Abstract |
Bax inhibitor-1 (BI-1) is an evolutionarily-conserved endoplasmic reticulum protein. The expression of BI-1 in mammalian cells suppresses apoptosis induced by Bax, a pro-apoptotic member of the Bcl-2 family. BI-1 has been shown to be associated with calcium (Ca(2+)) levels, reactive oxygen species (ROS) production, cytosolic acidification, and autophagy as well as endoplasmic reticulum stress signaling pathways. According to both in vitro and clinical studies, BI-1 promotes the characteristics of cancers. In other diseases, BI-1 has also been shown to regulate insulin resistance, adipocyte differentiation, hepatic dysfunction and depression. However, the roles of BI-1 in these disease conditions are not fully consistent among studies. Until now, the molecular mechanisms of BI-1 have not directly explained with regard to how these conditions can be regulated. Therefore, this review investigates the physiological role of BI-1 through molecular mechanism studies and its application in various diseases.
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Authors | B Li, R K Yadav, G S Jeong, H-R Kim, H-J Chae |
Journal | Current molecular medicine
(Curr Mol Med)
Vol. 14
Issue 5
Pg. 603-15
( 2014)
ISSN: 1875-5666 [Electronic] Netherlands |
PMID | 24894176
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Chemical References |
- Apoptosis Regulatory Proteins
- Membrane Proteins
- Reactive Oxygen Species
- TMBIM6 protein, human
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Topics |
- Animals
- Apoptosis Regulatory Proteins
(metabolism)
- Endoplasmic Reticulum Stress
(physiology)
- Humans
- Lysosomes
(metabolism)
- Membrane Proteins
(metabolism)
- Models, Biological
- Reactive Oxygen Species
(metabolism)
- Unfolded Protein Response
(physiology)
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