Bax Inhibitor 1 in apoptosis and disease

Robinson, K. S., Clements, A., Williams, A. C., Berger, Cedric N. ORCID: https://orcid.org/0000-0002-1316-5985 and Frankel, G. 2011. Bax Inhibitor 1 in apoptosis and disease. Oncogene 30 (21) , pp. 2391-2400. 10.1038/onc.2010.636

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Abstract

Bax inhibitor 1 (BI-1) was originally discovered as an inhibitor of Bax-induced apoptosis; this review highlights the fundamental importance of BI-1 in a wider context, including in tissue homeostasis and as a regulator of cellular stress. BI-1 has been shown to interact with a broad range of partners to inhibit many facets of apoptosis, such as reactive oxygen species production, cytosolic acidification and calcium levels as well as endoplasmic reticulum stress signalling pathways. BI-1's anti-apoptotic action initially enables the cell to adapt to stress, although if the stress is prolonged or severe the actions of BI-1 may promote apoptosis. This almost universal anti-apoptotic capacity has been shown to be manipulated during infection with enteropathogenic and enterohaemorrhagic Escherichia coli inhibiting host cell death through direct interaction between their effector NleH and BI-1. In addition, BI-1 activity is important in a large number of cancers, promoting metastasis by modulating actin dynamics, a process dependent upon the BI-1 C-terminus and BI-1:actin interaction. Manipulation of BI-1 therefore has the potential for significant therapeutic benefit in a wide range of human diseases.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Biosciences
Publisher:	Nature Publishing Group: Open Access Hybrid Model Option B
ISSN:	0950-9232
Last Modified:	24 Oct 2022 07:21
URI:	https://orca.cardiff.ac.uk/id/eprint/114711

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