Evidence map›Paper›PMID 22201672›Full record

ArticleOncotarget2011

TAp73alpha protects small cell lung carcinoma cells from caspase-2 induced mitochondrial mediated apoptotic cell death.

Naveen Muppani, Ulrika Nyman, Bertrand Joseph

Open access · hybridAbstract read
In one paragraph

Article in Oncotarget, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

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  14. p63 the guardian of human reproduction.Cell cycle (Georgetown, Tex.) · 2012
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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

3 authors at 2 institutions in 1 country.

Naveen MuppaniDepartment of Oncology-Pathology, Cancer Centrum Karolinska, Karolinska Institutet, 171 76 Stockholm, Sweden.
Ulrika Nyman
Bertrand Joseph
Karolinska Institutet · SELudwig Cancer Research · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Caspase-2 is ubiquitously expressed and the most evolutionarily conserved mammalian caspase. It can be activated by a range of death stimuli prior to Bax activation and the occurrence of apoptotic mitochondrial dysfunctions. Caspase-2 has also been reported to exert tumour suppressor function in vivo. The full length TAp73alpha isoform is found up-regulated in various tumour types, and is reported in a cell-type specific manner to repress drug-induced apoptosis. Here, we report that TAp73alpha represses caspase-2 enzymatic activity and by this means reduce caspase-2 induced Bax activation, loss of mitochondrial transmembrane potential and resulting apoptosis. The inhibitory effect on caspase-2 requires the presence of the DNA binding domain and SAM domain region of TAp73alpha. In conclusion, the ability of TAp73alpha to act as an inhibitor of caspase-2-induced cell death together with its up-regulation in certain tumour types strengthen the potential oncogenic activities for this protein.

Indexed as

Apoptosisbcl-2-Associated X ProteinCaspase 2Cell Line, TumorCysteine EndopeptidasesDNA-Binding ProteinsEnzyme ActivationHumansLung NeoplasmsMembrane Potential, MitochondrialMitochondriaNuclear ProteinsSmall Cell Lung CarcinomaTumor Protein p73Tumor Suppressor Proteinsbcl-2-Associated X ProteinCASP2 protein, humanCaspase 2Cysteine EndopeptidasesDNA-Binding ProteinsNuclear ProteinsTumor Protein p73Tumor Suppressor Proteins

Identifiers

PMID22201672
PMCPMC3282073
OpenAlexW1787205415

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.