Cheung K J, Li G
Division of Dermatology, University of British Columbia, Vancouver, British Columbia V6H 3Z6, Canada.
Exp Cell Res. 2001 Aug 1;268(1):1-6. doi: 10.1006/excr.2001.5258.
The biological functions of the tumor suppressor ING1 have been studied extensively in the past 5 years since it was cloned. Of the three alternatively spliced forms of ING1, p24(ING1) has been the focus of much of past research. Information on the other currently known isoforms, p47(ING1), p32(ING1), and p27(ING1), has been lacking. ING1 shares many biological functions with p53. It has been reported to mediate growth arrest, senescence, apoptosis, anchorage-dependent growth, and chemosensitivity. Some of these functions, such as cell-cycle arrest and apoptosis, have been shown to be dependent on the activity of both ING1 and p53 proteins. In this review, we will examine what is known about ING1 up to this point and clarify the cloning errors originating from the isolation of this gene.
自肿瘤抑制因子ING1被克隆以来,在过去5年里其生物学功能得到了广泛研究。ING1的三种可变剪接形式中,p24(ING1)一直是过去许多研究的重点。关于其他目前已知的同工型p47(ING1)、p32(ING1)和p27(ING1)的信息一直缺乏。ING1与p53具有许多生物学功能。据报道,它可介导生长停滞、衰老、凋亡、锚定依赖性生长和化学敏感性。其中一些功能,如细胞周期停滞和凋亡,已被证明依赖于ING1和p53蛋白的活性。在本综述中,我们将审视到目前为止关于ING1的已知情况,并澄清源于该基因分离的克隆错误。