Sit K H, Bay B H, Wong K P
Department of Anatomy, Faculty of Medicine, National University of Singapore, Kent Ridge.
In Vitro Cell Dev Biol Anim. 1993 May;29A(5):395-402. doi: 10.1007/BF02633988.
Cell rounding is generally regarded as a cytoskeletal change exemplified by the mitotic state of monolayer cell cultures in which mitosis-specific phosphorylation was recently cited as the molecular mechanism. Mechanistically, there appears a convergence with earlier suggestions of tyrosyl phosphorylation of cytoskeletal elements in growth-factor-induced rounding inasmuch as protein tyrosine kinase plays a major regulatory role in cell cycle progression. On the other hand, despite the permissive association between cell activation and intracellular alkalinization, inducing rounding via pH upshifts in the presence of even high concentrations (135 micrograms/ml) of a tyrosine specific protein kinase inhibitor, genistein, did not suppress the rounding response, although a distinct difference in phosphotyrosine level was demonstrated by monoclonal antiphosphotyrosine antibodies.
细胞变圆通常被视为一种细胞骨架变化，以单层细胞培养的有丝分裂状态为例，最近有研究认为有丝分裂特异性磷酸化是其分子机制。从机制上讲，这与早期关于生长因子诱导的细胞变圆过程中细胞骨架元件酪氨酸磷酸化的观点有相似之处，因为蛋白质酪氨酸激酶在细胞周期进程中起主要调节作用。另一方面，尽管细胞激活与细胞内碱化之间存在允许性关联，但在存在高浓度（135微克/毫升）酪氨酸特异性蛋白激酶抑制剂染料木黄酮的情况下，通过提高pH值诱导细胞变圆，并没有抑制细胞变圆反应，尽管单克隆抗磷酸酪氨酸抗体显示磷酸酪氨酸水平存在明显差异。
