Evidence map›Paper›PMID 31427815›Full record

ArticleNature chemical biology2019

Toll-like receptor mediated inflammation requires FASN-dependent MYD88 palmitoylation.

Young-Chan Kim, Sang Eun Lee, Somi K Kim, Hyun-Duk Jang, Injoo Hwang, Sooryeonhwa Jin, Eun-Byeol Hong, Kyoung-Soon Jang, Hyo-Soo Kim

Abstract read
PubMed Publisher
In one paragraph

Article in Nature chemical biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 3% 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

116 citing papers in PubMed, 1 synthesis or guideline pooled it, 185 citations in OpenAlex.

  1. Pooled it
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  5. ProteinJournal of pharmaceutical analysis · 2026
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  13. The Roles of ProteinCancer communications (London, England) · 2026
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56 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

9 authors at 5 institutions in 2 countries.

Young-Chan Kim *Strategic Center of Cell & Bio Therapy, Seoul National University Hospital, Seoul, Korea.ORCID http://orcid.org/0000-0002-6726-5957
Sang Eun Lee *Cardiology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.ORCID http://orcid.org/0000-0002-7290-2463
Somi K Kim *Strategic Center of Cell & Bio Therapy, Seoul National University Hospital, Seoul, Korea.ORCID http://orcid.org/0000-0001-7806-6200
Hyun-Duk Jang *Strategic Center of Cell & Bio Therapy, Seoul National University Hospital, Seoul, Korea.ORCID http://orcid.org/0000-0002-7126-3647
Injoo HwangStrategic Center of Cell & Bio Therapy, Seoul National University Hospital, Seoul, Korea.ORCID http://orcid.org/0000-0003-0209-5763
Sooryeonhwa JinStrategic Center of Cell & Bio Therapy, Seoul National University Hospital, Seoul, Korea.ORCID http://orcid.org/0000-0002-8588-1059
Eun-Byeol HongStrategic Center of Cell & Bio Therapy, Seoul National University Hospital, Seoul, Korea.ORCID http://orcid.org/0000-0002-8218-862X
Kyoung-Soon JangBiomedical Omics Center, Korea Basic Science Institute, Cheongju, South Korea.ORCID http://orcid.org/0000-0001-5451-5788
Hyo-Soo KimStrategic Center of Cell & Bio Therapy, Seoul National University Hospital, Seoul, Korea. hyosoo@snu.ac.kr.ORCID http://orcid.org/0000-0003-0847-5329
Seoul National University Hospital · KRKorea Basic Science Institute · KRSeoul National University · KRSeoul National University of Science and Technology · KRUlsan College · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toll-like receptor (TLR)/myeloid differentiation primary response protein (MYD88) signaling aggravates sepsis by impairing neutrophil migration to infection sites. However, the role of intracellular fatty acids in TLR/MYD88 signaling is unclear. Here, inhibition of fatty acid synthase by C75 improved neutrophil chemotaxis and increased the survival of mice with sepsis in cecal ligation puncture and lipopolysaccharide-induced septic shock models. C75 specifically blocked TLR/MYD88 signaling in neutrophils. Treatment with GSK2194069 that targets a different domain of fatty acid synthase, did not block TLR signaling or MYD88 palmitoylation. De novo fatty acid synthesis and CD36-mediated exogenous fatty acid incorporation contributed to MYD88 palmitoylation. The binding of IRAK4 to the MYD88 intermediate domain and downstream signal activation required MYD88 palmitoylation at cysteine 113. MYD88 was palmitoylated by ZDHHC6, and ZDHHC6 knockdown decreased MYD88 palmitoylation and TLR/MYD88 activation upon lipopolysaccharide stimulus. Thus, intracellular saturated fatty acid-dependent palmitoylation of MYD88 by ZDHHC6 is a therapeutic target of sepsis.

Indexed as

AnimalsCell LineFatty Acid Synthase, Type IHumansInflammationLipoylationMaleMiceMice, Inbred C57BLMyeloid Differentiation Factor 88NF-kappa BReal-Time Polymerase Chain ReactionToll-Like ReceptorsFatty Acid Synthase, Type IMyd88 protein, mouseMyeloid Differentiation Factor 88NF-kappa BToll-Like Receptors

Identifiers

PMID31427815
OpenAlexW2969892182

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.