Dismantling the autophagic arsenal when it is time to die: Concerted AMBRA1 degradation by caspases and calpains

Research output: Contribution to journalArticle

Abstract

Under stress conditions cells activate different response pathways which result in cell survival or apoptosis depending on: (1) the nature of the insults, (2) the type, if acute or chronic stress, and (3) how long the stress persists. Generally, autophagy is induced early to sustain cell survival and inhibit cell death. However, adverse conditions are able to overcome autophagy to promote cell death. Increasing evidence suggests that the inhibition of autophagy by the apoptotic machinery has been proposed as one of the crucial events responsible for the irreversible switch from survival to death. The mechanism seems to be related to the selective apoptotic protease-mediated degradation of key autophagic proteins. We recently found that AMBRA1, an important regulator of the autophagic process mediating the initial steps of autophagosome formation, is also irreversibly degraded by the combined activity of caspases and calpains. This phenomenon is not merely a consequence of apoptosis execution but represents a key step required to efficiently promote the autophagic vs apoptosis switch.

Original languageEnglish
Pages (from-to)1255-1257
Number of pages3
JournalAutophagy
Volume8
Issue number8
DOIs
Publication statusPublished - Aug 2012

Fingerprint

Calpain
Autophagy
Caspases
Apoptosis
Cell Survival
Cell Death
Peptide Hydrolases
Proteins

Keywords

  • Ambra1
  • Apoptosis
  • Autophagy
  • Calpains
  • Caspases

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology

Cite this

Dismantling the autophagic arsenal when it is time to die : Concerted AMBRA1 degradation by caspases and calpains. / Corazzari, Marco; Fimia, Gian Maria; Piacentini, Mauro.

In: Autophagy, Vol. 8, No. 8, 08.2012, p. 1255-1257.

Research output: Contribution to journalArticle

@article{dbfde0444a0847a49b81ce5cbef331b2,
title = "Dismantling the autophagic arsenal when it is time to die: Concerted AMBRA1 degradation by caspases and calpains",
abstract = "Under stress conditions cells activate different response pathways which result in cell survival or apoptosis depending on: (1) the nature of the insults, (2) the type, if acute or chronic stress, and (3) how long the stress persists. Generally, autophagy is induced early to sustain cell survival and inhibit cell death. However, adverse conditions are able to overcome autophagy to promote cell death. Increasing evidence suggests that the inhibition of autophagy by the apoptotic machinery has been proposed as one of the crucial events responsible for the irreversible switch from survival to death. The mechanism seems to be related to the selective apoptotic protease-mediated degradation of key autophagic proteins. We recently found that AMBRA1, an important regulator of the autophagic process mediating the initial steps of autophagosome formation, is also irreversibly degraded by the combined activity of caspases and calpains. This phenomenon is not merely a consequence of apoptosis execution but represents a key step required to efficiently promote the autophagic vs apoptosis switch.",
keywords = "Ambra1, Apoptosis, Autophagy, Calpains, Caspases",
author = "Marco Corazzari and Fimia, {Gian Maria} and Mauro Piacentini",
year = "2012",
month = "8",
doi = "10.4161/auto.20671",
language = "English",
volume = "8",
pages = "1255--1257",
journal = "Autophagy",
issn = "1554-8627",
publisher = "Taylor and Francis Inc.",
number = "8",

}

TY - JOUR

T1 - Dismantling the autophagic arsenal when it is time to die

T2 - Concerted AMBRA1 degradation by caspases and calpains

AU - Corazzari, Marco

AU - Fimia, Gian Maria

AU - Piacentini, Mauro

PY - 2012/8

Y1 - 2012/8

N2 - Under stress conditions cells activate different response pathways which result in cell survival or apoptosis depending on: (1) the nature of the insults, (2) the type, if acute or chronic stress, and (3) how long the stress persists. Generally, autophagy is induced early to sustain cell survival and inhibit cell death. However, adverse conditions are able to overcome autophagy to promote cell death. Increasing evidence suggests that the inhibition of autophagy by the apoptotic machinery has been proposed as one of the crucial events responsible for the irreversible switch from survival to death. The mechanism seems to be related to the selective apoptotic protease-mediated degradation of key autophagic proteins. We recently found that AMBRA1, an important regulator of the autophagic process mediating the initial steps of autophagosome formation, is also irreversibly degraded by the combined activity of caspases and calpains. This phenomenon is not merely a consequence of apoptosis execution but represents a key step required to efficiently promote the autophagic vs apoptosis switch.

AB - Under stress conditions cells activate different response pathways which result in cell survival or apoptosis depending on: (1) the nature of the insults, (2) the type, if acute or chronic stress, and (3) how long the stress persists. Generally, autophagy is induced early to sustain cell survival and inhibit cell death. However, adverse conditions are able to overcome autophagy to promote cell death. Increasing evidence suggests that the inhibition of autophagy by the apoptotic machinery has been proposed as one of the crucial events responsible for the irreversible switch from survival to death. The mechanism seems to be related to the selective apoptotic protease-mediated degradation of key autophagic proteins. We recently found that AMBRA1, an important regulator of the autophagic process mediating the initial steps of autophagosome formation, is also irreversibly degraded by the combined activity of caspases and calpains. This phenomenon is not merely a consequence of apoptosis execution but represents a key step required to efficiently promote the autophagic vs apoptosis switch.

KW - Ambra1

KW - Apoptosis

KW - Autophagy

KW - Calpains

KW - Caspases

UR - http://www.scopus.com/inward/record.url?scp=84866098743&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84866098743&partnerID=8YFLogxK

U2 - 10.4161/auto.20671

DO - 10.4161/auto.20671

M3 - Article

C2 - 22575990

AN - SCOPUS:84866098743

VL - 8

SP - 1255

EP - 1257

JO - Autophagy

JF - Autophagy

SN - 1554-8627

IS - 8

ER -