Bax inhibitor 1 in apoptosis and disease.

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.

• Authors: K S Robinson, A Clements, A C Williams, C N Berger, G Frankel
• Journal: Oncogene (Oncogene) Vol. 30 Issue 21 Pg. 2391-400 (May 26 2011) ISSN: 1476-5594 [Electronic] England
• PMID: 21297665 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Apoptosis Regulatory Proteins
• Membrane Proteins
• Reactive Oxygen Species
• TMBIM6 protein, human
• Calcium

Topics

• Amino Acid Sequence
• Apoptosis
• Apoptosis Regulatory Proteins (genetics, metabolism)
• Calcium (metabolism)
• Humans
• Membrane Proteins (genetics, metabolism)
• Models, Biological
• Molecular Sequence Data
• Neoplasms (genetics, metabolism, pathology)
• Reactive Oxygen Species (metabolism)
• Sequence Homology, Amino Acid