Neuronal repair: Apoptotic proteins make good

The potential of the central nervous system (CNS) to regenerate is regulated by a complex interaction of neuronal intrinsic and extrinsic factors that remain poorly understood. Significant research has been dedicated to identifying these factors to facilitate design of therapies that will treat the...

Full description

Bibliographic Details
Main Authors:	Reina, Christopher P., Driscoll, Monica, Gabel, Christopher V.
Format:	Online
Language:	English
Published:	Landes Bioscience 2013
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3704441/

id	pubmed-3704441
recordtype	oai_dc
spelling	pubmed-37044412013-09-19 Neuronal repair: Apoptotic proteins make good Reina, Christopher P. Driscoll, Monica Gabel, Christopher V. Commentary The potential of the central nervous system (CNS) to regenerate is regulated by a complex interaction of neuronal intrinsic and extrinsic factors that remain poorly understood. Significant research has been dedicated to identifying these factors to facilitate design of therapies that will treat the functional impairment associated with CNS injuries. Over the last decade, the development of in vivo laser severing of single axons in C. elegans has established an invaluable model for the genetic identification of novel regeneration factors. In a recent study we report the unexpected identification of the core apoptotic proteins CED-4/Apaf-1 and the executioner caspase CED-3 as important factors that promote early events in regeneration in C. elegans. Other upstream regulators of apoptosis do not influence regeneration, indicating the existence of a novel mechanism for activation of CED-4 and CED-3 in neuronal repair. CED-4 and CED-3 function downstream of injury-induced calcium transients and appear to act through the conserved DLK-1 pathway to promote regeneration. We propose a working model for calcium-dependent localized activation of CED-4 and CED-3 caspase and discuss questions raised including mechanisms for spatially regulating activated CED-3 and the possible substrates that it might cleave to initiate regeneration. Landes Bioscience 2013-04-01 2013-04-01 /pmc/articles/PMC3704441/ /pubmed/24058867 http://dx.doi.org/10.4161/worm.22285 Text en Copyright © 2013 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Reina, Christopher P. Driscoll, Monica Gabel, Christopher V.
spellingShingle	Reina, Christopher P. Driscoll, Monica Gabel, Christopher V. Neuronal repair: Apoptotic proteins make good
author_facet	Reina, Christopher P. Driscoll, Monica Gabel, Christopher V.
author_sort	Reina, Christopher P.
title	Neuronal repair: Apoptotic proteins make good
title_short	Neuronal repair: Apoptotic proteins make good
title_full	Neuronal repair: Apoptotic proteins make good
title_fullStr	Neuronal repair: Apoptotic proteins make good
title_full_unstemmed	Neuronal repair: Apoptotic proteins make good
title_sort	neuronal repair: apoptotic proteins make good
description	The potential of the central nervous system (CNS) to regenerate is regulated by a complex interaction of neuronal intrinsic and extrinsic factors that remain poorly understood. Significant research has been dedicated to identifying these factors to facilitate design of therapies that will treat the functional impairment associated with CNS injuries. Over the last decade, the development of in vivo laser severing of single axons in C. elegans has established an invaluable model for the genetic identification of novel regeneration factors. In a recent study we report the unexpected identification of the core apoptotic proteins CED-4/Apaf-1 and the executioner caspase CED-3 as important factors that promote early events in regeneration in C. elegans. Other upstream regulators of apoptosis do not influence regeneration, indicating the existence of a novel mechanism for activation of CED-4 and CED-3 in neuronal repair. CED-4 and CED-3 function downstream of injury-induced calcium transients and appear to act through the conserved DLK-1 pathway to promote regeneration. We propose a working model for calcium-dependent localized activation of CED-4 and CED-3 caspase and discuss questions raised including mechanisms for spatially regulating activated CED-3 and the possible substrates that it might cleave to initiate regeneration.
publisher	Landes Bioscience
publishDate	2013
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3704441/
_version_	1611992708940824576

Neuronal repair: Apoptotic proteins make good

Similar Items