胰岛素样生长因子I受体作为p53在白细胞介素-3撤除诱导的细胞凋亡中的生理相关靶点。
The insulin-like growth factor I receptor as a physiologically relevant target of p53 in apoptosis caused by interleukin-3 withdrawal.
作者信息
Prisco M, Hongo A, Rizzo M G, Sacchi A, Baserga R
机构信息
Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
出版信息
Mol Cell Biol. 1997 Mar;17(3):1084-92. doi: 10.1128/MCB.17.3.1084.
Abstract
The wild-type p53 protein is known to modulate apoptosis induced in 32D murine hemopoietic cells by interleukin-3 withdrawal. In 32D cells and in 32D cells constitutively expressing a temperature-sensitive mutant of p53 (32Dtsp53), overexpression of a wild-type (but not a mutant) insulin-like growth factor I receptor (IGF-IR) protects these cells from apoptosis. A tsp53 in its wild-type conformation causes a decrease in the levels of IGF-IRs, and this decrease is accompanied by increased sensitivity of these cells to apoptosis. However, when the expression of the IGF-IR cDNA is regulated by a viral promoter, IGF-IR levels are not decreased by a wild-type p53, and apoptosis does not occur. These findings show that, in 32Dtsp53 cells, the IGF-IR is a physiologically relevant target of p53 in the process of apoptosis.
摘要
已知野生型p53蛋白可调节因白细胞介素-3撤除而在32D小鼠造血细胞中诱导的细胞凋亡。在32D细胞以及组成性表达p53温度敏感突变体的32D细胞（32Dtsp53）中，野生型（而非突变型）胰岛素样生长因子I受体（IGF-IR）的过表达可保护这些细胞免于凋亡。处于野生型构象的tsp53会导致IGF-IR水平降低，而这种降低伴随着这些细胞对凋亡的敏感性增加。然而，当IGF-IR cDNA的表达受病毒启动子调控时，野生型p53不会降低IGF-IR水平，细胞凋亡也不会发生。这些发现表明，在32Dtsp53细胞中，IGF-IR是p53在细胞凋亡过程中的一个生理相关靶点。
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