Tsai S C, Pasumarthi K B, Pajak L, Franklin M, Patton B, Wang H, Henzel W J, Stults J T, Field L J
Krannert Institute of Cardiology and Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, Indiana 46202-5225, USA.
J Biol Chem. 2000 Feb 4;275(5):3239-46. doi: 10.1074/jbc.275.5.3239.
A 193-kDa SV40 large T antigen (T-Ag)-binding protein, designated p193, was identified and cloned. Inspection of the deduced amino acid sequence revealed the presence of a short motif similar to the Bcl-2 homology (BH) domain 3, suggesting that p193 may be a member of a family of apoptosis promoting proteins containing only BH3 motifs. In support of this, p193 expression promoted apoptosis in NIH-3T3 cells. Deletion of the BH3 motif abolished p193 apoptosis activity. p193-induced apoptosis was antagonized by co-expression of Bcl-X(L). Immune cytologic analysis indicated that p193 is localized to the cytoplasm of transfected cells. p193-induced apoptosis was also antagonized by co-expression of T-Ag, which resulted in the cytoplasmic localization of both proteins. The p193 binding site was mapped to an N-terminal region of T-Ag previously implicated in transforming activity. These results suggest that T-Ag possesses an antiapoptosis activity, independent of p53 sequestration, which is actuated by T-Ag/p193 binding in the cytoplasm.
一种分子量为193 kDa的SV40大T抗原(T-Ag)结合蛋白,命名为p193,已被鉴定并克隆。对推导的氨基酸序列进行检查发现,存在一个与Bcl-2同源(BH)结构域3相似的短基序,这表明p193可能是仅包含BH3基序的促凋亡蛋白家族的成员。与此相符的是,p193的表达促进了NIH-3T3细胞的凋亡。BH3基序的缺失消除了p193的凋亡活性。Bcl-X(L)的共表达拮抗了p193诱导的凋亡。免疫细胞分析表明,p193定位于转染细胞的细胞质中。T-Ag的共表达也拮抗了p193诱导的凋亡,这导致两种蛋白都定位于细胞质中。p193的结合位点定位于T-Ag的一个先前与转化活性有关的N端区域。这些结果表明,T-Ag具有一种不依赖于p53隔离的抗凋亡活性,该活性由细胞质中的T-Ag/p193结合激活。