Evidence map›Paper›PMID 41973923›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2026

SCD1 licenses STING signaling through fatty acid desaturation-mediated membrane remodeling.

Danhui Qin, Yanjie Gao, Haojia Jiang, Xintong Meng, Ying Qin, Hui Song, Yue Fu, Chengjiang Gao, Mutian Jia, Chunyuan Zhao and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

11 authors.

Danhui QinDepartment of Pathogenic Biology, Key Laboratory of Infection Immunity and Disease Intervention of Shandong Province, and Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.
Yanjie GaoDepartment of Pathogenic Biology, Key Laboratory of Infection Immunity and Disease Intervention of Shandong Province, and Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.ORCID 0009-0001-0290-5554
Haojia JiangDepartment of Pathogenic Biology, Key Laboratory of Infection Immunity and Disease Intervention of Shandong Province, and Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.
Xintong MengDepartment of Pathogenic Biology, Key Laboratory of Infection Immunity and Disease Intervention of Shandong Province, and Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.
Ying QinDepartment of Pathogenic Biology, Key Laboratory of Infection Immunity and Disease Intervention of Shandong Province, and Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.ORCID 0000-0001-6359-0886
Hui SongDepartment of Pathogenic Biology, Key Laboratory of Infection Immunity and Disease Intervention of Shandong Province, and Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.
Yue FuDepartment of Physiology and Pathophysiology, School of Basic Medical Science, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.
Chengjiang GaoDepartment of Immunology, School of Basic Medical Science, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.ORCID 0000-0002-9365-4497
Mutian JiaDepartment of Pathogenic Biology, Key Laboratory of Infection Immunity and Disease Intervention of Shandong Province, and Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.
Chunyuan ZhaoState Key Laboratory for Innovation and Transformation of Luobing Theory, Department of Cardiology, Qilu Hospital of Shandong University, Jinan 250012, China.
Wei ZhaoDepartment of Pathogenic Biology, Key Laboratory of Infection Immunity and Disease Intervention of Shandong Province, and Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.ORCID 0000-0001-8440-2274

Funding

MOST | National Natural Science Foundation of China (NSFC) 82125020MOST | National Natural Science Foundation of China (NSFC) 82321002
6 · The paper itself

Abstract

The stimulator of interferon genes (STING) is a critical mediator of innate immunity against cytosolic DNA pathogens, requiring precise regulation to balance antiviral defense and immune tolerance. While lipid metabolism influences immune signaling, the role of stearoyl-CoA desaturase 1 (SCD1), a key enzyme converting saturated fatty acids (SFAs) to monounsaturated fatty acids (MUFAs), in STING activation remains unexplored. Here, we identify SCD1 as a metabolic checkpoint that licenses STING activation through biophysical membrane remodeling. Mechanistically, SCD1-generated MUFAs incorporate into endoplasmic reticulum (ER) phospholipids, enhancing membrane curvature and fluidity. This biophysical remodeling facilitates cyclic guanosine monophosphate (GMP)-adenosine monophosphate (AMP) (cGAMP) binding to STING and promotes its dimerization, enabling downstream TBK1-IRF3 signaling and type I interferons (IFNs) production. Consequently,

Indexed as

Cell MembraneFatty AcidsMembrane ProteinsStearoyl-CoA DesaturaseAnimalscGAS-STING Signaling PathwayEndoplasmic ReticulumHerpesvirus 1, HumanHumansImmunity, InnateInterferon Type IMiceMice, KnockoutNucleotides, CyclicSignal TransductionSTING Proteincyclic guanosine monophosphate-adenosine monophosphateFatty AcidsInterferon Type IMembrane ProteinsNucleotides, CyclicScd1 protein, mouseStearoyl-CoA DesaturaseSTING1 protein, humanSting1 protein, mouseSTING Proteincellular lipid metabolisminnate immunitymembrane architectureSCD1STING

Identifiers

PMID41973923
PMCPMC13099626

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.