Evidence map›Paper›PMID 23815625›Full record

ArticleThe Biochemical journal2013

Caspase-2 is essential for c-Jun transcriptional activation and Bim induction in neuron death.

Ying Y Jean, Elena M Ribe, Maria Elena Pero, Marina Moskalenko, Zarah Iqbal, Lianna J Marks, Lloyd A Greene, Carol M Troy

Open access · greenAbstract read
In one paragraph

Article in The Biochemical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  14. Caspases: therapeutic targets in neurologic disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015
    Review
  15. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Ying Y Jean*Department of Pathology and Cell Biology, Columbia University College of Physicians and Surgeons, New York, NY 10032, U.S.A.
Elena M Ribe
Maria Elena Pero
Marina Moskalenko
Zarah Iqbal
Lianna J Marks
Lloyd A Greene
Carol M Troy
University of Naples Federico II · IT

Funding

NEUROTROPHIC FACTOR DEPRIVATION AND NEURONAL CELL DEATHR01NS033689 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GREENE, LLOYD A · 1995 to 2017
$8.9M
Downstream Regulators of Beta-Amyloid Induced Neuronal DeathR01NS043089 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TROY, CAROL M · 2001 to 2010
$2.2M
NEURONAL DEGENERATION: MECHANISMS AND PREVENTIONR01NS035933 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TROY, CAROL M · 2004 to 2007
$1.5M
Downstream Regulators of Beta-Amyloid Induced Neuronal DeathR56NS043089 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TROY, CAROL M · 2008 to 2008
$351k
NEURONAL DEGENERATION--MECHANISMS AND PREVENTIONR29NS035933 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TROY, CAROL M · 1997 to 2001
$237k
NINDS NIH HHS 2R01NS043089NINDS NIH HHS 5R01NS033689NINDS NIH HHS R01 NS033689NINDS NIH HHS R01 NS035933NINDS NIH HHS R01 NS043089NINDS NIH HHS R29 NS035933NINDS NIH HHS R56 NS043089
6 · The paper itself

Abstract

Neuronal apoptotic death generally requires de novo transcription, and activation of the transcription factor c-Jun has been shown to be necessary in multiple neuronal death paradigms. Caspase-2 has been implicated in death of neuronal and non-neuronal cells, but its relationship to transcriptional activation has not been clearly elucidated. In the present study, using two different neuronal apoptotic paradigms, β-amyloid treatment and NGF (nerve growth factor) withdrawal, we examined the hierarchical role of caspase-2 activation in the transcriptional control of neuron death. Both paradigms induce rapid activation of caspase-2 as well as activation of the transcription factor c-Jun and subsequent induction of the pro-apoptotic BH3 (Bcl-homology domain 3)-only protein Bim (Bcl-2-interacting mediator of cell death). Caspase-2 activation is dependent on the adaptor protein RAIDD {RIP (receptor-interacting protein)-associated ICH-1 [ICE (interleukin-1β-converting enzyme)/CED-3 (cell-death determining 3) homologue 1] protein with a death domain}, and both caspase-2 and RAIDD are required for c-Jun activation and Bim induction. The present study thus shows that rapid caspase-2 activation is essential for c-Jun activation and Bim induction in neurons subjected to apoptotic stimuli. This places caspase-2 at an apical position in the apoptotic cascade and demonstrates for the first time that caspase-2 can regulate transcription.

Indexed as

Amyloid beta-PeptidesAnimalsApoptosisApoptosis Regulatory ProteinsBcl-2-Like Protein 11Caspase 2CRADD Signaling Adaptor ProteinFetusMembrane ProteinsNerve Growth FactorNeuronsPrimary Cell CultureProto-Oncogene ProteinsProto-Oncogene Proteins c-junRatsRats, Sprague-DawleyAmyloid beta-PeptidesApoptosis Regulatory ProteinsBcl2l11 protein, ratBcl-2-Like Protein 11Caspase 2Cradd protein, ratCRADD Signaling Adaptor ProteinMembrane ProteinsNerve Growth FactorProto-Oncogene ProteinsProto-Oncogene Proteins c-jun

Identifiers

PMID23815625
PMCPMC3905453
OpenAlexW1979791199

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.