期刊文献+

酪蛋白激酶2相互作用蛋白1在心肌缺血再灌注损伤中的作用

下载PDF
导出
摘要 酪蛋白激酶2相互作用蛋白1(CKIP-1)是一种特殊的调控蛋白,自身不具有酶的活性,但是它通过其自身特殊的结构域或模体与其他蛋白质、脂质进行相互作用,因此具有很多非常重要的生物学功能,在癌变,凋亡等许多细胞行为中发挥着重要作用。心肌缺血再灌注损伤机制可能涉及细胞凋亡、炎性反应、钙离子超载、线粒体损伤、能量代谢障碍、氧自由基过度释放等^([1])。我们就CKIP-1参与调节心肌缺血再灌注损伤这一过程进行综述。
出处 《中华老年心脑血管病杂志》 CAS 北大核心 2019年第10期1099-1100,共2页 Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
基金 国家自然科学基金(8167020029)
  • 相关文献

参考文献2

二级参考文献54

  • 1Martinez FO, Helming L, Gordon S. Alternative activation of macrophages: an immunologic functional perspective. Annu Rev Immunol2009; 27:451-483.
  • 2Hamilton JA. Colony-stimulating factors in inflammation and autoimmunity. Nat Rev Immunol2008; 8:533-544.
  • 3Chitu V, Stanley ER. Colony-stimulating factor-l in immunity and inflammation. Curr Opin Immunol2006; 18:39-48.
  • 4Stanley ER, Berg KL, Einstein DB, et al. Biology and action of colony-stimulating factor-I. Mol Reprod Dev 1997; 46:4- 10.
  • 5Wiktor-Jedrzejczak W, Ratajczak MZ, Ptasznik A, Sell KW, Ahmed-Ansari A, Ostertag W. CSF-l deficiency in the op/op mouse has differential effects on macrophage populations and differentiation stages. Exp Hematol1992; 20: 1004-10 1 O.
  • 6Hamilton JA. CSF-l signal transduction. J Leukoc Biol 1997; 62:145-155.
  • 7Pixley FJ, Stanley ER. CSF-l regulation of the wandering macrophage: complexity in action. Trends Cell Biol 2004; 14:628-638.
  • 8Lee AW, States DJ. Colony-stimulating factor-l requires PI3- kinase-mediated metabolism for proliferation and survival in myeloid cells. Cell Death Differ 2006; 13: 1900-1914.
  • 9Smith JL, Schaffner AE, Hofmeister JK, et al. ets-2 is a target for an akt (protein kinase B)/jun N-terminal kinase signaling pathway in macrophages of motheaten-viable mutant mice. Mol Cell Biol 2000; 20:8026-8034.
  • 10Lee AW. Synergistic activation of mitogen-activated protein kinase by cyclic AMP and myeloid growth factors opposes cyclic AMP's growth-inhibitory effects. Blood 1999; 93:537- 553.

共引文献8

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部