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The N-terminal domain of tumor suppressor p53 is involved in the molecular interaction with the anti-apoptotic protein Bcl-Xl.

Abstract：

:Emerging evidences suggest that transcription-independent mechanism of p53 appears to make an important contribution to the overall p53-dependent apoptosis. Recently, it has been postulated that the DNA-binding domain of p53 can interact with Bcl-Xl, and subsequently the proposed molecular interaction has been shown by NMR studies. Interestingly, Chipuk et al. [Cancer Cell 4 (2003) 371] reported that the N-terminal domain of p53 (p53NTD) alone is necessary and sufficient to induce transcription-independent apoptosis. To further define and understand the nature of the molecular recognition between p53 and Bcl-Xl, our current study focuses on p53NTD. We first demonstrated the molecular interaction between p53NTD and Bcl-Xl by co-expressing and purifying the complex. Second, to define the binding interface of the molecular interaction, which is not previously characterized, in the current we employed a NMR-based binding study, showing that the binding site on Bcl-Xl is located in the region including alpha4, the N- and C-termini of alpha3, the N-terminus of alpha5, and the central part of alpha2. To further probe this observation, we then performed fluorescence resonance energy transfer (FRET) assay in cells. The FRET efficiency detected between the donor and acceptor molecules appears to suggest the presence of molecular interaction of p53NTD with Bcl-Xl in cells. Taken together, our data suggest that p53NTD interacts with Bcl-Xl but the characteristic of the molecular interaction appears to be different from that of the DNA-binding domain of p53.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Xu H,Tai J,Ye H,Kang CB,Yoon HS

doi

10.1016/j.bbrc.2005.12.227

subject

Has Abstract

pub_date

2006-03-24 00:00:00

pages

938-44

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(06)00114-8

journal_volume

341

pub_type

杂志文章

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