蛋白激酶C-δ参与DNA损伤诱导的细胞凋亡。
Involvement of protein kinase C-delta in DNA damage-induced apoptosis.
作者信息
Basu Alakananda
机构信息
Department of Molecular Biology & Immunology, University of North Texas Health Science Center, Fort Worth, Texas 76107, USA.
出版信息
J Cell Mol Med. 2003 Oct-Dec;7(4):341-50. doi: 10.1111/j.1582-4934.2003.tb00237.x.
Apoptosis is a highly orchestrated cell suicidal program required to maintain a balance between cell proliferation and cell death. A defect in apoptotic machinery can cause cancer. Many anticancer drugs are known to kill tumor cells by inducing apoptosis, and a defect in apoptosis can lead to anticancer drug resistance. Apoptosis is regulated by a complex cellular signaling network. Several members of the protein kinase C (PKC) family serve as substrates for caspases and PKCdelta isozyme has been intimately associated with DNA damage-induced apoptosis. It can act both upstream and downstream of caspases. In response to apoptotic stimuli, the full-length and the catalytic fragment of PKCdelta may translocate to distinct cellular compartments, including mitochondria and the nucleus, to reach their targets. Both activation and intracellular distribution of PKCdelta may have significant impact on apoptosis. This review intends to assimilate recent views regarding the involvement of PKCdelta in DNA damage-induced apoptosis.
细胞凋亡是一种高度有序的细胞自杀程序，对于维持细胞增殖与细胞死亡之间的平衡至关重要。凋亡机制的缺陷可导致癌症。已知许多抗癌药物通过诱导细胞凋亡来杀死肿瘤细胞，而凋亡缺陷可导致抗癌药物耐药性。细胞凋亡受复杂的细胞信号网络调控。蛋白激酶C（PKC）家族的几个成员作为半胱天冬酶的底物，PKCδ同工酶与DNA损伤诱导的细胞凋亡密切相关。它可在半胱天冬酶的上游和下游发挥作用。响应凋亡刺激时，PKCδ的全长和催化片段可能会转移到不同的细胞区室，包括线粒体和细胞核，以到达其靶点。PKCδ的激活和细胞内分布可能对细胞凋亡产生重大影响。本综述旨在综合有关PKCδ参与DNA损伤诱导细胞凋亡的最新观点。
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