Overproduced p73α activates a minimal promoter through a mechanism independent of its transcriptional activity

FEBS Letters

Shimotohno, Kunitada¹  Hijikata, Makoto¹  Takagi, Shinji¹  Ueda, Yoshihide¹ 

[1] Department of Viral Oncology, Institute for Virus Research, Kyoto University, Sakyo-ku, Kyoto 606-8507, Japan

关键词: p73;    Splicing variant;    Transcription;    p53;    p53BCS;    p53-binding consensus sequence;    GAPDH;    glyceraldehyde-3-phosphate dehydrogenase;    SV40;    simian virus 40;    MDM2;    murine double minute clone 2 oncoprotein;    HBV;    hepatitis B virus;    IGF-I-R;    insulin-like growth factor receptor I;   

DOI  :  10.1016/S0014-5793(01)03141-6

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

p73, the gene for a protein related to the tumor suppressor p53, encodes several variants which bear distinct carboxy-terminal structures as a result of alternative splicing. We and others showed that these splicing variants have different transcriptional effects on promoters with a p53-binding consensus sequence (p53BCS). Here we show that when transiently overexpressed, p73α but not p73β activated several minimal promoters without the p53BCS, while p73γ and p73ϵ activated them to a much lesser extent than p73α, and p53 suppressed the promoters without p53BCS as reported previously. Moreover, the results of RNase protection and RNA transfection assays suggested that this activation occurred at the transcriptional level. Deletion analysis of p73α revealed that the transactivation domain of p73 was not involved in this activity and the C-terminal region of p73α which is a specific structure of this variant was essential, suggesting that this phenomenon occurs independent of the transactivation activity of p73α and that the C-terminal extension of p73α may affect the basal level of transcription.

【 授权许可】

Unknown