细胞生物学
核板
上睑下垂
内膜
核膜
程序性细胞死亡
染色质
细胞质
核蛋白
核定位序列
生物
细胞核
死亡相关蛋白6
核DNA
DNA损伤
核心
核运输
胞浆
拉明
细胞凋亡
转录因子
DNA
生物化学
线粒体
基因
线粒体DNA
酶
作者
Weidong Chen,Jiin Byun,Han Chang Kang,Hye Suk Lee,Joo Young Lee,Young Jik Kwon,Yong‐Yeon Cho
标识
DOI:10.1080/10715762.2024.2433986
摘要
Karyoptosis is a type of regulated cell death (RCD) characterized by explosive nuclear rupture caused by a loss of nuclear membrane integrity, resulting in the release of genomic DNA and other nuclear components into the cytosol and extracellular environment. The mechanism underlying karyoptosis involves a delicate balance between the following forces: the expansion force exerted by the tightly packed DNA in the nucleus, the resistance provided by the nuclear lamina at the inner nuclear membrane (INM), and the tensile force from the cytoskeleton that helps position the nucleus at the center of the cytoplasm, allowing it to remain maximally expanded. In addition, CREB3, a type II integral membrane protein with DNA-binding ability, tethers chromatin to the INM, providing a tightening force through chromatin interactions that prevent nuclear membrane rupture. UVB radiation can trigger this process, inducing CREB3-FL cleavage and producing CREB3-CF. Therefore, UVB acts as an intrinsic factor in the induction of karyoptosis. Importantly, biochemical analysis of RCD markers shows that karyoptosis is distinct from other forms of cell death, such as apoptosis, autophagy, necroptosis, and pyroptosis. This review explores the mechanisms involved in maintaining nuclear membrane integrity and the role of CREB3 in triggering karyoptosis and provides brief suggestions on the potential implications for targeting cancer cells.
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