Evidence map›Paper›PMID 28098138›Full record

ArticleNature communications2017

SCIMP is a transmembrane non-TIR TLR adaptor that promotes proinflammatory cytokine production from macrophages.

Lin Luo, Nilesh J Bokil, Adam A Wall, Ronan Kapetanovic, Natalie M Lansdaal, Faustine Marceline, Belinda J Burgess, Samuel J Tong, Zhong Guo, Kirill Alexandrov and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

38 citing papers in PubMed, 58 citations in OpenAlex.

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  14. Re-identification and characterization of grass carpFish and shellfish immunology reports · 2023
    Article
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  20. ERK1/2 in immune signalling.Biochemical Society transactions · 2022
    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

14 authors at 2 institutions in 1 country.

Lin LuoInstitute for Molecular Bioscience (IMB), The University of Queensland, Brisbane, Queensland 4072, Australia.
Nilesh J BokilInstitute for Molecular Bioscience (IMB), The University of Queensland, Brisbane, Queensland 4072, Australia.
Adam A WallInstitute for Molecular Bioscience (IMB), The University of Queensland, Brisbane, Queensland 4072, Australia.
Ronan KapetanovicInstitute for Molecular Bioscience (IMB), The University of Queensland, Brisbane, Queensland 4072, Australia.
Natalie M LansdaalInstitute for Molecular Bioscience (IMB), The University of Queensland, Brisbane, Queensland 4072, Australia.
Faustine MarcelineInstitute for Molecular Bioscience (IMB), The University of Queensland, Brisbane, Queensland 4072, Australia.
Belinda J BurgessInstitute for Molecular Bioscience (IMB), The University of Queensland, Brisbane, Queensland 4072, Australia.
Samuel J TongInstitute for Molecular Bioscience (IMB), The University of Queensland, Brisbane, Queensland 4072, Australia.
Zhong GuoInstitute for Molecular Bioscience (IMB), The University of Queensland, Brisbane, Queensland 4072, Australia.
Kirill AlexandrovInstitute for Molecular Bioscience (IMB), The University of Queensland, Brisbane, Queensland 4072, Australia.
Ian L RossInstitute for Molecular Bioscience (IMB), The University of Queensland, Brisbane, Queensland 4072, Australia.ORCID 0000-0002-2389-4292
Margaret L HibbsDepartment of Immunology and Pathology, Alfred Medical Research and Education Precinct, Monash University, Commercial Road, Melbourne, Victoria 3004, Australia.
Jennifer L StowInstitute for Molecular Bioscience (IMB), The University of Queensland, Brisbane, Queensland 4072, Australia.
Matthew J SweetInstitute for Molecular Bioscience (IMB), The University of Queensland, Brisbane, Queensland 4072, Australia.
The University of Queensland · AUMonash Alfred Psychiatry Research centre · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Danger signals activate Toll-like receptors (TLRs), thereby initiating inflammatory responses. Canonical TLR signalling, via Toll/Interleukin-1 receptor domain (TIR)-containing adaptors and proinflammatory transcription factors such as NF-κB, occurs in many cell types; however, additional mechanisms are required for specificity of inflammatory responses in innate immune cells. Here we show that SCIMP, an immune-restricted, transmembrane adaptor protein (TRAP), promotes selective proinflammatory cytokine responses by direct modulation of TLR4. SCIMP is a non-TIR-containing adaptor, binding directly to the TLR4-TIR domain in response to lipopolysaccharide. In macrophages, SCIMP is constitutively associated with the Lyn tyrosine kinase, is required for tyrosine phosphorylation of TLR4, and facilitates TLR-inducible production of the proinflammatory cytokines IL-6 and IL-12p40. Point mutations in SCIMP abrogating TLR4 binding also prevent SCIMP-mediated cytokine production. SCIMP is, therefore, an immune-specific TLR adaptor that shapes host defence and inflammation.

Indexed as

AnimalsCytokinesInterleukin-12 Subunit p40Interleukin-6MacrophagesMiceMice, Inbred C57BLProtein BindingProtein Domainssrc-Family KinasesToll-Like Receptor 4CytokinesInterleukin-12 Subunit p40Interleukin-6lyn protein-tyrosine kinasesrc-Family KinasesToll-Like Receptor 4

Identifiers

PMID28098138
PMCPMC5253658
OpenAlexW2579687242

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.