Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1996 Nov 15;15(22):6205-12.

HGF receptor associates with the anti-apoptotic protein BAG-1 and prevents cell death

A Bardelli  1 , P Longati, D Albero, S Goruppi, C Schneider, C Ponzetto, P M Comoglio
Affiliations

HGF receptor associates with the anti-apoptotic protein BAG-1 and prevents cell death

A Bardelli et al. EMBO J. .

Abstract

The mechanisms by which apoptosis is prevented by survival factors are largely unknown. Using an interaction cloning approach, we identified a protein that binds to the intracellular domain of the hepatocyte growth factor (HGF) receptor. This protein was identified as BAG-1, a recently characterized Bcl-2 functional partner, which prolongs cell survival through unknown mechanisms. Overexpression of BAG-1 in liver progenitor cells enhances protection from apoptosis by HGF. Association of the receptor with BAG-1 occurs in intact cells, is mediated by the C-terminal region of BAG-1 and is independent from tyrosine phosphorylation of the receptor. Formation of the complex is increased rapidly following induction of apoptosis. BAG-1 also enhances platelet-derived growth factor (PDGF)-mediated protection from apoptosis and associates with the PDGF receptor. Microinjection or transient expression of BAG-1 deletion mutants shows that both the N- and the C-terminal domains are required for protection from apoptosis. The finding of a link between growth factor receptors and the anti-apoptotic machinery fills a gap in the understanding of the molecular events regulating programmed cell death.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Proc Natl Acad Sci U S A. 1986 Sep;83(17):6489-93 - PubMed
    1. J Biol Chem. 1995 Jan 13;270(2):603-11 - PubMed
    1. J Mol Biol. 1987 Apr 5;194(3):531-44 - PubMed
    1. Proc Natl Acad Sci U S A. 1988 Feb;85(3):851-5 - PubMed
    1. Nature. 1989 May 11;339(6220):155-6 - PubMed

Publication types

MeSH terms

LinkOut - more resources