliferation and differentiation. Within mammalian melanocytes, the expression of genes regulating cell growth and/or differentiation can be controlled by alpha-melanocyte-stimulating hormone (alphaMSH) and other melanogenesis modulating agents. In the B16 mouse melanoma model, alphaMSH stimulates melanogenesis by upmodulation of tyrosinase (tyr) activity, whereas the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) inhibits melanin synthesis. Therefore, we analyzed the regulation of ODC by these agents, as related to changes in the melanogenic pathway. Treatment of B16 cells with TPA or alphaMSH rapidly stimulated ODC activity. The effect was stronger for TPA and appeared mainly posttranslational. Irreversible inhibition of ODC with the active site-directed inhibitor alpha-difluoromethylornithine (DFMO) did not block TPA-mediated inhibition of tyr. Conversely, prolonged treatment of B16 cells with DFMO stimulated tyr activity by a posttranslational mechanism, probably requiring polyamine depletion. Combination treatment with alphaMSH and DFMO synergistically activated tyr. Therefore, ODC induction is not involved in the melanogenic response of B16 cells to alphaMSH. Rather, increased intracellular concentrations of polyamines following ODC induction might constitute a feedback mechanism to limit melanogenesis activation by alphaMSH. 相似文献
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