Evidence map›Paper›PMID 21119681›Full record

ReviewCell research2011

Regulation of NF-κB signaling by caspases and MALT1 paracaspase.

Jens Staal, Tine Bekaert, Rudi Beyaert

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

40 citing papers in PubMed, 114 citations in OpenAlex.

  1. Article
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  5. Review
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  10. Food & nutrition research · 2023
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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 1 institution in 1 country.

Jens StaalDepartment for Molecular Biomedical Research - VIB, Department of Biomedical Molecular Biology - Ghent University, Technologiepark 927, Ghent B-9052, Belgium.
Tine Bekaert
Rudi Beyaert
Ghent University · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Caspases are intracellular proteases that are best known for their function in apoptosis signaling. It has become evident that many caspases also function in other signaling pathways that propagate cell proliferation and inflammation, but studies on the inflammatory function of caspases have mainly been limited to caspase-1-mediated cytokine processing. Emerging evidence, however, indicates an important contribution of caspases as mediators or regulators of nuclear factor-κB (NF-κB) signaling, which plays a key role in inflammation and immunity. Much still needs to be learned about the mechanisms that govern the activation and regulation of NF-κB by caspases, and this review provides an update of this area. Whereas apoptosis signaling is dependent on the catalytic activity of caspases, they mainly act as scaffolding platforms for other signaling proteins in the case of NF-κB signaling. Caspase proteolytic activity, however, counteracts the pro-survival function of NF-κB by cleaving specific signaling molecules. A striking exception is the paracaspase mucosa-associated lymphoid tissue 1 (MALT1), whose adaptor and proteolytic activity are both needed to initiate a full blown NF-κB response in antigen-stimulated lymphocytes. Understanding the role of caspases and MALT1 in the regulation of NF-κB signaling is of high interest for therapeutic immunomodulation.

Indexed as

ApoptosisCaspasesHumansMucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinNeoplasm ProteinsNF-kappa BSignal TransductionCaspasesMALT1 protein, humanMucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinNeoplasm ProteinsNF-kappa B

Identifiers

PMID21119681
PMCPMC3193404
OpenAlexW2088591345

What OpenQuestion holds

Textmetadata
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.