2-Aminopurine overrides a late telophase delay created by ectopic expression of the PITSLRE beta 1 protein kinase.
2-Aminopurine overrides a late telophase delay created by ectopic expression of the PITSLRE beta 1 protein kinase.
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2-氨基嘌呤可以克服 PITSLRE beta 1 蛋白激酶异位表达造成的末期晚期延迟。
DOI：
10.1006/bbrc.1994.1353
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发表时间：
1994
影响因子：
3.1
通讯作者：
Kidd,VJ
中科院分区：
文献类型：
--
作者：
Xiang,J;Lahti,JM;Kidd,VJ
CHO细胞中PITSLREβ1蛋白激酶的最小过表达导致晚期有丝分裂显著延迟。我们以前已经表明，这种延迟的特点是存在大量增加的微管蛋白中间体，抑制胞质分裂，和许多多核和微核细胞。其他研究表明，蛋白激酶抑制剂2-氨基嘌呤（2-AP）能够克服药物诱导的细胞周期阻滞。在这项研究中，我们证明了由PITSLREβ1蛋白激酶异位表达引起的晚期有丝分裂延迟和细胞形态改变可以通过2-氨基嘌呤治疗来克服。此外，2-氨基嘌呤在体内抑制PITSLREβ1蛋白激酶活性，但不影响p34 cdc 2蛋白激酶活性。
Minimal overexpression of the PITSLREβ1 protein kinase in CHO cells to a marked delay in late mitosis. We have previously shown that this delay is characterized by the presence of substantially increased numbers of tubulin midbodies, inhibition of cytokinesis, and numerous multinucleated and micronucleated cells. Others have shown that the protein kinase inhibitor 2-aminopurine (2-AP) is capable of overriding drug induced cell cycle blocks. In this study we demonstrate that the late mitotic delay and altered cellular morphology caused by ectopic expression of the PITSLREβ1 protein kinase can be overcome by 2-aminopurine treatment. Furthermore, 2-aminopurine inhibits PITSLREβ1 protein kinase activityin vivo, but does not effect p34cdc2protein kinase activity in a similar manner.