Neuroglobin as a regulator of mitochondrial-dependent apoptosis: a bioinformatics analysis.

Apoptosis represents the key mechanism for the removal of surplus, damaged, or aged cells, and deregulated apoptosis has been implicated in the etiology of diverse pathologies. There are two main pathways which are known to initiate apoptosis: the death receptor-dependent (extrinsic) pathway and the mitochondrial-dependent (intrinsic) pathway. In the intrinsic pathway, as a response to diverse signals from the cellular environment, a permeabilization of the mitochondrial outer membrane occurs, followed by the release of cytochrome c and the activation of the effector caspases, which leads to cell death. Recently, increased attention has been paid to the possible role of the protein neuroglobin, in the regulation of the apoptotic process, and data have been provided, demonstrating the ability of the protein to inhibit the intrinsic pathway of apoptosis by interacting with mitochondrial proteins. The molecular details of these interactions, however, remain largely undefined. In the present study, well recognized bioinformatics methods were applied to predict the possible interaction interfaces which the protein can exploit to interact with relevant proteins of the mitochondrial-dependent pathway of apoptosis. In the search for therapeutic approaches based on the modulation of apoptosis, such a computational prediction could represent a first, guiding step, for the design of strategies aimed at modulating these interactions, and tune the apoptotic process.