PREMATURE P34(CDC2) ACTIVATION REQUIRED FOR APOPTOSIS
PREMATURE P34(CDC2) ACTIVATION REQUIRED FOR APOPTOSIS
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DOI：
10.1126/science.8108732
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发表时间：
1994-02-25
期刊：
影响因子：
56.9
通讯作者：
GREENBERG, AH
中科院分区：
文献类型：
--
作者：
SHI, L;NISHIOKA, WK;GREENBERG, AH
丝氨酸-苏氨酸激酶p34 cdc 2在细胞周期中的不适当时间激活导致类似于凋亡的细胞死亡。p34 cdc 2的过早激活被证明是由淋巴细胞颗粒蛋白酶诱导的细胞凋亡所必需的。在细胞凋亡开始时，激酶被迅速激活，酪氨酸去磷酸化。DNA断裂和核崩溃可以通过阻断p34 cdc 2活性与过量的肽底物，或通过失活p34 cdc 2在温度敏感的突变体。p34 cdc 2过早激活可能是诱导细胞凋亡引发细胞核破裂的一般机制。
Activation of the serine-threonine kinase p34cdc2 at an inappropriate time during the cell cycle leads to cell death that resembles apoptosis. Premature activation of p34cdc2 was shown to be required for apoptosis induced by a lymphocyte granule protease. The kinase was rapidly activated and tyrosine dephosphorylated at the initiation of apoptosis. DNA fragmentation and nuclear collapse could be prevented by blocking p34cdc2 activity with excess peptide substrate, or by inactivating p34cdc2 in a temperature-sensitive mutant. Premature p34cdc2 activation may be a general mechanism by which cells induced to undergo apoptosis initiate the disruption of the nucleus.