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肿瘤抑制蛋白p53通过泛素介导的蛋白水解系统降解需要一种新型的泛素载体蛋白E2。

Degradation of the tumor suppressor protein p53 by the ubiquitin-mediated proteolytic system requires a novel species of ubiquitin-carrier protein, E2.

作者信息

Ciechanover A, Shkedy D, Oren M, Bercovich B

机构信息

Department of Biochemistry, Faculty of Medicine, Technion-Israel Institute of Technology, Haifa.

出版信息

J Biol Chem. 1994 Apr 1;269(13):9582-9.

PMID:8144545
Abstract

The tumor suppressor protein p53 is extremely unstable in most cell lines. In contrast, many mutant and oncogenic species of the protein are stable. The degradation of p53 in vivo requires metabolic energy; however, the proteolytic system(s) involved have not been identified. The ubiquitin system has been implicated in the degradation of p53 in vitro. The degradation is stimulated significantly by the human papillomavirus (HPV) oncoprotein E6 that associates with p53 and facilitates conjugate formation and subsequent degradation. Complex formation between E6 and p53 is promoted by a cellular protein designated E6-associated protein (E6-AP). Initial dissection of the conjugation process have demonstrated a role for the ubiquitin-activating enzyme, E1, but the ubiquitin-carrier protein (E2, UBC) and the ubiquitin protein ligase, E3, have not been identified. In this study, we report that a novel species of ubiquitin-carrier protein designated E2-F1 (Blumenfeld, N., Gonen, H., Mayer, A., Smith, C., Siegel, N.R., Schwartz, A.L., and Ciechanover, A. (1994) J. Biol. Chem. 269, 9574-9581) is involved in the conjugation and degradation of p53. This E2 enzyme recognizes non-"N-end rule" protein substrates and appears to mediate their conjugation via a novel species of E3. The process of recognition appears to be selective; E2-F1 is not required for the conjugation and degradation of human N-myc. The involvement of E2-F1 in the in vitro process appears to be physiologically meaningful and to reproduce the in vivo process; mutant species of p53 that do not interact with E6 and are stable in vivo are not recognized by the cell free system.

摘要

肿瘤抑制蛋白p53在大多数细胞系中极不稳定。相比之下,该蛋白的许多突变体和致癌物种则较为稳定。p53在体内的降解需要代谢能量;然而,所涉及的蛋白水解系统尚未明确。泛素系统在体外p53的降解中发挥作用。人乳头瘤病毒(HPV)癌蛋白E6与p53结合并促进共轭物形成及后续降解,从而显著刺激这种降解。细胞蛋白E6相关蛋白(E6-AP)促进E6与p53之间的复合物形成。对共轭过程的初步剖析表明泛素激活酶E1发挥了作用,但泛素载体蛋白(E2,UBC)和泛素蛋白连接酶E3尚未明确。在本研究中,我们报告一种名为E2-F1的新型泛素载体蛋白(布卢门菲尔德,N.,戈嫩,H.,迈耶,A.,史密斯,C.,西格尔,N.R.,施瓦茨,A.L.,和齐查诺弗,A.(1994年)《生物化学杂志》269,9574 - 9581)参与p53的共轭和降解。这种E2酶识别非“N端规则”蛋白底物,并且似乎通过一种新型E3介导它们的共轭。识别过程似乎具有选择性;人N - myc的共轭和降解不需要E2-F1。E2-F1参与体外过程似乎具有生理意义并重现了体内过程;不与E6相互作用且在体内稳定的p53突变体不被无细胞系统识别。

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