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Volume 10, Pages 924-929
Directions in Science

Autophagy Regulates the Post-Translational Cleavage of BCL-2 and Promotes Neuronal Survival

Dipartimento di Morfofisiologia Veterinaria e Istituto Nazionale di Neuroscienze (INN), Università degli Studi di Torino, Grugliasco (TO), Italy

Received 22 December 2009; Revised 12 April 2010; Accepted 14 April 2010

Academic Editor: Sergi Ferre

Copyright © 2010 Laura Lossi et al.


B-cell lymphoma 2 protein (BCL-2) is one of the more widely investigated anti-apoptotic protein in mammals, and its levels are critical for protecting from programmed cell death. We report here that the cellular content of BCL-2 is regulated at post-translational level along the autophagy/lysosome pathways in organotypic cultures of post-natal mouse cerebellar cortex. Specifically this mechanism appears to be effective in the cerebellar granule cells (CGCs) that are known to undergo massive programmed cell death (apoptosis) during post-natal maturation. By the use of specific agonists/antagonist of calcium channels at the endoplasmic reticulum it was possible to understand the pivotal role of calcium release from intracellular stores in CGC neuroprotection. The more general significance of these findings is supported by a very recent study Niemann-Pick transgenic mice.