摘要
选定的转录因子通过调节控制应对压力条件所需适应性的基因表达,在生物体生存中发挥关键作用。与 E2F 转录因子家族结合的成视网膜细胞瘤 (Rb) 蛋白被证明在冷冻和相关环境压力(缺氧、脱水)期间控制细胞周期中起作用。不同位点的 Rb 磷酸化或乙酰化提供了一种抑制细胞增殖的机制,在面临破坏细胞能量学或细胞体积控制的压力的动物中,该机制受 E2F 转录因子的控制。细胞周期的其他中央调节剂,包括细胞周期蛋白、细胞周期蛋白依赖性激酶 (Cdks) 和检查点蛋白,可检测 DNA 损伤或任何不正确的复制,阻止细胞周期的进一步进展并中断细胞增殖。这篇综述深入探讨了细胞周期控制的分子调控机制,重点关注 Rb-E2F 以及通常参与发育和分化的细胞周期蛋白-Cdk 复合物,这些复合物需要受到调控才能在极端细胞压力下生存。
关键词: 细胞周期、视网膜母细胞瘤、E2F 转录因子、染色质重塑、细胞周期蛋白-Cdk、压力。
Current Molecular Medicine
Title:The Role of Retinoblastoma Protein in Cell Cycle Regulation: An Updated Review
Volume: 21 Issue: 8
关键词: 细胞周期、视网膜母细胞瘤、E2F 转录因子、染色质重塑、细胞周期蛋白-Cdk、压力。
摘要: Selected transcription factors have critical roles to play in organism survival by regulating the expression of genes that control the adaptations needed to handle stress conditions. The retinoblastoma (Rb) protein coupled with the E2F transcription factor family was demonstrated to have roles in controlling the cell cycle during freezing and associated environmental stresses (anoxia, dehydration). Rb phosphorylation or acetylation at different sites provides a mechanism for repressing cell proliferation that is under the control of E2F transcription factors in animals facing stresses that disrupt cellular energetics or cell volume controls. Other central regulators of the cell cycle including Cyclins, Cyclin-dependent kinases (Cdks), and checkpoint proteins detect DNA damage or any improper replication, blocking further progression of cell cycle and interrupting cell proliferation. This review provides an insight into the molecular regulatory mechanisms of cell cycle control, focusing on Rb-E2F along with Cyclin-Cdk complexes typically involved in development and differentiation that need to be regulated in order to survive extreme cellular stress.
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Cite this article as:
The Role of Retinoblastoma Protein in Cell Cycle Regulation: An Updated Review, Current Molecular Medicine 2021; 21 (8) . https://dx.doi.org/10.2174/1566524020666210104113003
DOI https://dx.doi.org/10.2174/1566524020666210104113003 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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