Shiseki Masayuki, Nagashima Makoto, Pedeux Remy M, Kitahama-Shiseki Mariko, Miura Koh, Okamura Shu, Onogi Hitoshi, Higashimoto Yuichiro, Appella Ettore, Yokota Jun, Harris Curtis C
Laboratories of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892-4255, USA.
Cancer Res. 2003 May 15;63(10):2373-8.
We identified and characterized two new ING family genes, p29ING4 and p28ING5,coding for two proteins of 249 and 240 amino acids, respectively. Both p29ING4 and p28ING5 proteins have a plant homeodomain finger motif also found in other ING proteins, and which is common in proteins involved in chromatin remodeling. p29ING4 or p28ING5 overexpression resulted in a diminished colony-forming efficiency, a decreased cell population in S phase, and the induction of apoptosis in a p53-dependent manner. Both p29ING4 and p28ING5 activate the p21/waf1 promoter, and induce p21/WAF1 expression. p29ING4 and p28ING5 enhance p53 acetylation at Lys-382 residues, and physically interact with p300, a member of histone acetyl transferase complexes, and p53 in vivo. These results indicate that p29ING4 and p28ING5 may be significant modulators of p53 function.
我们鉴定并表征了两个新的ING家族基因,即p29ING4和p28ING5,它们分别编码由249个和240个氨基酸组成的两种蛋白质。p29ING4和p28ING5蛋白均具有一个植物同源异型域手指基序,该基序也存在于其他ING蛋白中,并且在参与染色质重塑的蛋白质中很常见。p29ING4或p28ING5的过表达导致集落形成效率降低、S期细胞数量减少,并以p53依赖的方式诱导细胞凋亡。p29ING4和p28ING5均激活p21/waf1启动子,并诱导p21/WAF1表达。p29ING4和p28ING5增强p53在赖氨酸382残基处的乙酰化,并在体内与组蛋白乙酰转移酶复合物成员p300和p53发生物理相互作用。这些结果表明,p29ING4和p28ING5可能是p53功能的重要调节因子。