Title Role of Mitochondria in Apoptosis
Authors Gülhan ATAGÜN, Zafer EREN, İrem GÜRKANLI
Abstract Apoptosis is the cell death type monitored and studied for more than one century. Apoptosis process was defined as ‘programmed cell death’ in 1964. The term apoptosis that means ‘a leaf falls from the tree or petal leaves the flower’ in Greek was first defined by Kerr et al. in 1972. This cell death type has been investigated widely during the last 36 years and molecular mechanisms underlying the self destruction of the cells were explained. Additionally, an increase occured in understanding the role of mitochondria in cell death in the last few years. Mitochondrial metabolic pathway of apoptosis is regulated by Bcl-2 family members. This family is consisted of pro-apoptotic and antiapoptotic proteins sharing 4 protected areas known as Bcl-2 homolog areas. Anti-apoptotic members as Bcl-2 and Bcl-XL support cell living by inhibiting the functions of pro-apoptotic Bcl-2 proteins. Anti-apoptotic Bcl-2 proteins have been reported to protect the cells from various apoptotic stimulus and to be important for cell living. Mitochondria includes the intermembranous area holocytochrome c, certain procaspases, endonuclease G, HtrA2/Omi, Smac/Diablo and apoptosis- stimulating factor. Permeabilization of the outer membrane is resulted in release of these molecules into cytoplasma. Release of cytochrome c is one of the important steps in the mitochondrial metabolic pathway of apoptosis. Release of cytochrome c supports the occurence of apoptosis activating killer caspases managing apoptosis. Components of apoptosis are cytochrome c, an adaptor molecule Apaf-1 and procaspase 9. Binding cytochrome c to Apaf-1 in the presence of ATP and dATP results in activation of procaspase 9. Thereafter, activated procaspase 9 activates killer caspases achieving apoptosis. Endonuclease G and apoptosis-stimulating factor settle in nucleus from mitochondria and cause caspaseindependent DNA fragmentation. Smac/Diablo and HtrA2/Omi play critical roles in regulation of apoptosis by binding caspases and inhibiting apoptosis protein inhibitors.
Keywords Apoptosis, Apaf-1, caspase, mitochondria, cytochrome c
Journal DERLEME - Turkish Journal of Scientific Reviews
Issue Issue 2
Page 009-53
Year 2011
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