当前位置： SCI文献检索 > PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA期刊下所有文献 > A proline-rich motif in p53 is required for transactivation-independent growth arrest as induced by Gas1.

A proline-rich motif in p53 is required for transactivation-independent growth arrest as induced by Gas1.

Abstract：

:The involvement of p53 in regulating diverse cellular processes dictates that it must respond to multiple signaling mechanisms, thus coordinating the response to various "stress conditions." Genotoxic stress has served as a paradigm to dissect the transactivation-dependent branch of the pathway by which p53 can induce growth arrest. Alternate mechanisms have been invoked to explain transactivation-independent effects of p53, especially in the context of apoptosis. We have identified a p53-dependent pathway initiated by the gas1 product, a plasma membrane protein highly expressed during G0, which activates a transactivation-independent p53 growth arrest function. Through a detailed deletional analysis and site-specific mutagenesis of p53 we show that the Gas1-dependent signal transduction relies on a proline-rich region (amino acids 63-85) of murine p53. In vivo competition experiments using combinations of such mutants implicate this functional domain of p53 as a docking site in the transmission of antiproliferative signals.

journal_name

Proc Natl Acad Sci U S A

journal_title

Proceedings of the National Academy of Sciences of the United States of America

authors

Ruaro EM,Collavin L,Del Sal G,Haffner R,Oren M,Levine AJ,Schneider C

doi

10.1073/pnas.94.9.4675

subject

Has Abstract

pub_date

1997-04-29 00:00:00

pages

4675-80

issue

9

eissn

0027-8424

issn

1091-6490

journal_volume

94

pub_type

杂志文章

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