Evidence map›Paper›PMID 27761594›Full record

ReviewCellular and molecular life sciences : CMLS2017

Assembly and regulation of ASC specks.

Florian Hoss, Juan F Rodriguez-Alcazar, Eicke Latz

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

89 citing papers in PubMed, 146 citations in OpenAlex.

  1. Article
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  11. Frontiers in pharmacology · 2026
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29 more citing papers are in PubMed but not listed here.

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 3 countries.

Florian HossInstitute of Innate Immunity, University Hospitals, University of Bonn, Sigmund-Freud-Straße 25, 53127, Bonn, Germany.
Juan F Rodriguez-AlcazarInstitute of Innate Immunity, University Hospitals, University of Bonn, Sigmund-Freud-Straße 25, 53127, Bonn, Germany.
Eicke LatzInstitute of Innate Immunity, University Hospitals, University of Bonn, Sigmund-Freud-Straße 25, 53127, Bonn, Germany. eicke.latz@uni-bonn.de.ORCID 0000-0003-1488-5666
University of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The inflammasome adapter ASC links activated inflammasome sensors to the effector molecule pro-caspase-1. Recruitment of pro-caspase-1 to ASC promotes the autocatalytic activation of caspase-1, which leads to the release of pro-inflammatory cytokines, such as IL-1β. Upon triggering of inflammasome sensors, ASC assembles into large helical fibrils that interact with each other serving as a supramolecular signaling platform termed the ASC speck. Alternative splicing, post-translational modifications of ASC, as well as interaction with other proteins can perturb ASC function. In several inflammatory diseases, ASC specks can be found in the extracellular space and its presence correlates with poor prognosis. Here, we review the role of ASC in inflammation, and focus on the structural mechanisms that lead to ASC speck formation, the regulation of ASC function during inflammasome assembly, and the importance of ASC specks in disease.

Indexed as

Apoptosis Regulatory ProteinsCarrier ProteinsExtracellular MatrixHumansInflammasomesInflammationProtein IsoformsProtein MultimerizationProtein Processing, Post-TranslationalRNA SplicingApoptosis Regulatory ProteinsCarrier ProteinsInflammasomesLLID-114769 protein, humanProtein IsoformsCARDCOPFibrilPOPPrionoidPTMPYDSpeck

Identifiers

PMID27761594
PMCPMC11107573
OpenAlexW2538561584

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.