Baculovirus Regulation of Apoptosis

Lois K. Miller, William J. Kaiser, Somasekar Seshagiri
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引用次数: 30

Abstract

The baculovirus AcMNPV induces apoptosis in a host-specific manner which involves the activation of host caspases (cysteine-dependent, aspartate-specific proteases). AcMNPV carries a novel gene, p35, which encodes a stoichiometric inhibitor of active caspases, thereby blocking apoptosis. P35 is cleaved by caspases and the cleavage products form a stable complex with the caspase. Baculoviruses also carry genes known as iaps (inhibitors of apoptosis), some of which can actively suppress apoptosis by inhibiting the activation of caspases. Members of the IAP family are found in both viral and animal genomes and interact physically with a variety of proteins associated with apoptotic pathways including Reaper, Doom, TRAF2, and some caspases. The ability of baculoviruses to block apoptosis influences their pathogenicity and host range.

杆状病毒调控细胞凋亡
杆状病毒AcMNPV以宿主特异性方式诱导细胞凋亡,涉及宿主半胱天冬酶(半胱氨酸依赖,天冬氨酸特异性蛋白酶)的激活。AcMNPV携带一个新的基因p35,该基因编码活性半胱天冬酶的化学计量抑制剂,从而阻断细胞凋亡。P35被半胱天冬酶裂解,裂解产物与半胱天冬酶形成稳定的复合物。杆状病毒还携带iaps(细胞凋亡抑制剂)基因,其中一些基因可以通过抑制半胱天蛋白酶的激活来积极抑制细胞凋亡。IAP家族成员存在于病毒和动物基因组中,并与多种与凋亡途径相关的蛋白质相互作用,包括Reaper、Doom、TRAF2和一些半胱天冬酶。杆状病毒阻断细胞凋亡的能力影响其致病性和宿主范围。
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