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BH3-Only Proteins and Their Effects on Cancer

  • Chapter
BCL-2 Protein Family

Part of the book series: Advances in Experimental Medicine and Biology ((volume 687))

Abstract

Apoptosis, a form of cellular suicide is a key mechanism involved in the clearance of cells that are dysfunctional, superfluous or infected. For this reason, the cell needs mechanisms to sense death cues and relay death signals to the apoptotic machinery involved in cellular execution. In the intrinsic apoptotic pathway, a subclass of BCL-2 family proteins called the BH3-only proteins are responsible for triggering apoptosis in response to varied cellular stress cues. The mechanisms by which they are regulated are tied to the type of cellular stress they sense. Once triggered, they interact with other BCL-2 family proteins to cause mitochondrial outer membrane permeabilization which in turn results in the activation of serine proteases necessary for cell killing. Failure to properly sense death cues and relay the death signal can have a major impact on cancer. This chapter will discuss our current models of how BH3-only proteins function as well as their impact on carcinogenesis and cancer treatment.

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Authors and Affiliations

  1. Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, 02115, USA

    Thanh-Trang Vo & Anthony Letai

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  1. Thanh-Trang Vo
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  2. Anthony Letai
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Correspondence to Anthony Letai .

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Editors and Affiliations

  1. Institute of Biomedical Sciences, FONDAP Center for Molecular Studies of the Cell (CEMC) Millennium Nucleus for Neural Morphogenesis (NEMO), University of Chile, Santiago, Chile

    Claudio Hetz PhD

  2. Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, USA

    Claudio Hetz PhD

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© 2010 Landes Bioscience and Springer Science+Business Media

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Vo, TT., Letai, A. (2010). BH3-Only Proteins and Their Effects on Cancer. In: Hetz, C. (eds) BCL-2 Protein Family. Advances in Experimental Medicine and Biology, vol 687. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-6706-0_3

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