Selkirk J K, Merrick B A, Stackhouse B L, He C
Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709.
Appl Theor Electrophor. 1994;4(1):11-8.
At least eleven isoforms of p53 protein were observed in a human mammary tumor cell line. T47D. Comparative 33P and 35S incorporation analysis showed an equal distribution of P53 isoforms within cytoplasmic and nuclear compartments, although phosphorylation was unequal among isoforms and the most basic p53 species was unphosphorylated. Using a combination of immunoprecipitation with monoclonal antibodies for p53 and heat shock proteins Hsp70 & Hsp90, and two-dimensional gel electrophoretic analysis, T47D p53 protein oligomers were observed with several species of Hsp70 and Hsp90. The p53/Hsp70/Hsp90 aggregate dissociates after nuclear translocation. Immunoprecipitation of Hsp70 and Hsp90 using monoclonal antibodies showed formation of a heteroligomer between Hsp70 and Hsp90 in cytoplasm but not nucleus. This suggests these Hsp proteins can form a complex in the cytoplasm but undergo a conformational change after nuclear translocation such that Hsp/Hsp binding sites are no longer recognized. These data indicate T47D cells have multiple p53 precursor molecules probably at different stages of phosphorylation, and which may be sequestered from proteases by binding to Hsp proteins. Hsp proteins also can heterocomplex in the cytoplasm, also possibly as protection against protease degradation until bound to p53. After translocation, p53 is freed from Hsp proteins for binding to DNA where Hsp70 and Hsp90 are no longer able to form a nuclear complex probably rendering Hsp's labile to proteolysis.
在人乳腺肿瘤细胞系T47D中观察到至少11种p53蛋白异构体。33P和35S掺入的比较分析表明,P53异构体在细胞质和细胞核区室中分布均匀,尽管异构体之间的磷酸化情况不同,且最碱性的p53种类未被磷酸化。通过使用针对p53以及热休克蛋白Hsp70和Hsp90的单克隆抗体进行免疫沉淀,结合二维凝胶电泳分析,在T47D细胞中观察到p53蛋白寡聚体与几种Hsp70和Hsp90种类相关。p53/Hsp70/Hsp90聚集体在核转位后解离。使用单克隆抗体对Hsp70和Hsp90进行免疫沉淀显示,Hsp70和Hsp90在细胞质中形成异源寡聚体,但在细胞核中不形成。这表明这些热休克蛋白可在细胞质中形成复合物,但在核转位后发生构象变化,使得Hsp/Hsp结合位点不再被识别。这些数据表明,T47D细胞具有多个可能处于不同磷酸化阶段的p53前体分子,它们可能通过与热休克蛋白结合而免受蛋白酶的作用。热休克蛋白也可在细胞质中形成异源复合物,也可能是作为一种防止蛋白酶降解的保护机制,直到与p53结合。转位后,p53从热休克蛋白中释放出来以结合DNA,此时Hsp70和Hsp90不再能够形成核复合物,这可能使热休克蛋白易于被蛋白水解。