Absence of the BH3 domain mutation of proapoptotic Bcl-2 family gene BAD in serous and mucinous tumors of ovary

Abstract

Apoptosis is defined as a physiological process that plays a critical role in the normal development and maintenance of tissue homeostasis [ [1] Reed J.C. Mechanisms of apoptosis. Am J Pathol. 2000; 157: 1415-1430 Abstract Full Text Full Text PDF PubMed Google Scholar ]. Proteins in the Bcl-2 family, which operate immediately upstream of mitochondria, are central regulators of apoptosis. Both proapoptotic and antiapoptotic Bcl-2 family proteins exist, and many of Bcl-2 family proteins bind each other, forming a complex network of homo- and heterodimers [ [1] Reed J.C. Mechanisms of apoptosis. Am J Pathol. 2000; 157: 1415-1430 Abstract Full Text Full Text PDF PubMed Google Scholar ]. Proapoptotic Bcl-2 family proteins have in common the Bcl-2 homology 3 (BH3) domain—an interacting domain that is both necessary and sufficient for the killing action. BAD is a proapoptotic Bcl-2 family member, and the function of BAD is regulated primarily by rapid changes of its phosphorylation state that modulates its protein–protein interactions and subcellular localization [ [2] Datta S.R. Katsov A. Hu L. et al. 14-3-3 Proteins and survival kinases cooperate to inactivate BAD by BH3 domain phosphorylation. Mol Cell. 2000; 6: 41-51 Abstract Full Text Full Text PDF PubMed Scopus (544) Google Scholar ].