Wienzek S, Roth J, Dobbelstein M
Institut für Virologie, Zentrum für Mikrobiologie und Hygiene, Philipps-Universität Marburg, 35037 Marburg, Germany.
J Virol. 2000 Jan;74(1):193-202. doi: 10.1128/jvi.74.1.193-202.2000.
The p53 tumor suppressor protein represents a target for viral and cellular oncoproteins, including adenovirus gene products. Recently, it was discovered that several proteins with structural and functional homologies to p53 exist in human cells. Two of them were termed p51 and p73. We have shown previously that the E1B 55-kDa protein (E1B-55 kDa) of adenovirus type 5 (Ad5) binds and inactivates p53 but not p73. Further, p53 is rapidly degraded in the presence of E1B-55 kDa and the E4orf6 protein of this virus. Here, it is demonstrated that p51 does not detectably associate with E1B-55 kDa. While p53 is relocalized to the cytoplasm by E1B-55 kDa, p51's location is unaffected. Finally, p51 retains its full transcriptional activity in the presence of E1B-55 kDa. Apparently, p51 does not represent a target of Ad5 E1B-55 kDa, suggesting that the functions of p51 are distinct from p53-like tumor suppression. E1B-55 kDa from highly oncogenic adenovirus type 12 (Ad12) was previously shown to surpass the oncogenic activity of Ad5 E1B-55 kDa in various assay systems, raising the possibility that Ad12 E1B-55 kDa might target a broader range of p53-like proteins. However, we show here that Ad12 E1B-55 kDa also inhibits p53's transcriptional activity without measurably affecting p73 or p51. Moderate inhibition of p51's transcriptional activity was observed in the presence of the E4orf6 proteins from Ad5 and Ad12. p53 and Ad12-E1B-55 kDa colocalize in the nucleus and also in cytoplasmic clusters when transiently coexpressed. Finally, E1B-55 kDa and E4orf6 of Ad12 mediate rapid degradation of p53 with an efficiency comparable to that of the Ad5 proteins in human and rodent cells. Our results suggest that E1B-55 kDa of either virus type has similar effects on p53 but does not affect p73 and p51.
p53肿瘤抑制蛋白是病毒和细胞癌蛋白的作用靶点,包括腺病毒基因产物。最近,人们发现在人类细胞中存在几种与p53具有结构和功能同源性的蛋白质。其中两种被命名为p51和p73。我们之前已经表明,5型腺病毒(Ad5)的E1B 55 kDa蛋白(E1B-55 kDa)能结合并使p53失活,但对p73无此作用。此外,在E1B-55 kDa和该病毒的E4orf6蛋白存在的情况下,p53会迅速降解。在此,我们证明p51与E1B-55 kDa没有可检测到的结合。当p53被E1B-55 kDa重新定位到细胞质中时,p51的定位不受影响。最后,在E1B-55 kDa存在的情况下,p51保留了其全部转录活性。显然,p51不是Ad5 E1B-55 kDa的作用靶点,这表明p51的功能与p53样的肿瘤抑制功能不同。之前在各种检测系统中已表明,高致癌性12型腺病毒(Ad12)的E1B-55 kDa超过了Ad5 E1B-55 kDa的致癌活性,这增加了Ad12 E1B-55 kDa可能作用于更广泛的p53样蛋白的可能性。然而,我们在此表明,Ad12 E1B-55 kDa也能抑制p53的转录活性,而对p73或p51没有明显影响。在Ad5和Ad12的E4orf6蛋白存在的情况下,观察到对p51转录活性有适度抑制。当瞬时共表达时,p53和Ad12-E1B-55 kDa在细胞核以及细胞质聚集体中都共定位。最后,Ad12的E1B-55 kDa和E4orf6在人和啮齿动物细胞中介导p53的快速降解,其效率与Ad proteins相当。我们的结果表明,两种病毒类型的E1B-55 kDa对p53有相似的作用,但不影响p73和p51。