Yen A, Sturgill R
Department of Pathology, Cornell University, Ithaca, New York, 14853, USA.
Exp Cell Res. 1998 Jun 15;241(2):324-31. doi: 10.1006/excr.1998.4007.
The RB tumor suppressor protein is a cell cycle regulator, where hypophosphorylated RB is associated with G1/0 arrest and its cyclin-dependent phosphorylation in G1 allows progression from G1 to S. The present report shows that in human leukemia cells induced to undergo growth arrest with sodium butyrate or DMSO, hypophosphorylation of the RB protein is not G1 restricted and also occurs in S and G2/M cells as well as in G1 cells when growth is inhibited. While all of the RB protein in G1/0 cells is hypophosphorylated, residual cells in S and G2 have significant detectable amounts of hypophosphorylated RB as well as still hyperphosphorylated RB protein. Thus RB hypophosphorylation can be induced in S and G2 as well as the G1 phase. The results show that growth retardation in other than the G1 phase is associated with occurrence of hypophosphorylated RB. RB may thus have a broader capability to inhibit proliferation than just in G1.
视网膜母细胞瘤抑制蛋白是一种细胞周期调节因子，其中低磷酸化的RB与G1/0期停滞相关，其在G1期的细胞周期蛋白依赖性磷酸化允许细胞从G1期进入S期。本报告表明，在用人丁酸钠或二甲基亚砜诱导生长停滞的人白血病细胞中，RB蛋白的低磷酸化并不局限于G1期，在S期、G2/M期细胞以及生长受抑制时的G1期细胞中也会发生。虽然G1/0期细胞中的所有RB蛋白都是低磷酸化的，但S期和G2期的残余细胞中也有大量可检测到的低磷酸化RB以及仍处于高磷酸化状态的RB蛋白。因此，RB的低磷酸化可在S期、G2期以及G1期诱导产生。结果表明，除G1期外的其他时期生长迟缓与低磷酸化RB的出现有关。因此，RB可能具有比仅在G1期更广泛的抑制增殖的能力。
