Heterotrimeric G Proteins and Apoptosis: Intersecting Signaling Pathways Leading to Context Dependent Phenotypes

The Intrinsic pathway is triggered by various stresses including hypoxia/ischemia, growth factor deprivation, and cell damage. These stimuli cause a disruption in the ratio of pro-apoptotic (BAX, BAK) to anti-apoptotic (Bcl-2, Bcl-xL) Bcl-2 family proteins at the mitochondria. Relative increase in the levels of the pro-apoptotic proteins allows for their homodimerization, and subsequent Cytochrome C efflux into the cytoplasm activates Apaf-1. Apaf-1 triggers Caspase-9 aggregation and activation and the subsequent caspase cascade. The extrinsic pathway is triggered by ligand binding to the death receptors, which causes receptor trimerization and activation. Activated receptors recruit adapter proteins, such as FADD, leading ultimately to the activation of Caspase-8 and the subsequent caspase cascade. Both pathways converge on Caspase-3, leading to apoptosis.

Publication

Heterotrimeric G Proteins and Apoptosis: Intersecting Signaling Pathways Leading to Context Dependent Phenotypes. () Vijay Yanamadala, et al. Curr Mol Med. ;9(5):527. Figure: F1. All organisms Mus musculus Rattus norvegicus Bos taurus Cricetulus griseus Homo sapiens Canis lupus familiaris Drosophila melanogaster

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