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组蛋白去乙酰化酶3研究进展(4)
http://www.100md.com 2017年7月23日 《健康周刊》 201729
     [25]Saad M I, Abdelkhalek T M, Saleh M M, et al. Insights into the molecular mechanisms of diabetes-induced endothelial dysfunction: focus on oxidative stress and endothelial progenitor cells.[J]. Endocrine, 2015, 50(3):537-567.

    [26]Fernandesfreitas I, Owen B M. Metabolic roles of endocrine fibroblast growth factors.[J]. Current Opinion in Pharmacology, 2015, 25:30.

    [27]Gourlaouen M, Welti J C, Vasudev N S, et al. Essential Role for Endocytosis in the Growth Factor-stimulated Activation of ERK1/2 in Endothelial Cells[J]. Journal of Biological Chemistry, 2013, 288(11):7467.

    [28]Kaluza D, Kroll J, Gesierich S, et al. Class IIb HDAC6 regulates endothelial cell migration and angiogenesis by deacetylation of cortactin[J]. Embo Journal, 2011, 30(20):4142.

    [29]Jeon H W, Lee Y M. Inhibition of histone deacetylase attenuates hypoxia-induced migration and invasion of cancer cells via the restoration of RECK expression.[J]. Molecular Cancer Therapeutics, 2010, 9(5):1361.

    [30]Li D, Xie S, Ren Y, et al. Microtubule-associated deacetylase HDAC6 promotes angiogenesis by regulating cell migration in an EB1-dependent manner[J]. Protein & Cell, 2011, 2(2):150-160.

    基金項目:

    温州医科大学本专科学生科研项目(wyx2017101014)

    通讯作者:

    金利泰,教授, http://www.100md.com(张思怡 梁洋志 吕淑楠 朱坤选 金利泰)
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