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A study involving the Consejo Superior de Investigaciones Científicas (CSIC) describes a new molecular mechanism capable of inducing programmed cell death or apoptosis. This phenomenon occurs naturally in many biological processes, from embryonic development to respond to cell damage, and is associated with abnormal pathologies such as cancer. The results of the work published in the EMBO journal.

The work has been performed by the team led Felipe X. Pimentel- uiños at the Institute of Molecular and Cell Biology of Cancer (center joint CSIC and Universidad de Salamanca). Specifically, the authors identify a novel signaling route of apoptosis, which is initiated and integrated into the endoplasmic reticulum.

Discovered the mechanism operates independently of the mitochondrial machinery that, until now, was supposed to be instrumental in integrating apoptotic signals. Understanding the molecular mechanisms that regulate and facilitate this process may lead in future to design strategies to address its effective manipulation for therapeutic purposes.

The molecules belonging to the BCL2 family play an important role in the regulation and execution of apoptotic cell death. After years of study, the scientific community knows today, that the presence of some of these proteins (eg Bak and Bax) in the mitochondrial membrane critically regulates the release of cytochrome c to the cytoplasm. This is configured as a point of no return in the process of cell death induced by natural activators of Bax and Bak: BH3-only proteins.

The group led by Pimentel Muiños-Bak has been found that, in the endoplasmic reticulum, usually responds to BH3-only activators inducing apoptotic signaling pathway completely independent and autonomous mitochondrial function of these molecules. Similarly, researchers have found that this effect is channeled through a novel signaling molecular machinery that involves both calcium flows molecules IRE1 and TRAF2, previously involved in the response of the reticular cell stress. "Thus, the entire molecular system, which activates apoptosis seems to function normally only in the presence of BCL2 protein expressed in the reticulum and mitochondria in the absence of expression of these molecules, something that really was very surprising to us at the beginning of our investigation," said the scientist.