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Changes in cIAP2, survivin and BimEL expression characterize the switch from autophagy to apoptosis in prolonged starvation.

Abstract Autophagy is a catabolic process involving the engulfment of cytoplasmic content within autophagosomes followed by their delivery to lysosomes. This process is a survival mechanism, enabling cells to cope with nutrient deprivation by degradation and recycling of macromolecules. Yet during continued stress such as prolonged starvation, a switch from autophagy to apoptosis is often detected.
PMID
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Authors

Mayor MeshTerms
Keywords

Bcl-2-like protein 11

apoptosis

autophagy

beta-transducin repeat-containing proteins

inhibitor of apoptosis proteins

Journal Title journal of internal medicine
Publication Year Start




PMID- 28425584
OWN - NLM
STAT- MEDLINE
DA  - 20170420
DCOM- 20170501
LR  - 20170501
IS  - 1365-2796 (Electronic)
IS  - 0954-6820 (Linking)
VI  - 281
IP  - 5
DP  - 2017 May
TI  - Changes in cIAP2, survivin and BimEL expression characterize the switch from
      autophagy to apoptosis in prolonged starvation.
PG  - 458-470
LID - 10.1111/joim.12616 [doi]
AB  - BACKGROUND: Autophagy is a catabolic process involving the engulfment of
      cytoplasmic content within autophagosomes followed by their delivery to
      lysosomes. This process is a survival mechanism, enabling cells to cope with
      nutrient deprivation by degradation and recycling of macromolecules. Yet during
      continued stress such as prolonged starvation, a switch from autophagy to
      apoptosis is often detected. OBJECTIVE: In this work, we characterized the
      temporal dynamics of the transition from autophagy towards apoptosis with the aim
      of elucidating the molecular mechanism regulating the switch from survival
      autophagy to apoptotic cell death. RESULTS AND CONCLUSIONS: We defined an inverse
      relationship between apoptosis and autophagy spanning a period of 72 h,
      manifested by the sequential reduction in LC3 lipidation and the activation of
      caspase-3. The transition to apoptosis correlated with a selective decline in the
      mRNA and protein levels of two anti-apoptotic IAP family proteins, survivin and
      cIAP2 and a selective increase in the BH3-only protein, BimEL. This 'molecular
      signature' was common to several cell lines undergoing the switch from autophagy 
      to apoptosis during prolonged starvation. Mechanistically, the increased BimEL
      protein levels resulted from its reduced binding to its specific E3 ligase,
      betaTrCP, leading to protein stabilization. Consistent with this, BimEL showed
      decreased phosphorylation at critical sites previously reported to be essential
      for binding to the E3 ligase. The decrease in the anti-apoptotic IAPs and the
      increase in the pro-apoptotic BimEL may thus constitute a molecular switch from
      autophagy to apoptosis during prolonged starvation.
CI  - (c) 2017 The Association for the Publication of the Journal of Internal Medicine.
FAU - Hay-Koren, A
AU  - Hay-Koren A
AD  - Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
FAU - Bialik, S
AU  - Bialik S
AD  - Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
FAU - Levin-Salomon, V
AU  - Levin-Salomon V
AD  - Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
FAU - Kimchi, A
AU  - Kimchi A
AUID- ORCID: http://orcid.org/0000-0002-8236-8989
AD  - Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
LA  - eng
PT  - Journal Article
PL  - England
TA  - J Intern Med
JT  - Journal of internal medicine
JID - 8904841
RN  - 0 (Autophagy-Related Proteins)
RN  - 0 (BCL2L11 protein, human)
RN  - 0 (BIRC5 protein, human)
RN  - 0 (BTRC protein, human)
RN  - 0 (Bcl-2-Like Protein 11)
RN  - 0 (Inhibitor of Apoptosis Proteins)
RN  - 0 (beta-Transducin Repeat-Containing Proteins)
RN  - EC 2.3.2.27 (BIRC3 protein, human)
RN  - EC 2.3.2.27 (Ubiquitin-Protein Ligases)
SB  - IM
MH  - A549 Cells
MH  - Apoptosis/*physiology
MH  - Autophagy/*physiology
MH  - Autophagy-Related Proteins/metabolism
MH  - Bcl-2-Like Protein 11/*metabolism
MH  - Cells, Cultured
MH  - Humans
MH  - Inhibitor of Apoptosis Proteins/*metabolism
MH  - Starvation/*physiopathology
MH  - Ubiquitin-Protein Ligases/*metabolism
MH  - beta-Transducin Repeat-Containing Proteins/metabolism
OTO - NOTNLM
OT  - Bcl-2-like protein 11
OT  - apoptosis
OT  - autophagy
OT  - beta-transducin repeat-containing proteins
OT  - inhibitor of apoptosis proteins
EDAT- 2017/04/21 06:00
MHDA- 2017/05/02 06:00
CRDT- 2017/04/21 06:00
AID - 10.1111/joim.12616 [doi]
PST - ppublish
SO  - J Intern Med. 2017 May;281(5):458-470. doi: 10.1111/joim.12616.

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