TRAP1: A Regulator of Mitochondrial Functions and Apoptosis

Yutaka Masuda (Editor)
Hiroyuki Itabe (Editor)
Showa Pharmaceutical University, Tokyo, Japan

Series: Cell Biology Research Progress
BISAC: SCI017000

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Volume 10

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Special issue: Resilience in breaking the cycle of children’s environmental health disparities
Edited by I Leslie Rubin, Robert J Geller, Abby Mutic, Benjamin A Gitterman, Nathan Mutic, Wayne Garfinkel, Claire D Coles, Kurt Martinuzzi, and Joav Merrick

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In recent years, the role of mitochondria in apoptotic cell death has received considerable attention. One of the key events in apoptosis is the increase in mitochondrial membrane permeability, which leads to the release of apoptogenic factors from mitochondria into the cytoplasm. Cytochrome c released from mitochondria activates the cascade of caspases and downstream targets of apoptotic cell death.

Tumor necrosis factor receptor-associated protein 1 (TRAP1) is a member of the heat-shock family of mitochondrial proteins, and is homologous to the members of the 90-kDa family of heat-shock proteins (HSP90). TRAP1 appears to have specific functions different from those of other members of the HSP90 family. Reduced expression of TRAP1 enhances cytochrome c release from mitochondria. This new book discusses the mechanism by which TRAP1 controls mitochondrial functions during apoptosis. (Imprint: Nova Biomedical)

Abstract

Introduction

1. Role of Mitochondria in Apoptosis

2. Involvement of HSP Family of Proteins in Mitochondrial Function

3. Regulation of Mitochondrial Function by TRAP1

4. Possible Role of TRAP1 in Diseases

Conclusion

References

Index

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