期刊
ONCOGENESIS
卷 9, 期 9, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41389-020-00266-y
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资金
- Breast Cancer Research Program [W81XWH1810605]
- Wistar Cancer Center Support Grant [P30 CA10815, R01CA188575]
- [R01CA132115]
The essential G(1)-cyclin,CCND1, is a collaborative nuclear oncogene that is frequently overexpressed in cancer. D-type cyclins bind and activate CDK4 and CDK6 thereby contributing to G(1)-S cell-cycle progression. In addition to the nucleus, herein cyclin D1 was also located in the cytoplasmic membrane. In contrast with the nuclear-localized form of cyclin D1 (cyclin D1(NL)), the cytoplasmic membrane-localized form of cyclin D1 (cyclin D1(MEM)) induced transwell migration and the velocity of cellular migration. The cyclin D1(MEM)was sufficient to induce G(1)-S cell-cycle progression, cellular proliferation, and colony formation. The cyclin D1(MEM)was sufficient to induce phosphorylation of the serine threonine kinase Akt (Ser473) and augmented extranuclear localized 17 beta-estradiol dendrimer conjugate (EDC)-mediated phosphorylation of Akt (Ser473). These studies suggest distinct subcellular compartments of cell cycle proteins may convey distinct functions.
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