当前位置: 首页 > 期刊 > 《中国实用医药》 > 2010年第16期
编号:11935974
氯化钆诱导大鼠腹腔巨噬细胞内质网应激和凋亡的研究(3)
http://www.100md.com 2010年6月5日 黄学桂 赵隽
第1页

    参见附件(1966KB,3页)。

     [4] Voeltz G K, Rolls M M, Rapoport T A. Structural organization of the endoplasmic reticulum. EMBO Rep, 2002, 3(10):944-950.

    [5] Hampton R Y. ER-associated degradation in protein quality control and cellular regulation. Curr Opin Cell Biol, 2002,14(4): 476-482.

    [6] Rutkowski D T. A trip to the ER: coping with stress. Trends Cell Biol, 2004, 14(1):20-28.

    [7] Liu CY, et al.Structure and intermolecular interactions of the luminal dimerization domain of human IRE1 alpha. J Biol Chem 2003, 278(20):17680-17687.

    [8] Kadowaki H, et al. Survival and apoptosis signals in ER stress: the role of protein kinases. J Chem Neuroanat,2004, 28(1-2):93-100.

    [9] Brown EM, Bai M, Pollak MR, et al. Familial benign hypocalciuric hypercalcemia and other syndromes of altered responsiveness toextracellular calcium //L V Avioli, S M Krane(Eds.), Metabolic bone disease. New York: Academic Press,1998:12-18.

    [10] Orrenius S,Zhivotovsky B, and Nicotera P. Regulation of cell death: the calcium-apoptosis link. Nat Rev Mol Cell Biol, 2003,4:552-565.

您现在查看是摘要介绍页,详见PDF附件(1966KB,3页)