Evidence map›Paper›PMID 38369277›Full record

ArticleJournal of molecular biology2024

RNA Binding Proteins that Mediate LPS-induced Alternative Splicing of the MyD88 Innate Immune Regulator.

Frank Fang Yao Lee, Chelsea Harris, Scott Alper

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

  1. Innate immunity: current understandings and future perspectives.Signal transduction and targeted therapy · 2026
    Review
  2. Alternative splicing of toll-like receptor pathway mRNAs in lung immune cells from patients with ARDS.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
  3. Review
  4. Integrative transcriptomic analysis reveals alternative splicing programs in sepsis-induced myocardial injury across dual mouse models.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  5. Review
  6. Article
  7. Macrophage Zc3h12c Limits Tissue Inflammation and Injury via Alternative Splicing of Pre-mRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Tumor-promoting effect and tumor immunity of SRSFs.Frontiers in cell and developmental biology · 2025
    Review
  13. 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

3 authors at 1 institution in 1 country.

Frank Fang Yao LeeDepartment of Immunology and Genomic Medicine, National Jewish Health, Denver, CO 80206, USA; Center for Genes, Environment and Health, National Jewish Health, Denver, CO 80206, USA; Department of Immunology and Microbiology, University of Colorado School of Medicine, Anschutz, CO 80045, USA.
Chelsea HarrisDepartment of Immunology and Genomic Medicine, National Jewish Health, Denver, CO 80206, USA; Center for Genes, Environment and Health, National Jewish Health, Denver, CO 80206, USA; Department of Immunology and Microbiology, University of Colorado School of Medicine, Anschutz, CO 80045, USA.
Scott AlperDepartment of Immunology and Genomic Medicine, National Jewish Health, Denver, CO 80206, USA; Center for Genes, Environment and Health, National Jewish Health, Denver, CO 80206, USA; Department of Immunology and Microbiology, University of Colorado School of Medicine, Anschutz, CO 80045, USA. Electronic address: alpers@njhealth.org.
National Jewish Health · US

Funding

MDS-Associated Spliceosome Mutations Regulate Host DefenseR01AI155749 · NIAID · NATIONAL JEWISH HEALTH · PI ALPER, SCOTT · 2021 to 2025
$2.7M
Temporal regulation of pulmonary inflammation by MyD88 alternative pre-mRNA splicingR01HL148335 · NHLBI · NATIONAL JEWISH HEALTH · PI ALPER, SCOTT · 2019 to 2022
$2.3M
NHLBI NIH HHS R01 HL148335NIAID NIH HHS R01 AI155749
6 · The paper itself

Abstract

Inflammation driven by Toll-like receptor (TLR) signaling pathways is required to combat infection. However, inflammation can damage host tissues; thus it is essential that TLR signaling ultimately is terminated to prevent chronic inflammatory disorders. One mechanism that terminates persistent TLR signaling is alternative splicing of the MyD88 signaling adaptor, which functions in multiple TLR signaling pathways. While the canonical long isoform of MyD88 (MyD88-L) mediates TLR signaling and promotes inflammation, an alternatively-spliced shorter isoform of MyD88 (MyD88-S) produces a dominant negative inhibitor of TLR signaling. MyD88-S production is induced by inflammatory agonists including lipopolysaccharide (LPS), and thus MyD88-S induction is thought to act as a negative feedback loop that prevents chronic inflammation. Despite the potential role that MyD88-S production plays in inflammatory disorders, the mechanisms controlling MyD88 alternative splicing remain unclear. Here, we identify two RNA binding proteins, SRSF1 and HNRNPU, that regulate LPS-induced alternative splicing of MyD88.

Indexed as

Alternative SplicingHeterogeneous-Nuclear Ribonucleoprotein UMyeloid Differentiation Factor 88RNA-Binding ProteinsSerine-Arginine Splicing FactorsAnimalsHEK293 CellsHumansImmunity, InnateInflammationLipopolysaccharidesMiceProtein IsoformsRAW 264.7 CellsHeterogeneous-Nuclear Ribonucleoprotein ULipopolysaccharidesMyeloid Differentiation Factor 88Protein IsoformsRNA-Binding ProteinsSerine-Arginine Splicing FactorsInflammationMacrophagePre-mRNA splicingRNA binding proteinsToll-like receptor signaling

Identifiers

PMID38369277
PMCPMC11001520
OpenAlexW4392439332

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.