Evidence map›Paper›PMID 40664791›Full record

ArticleNature chemical biology2025

Lipoyl deglutarylation by ABHD11 regulates mitochondrial and T cell metabolism.

Guinevere L Grice, Eleanor Minogue, Hudson W Coates, Mekdes Debela, Richard J Stopforth, Niek Wit, Zongyu Li, Joseph P Crowley, Arthur Kaser, Nicole Kaneider-Kaser and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature chemical biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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.

Guinevere L Grice *Cambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Jeffrey Cheah Biomedical Centre, Department of Medicine, University of Cambridge, Cambridge, UK.
Eleanor Minogue *Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, UK.
Hudson W Coates *Cambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Jeffrey Cheah Biomedical Centre, Department of Medicine, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-6506-5249
Mekdes DebelaCambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Jeffrey Cheah Biomedical Centre, Department of Medicine, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0009-0004-6659-2106
Richard J StopforthCambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Jeffrey Cheah Biomedical Centre, Department of Medicine, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-0054-7503
Niek WitCambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Jeffrey Cheah Biomedical Centre, Department of Medicine, University of Cambridge, Cambridge, UK.
Zongyu LiDepartment of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA, USA.
Joseph P CrowleyDepartment of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA, USA.
Arthur KaserCambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Jeffrey Cheah Biomedical Centre, Department of Medicine, University of Cambridge, Cambridge, UK.
Nicole Kaneider-KaserCambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Jeffrey Cheah Biomedical Centre, Department of Medicine, University of Cambridge, Cambridge, UK.
P Robin AntrobusCambridge Institute for Medical Research, University of Cambridge, Cambridge, UK.
Marcia C HaigisDepartment of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0003-2530-2681
Randall S JohnsonDepartment of Cell and Molecular Biology, Karolinska Institute, Stockholm, Sweden. randall.johnson@ki.se.
James A NathanCambridge Institute of Therapeutic Immunology & Infectious Disease (CITIID), Jeffrey Cheah Biomedical Centre, Department of Medicine, University of Cambridge, Cambridge, UK. jan33@cam.ac.uk.ORCID http://orcid.org/0000-0002-0248-1632

Funding

RCUK | Medical Research Council (MRC) MR/X008118/1Wellcome TrustWellcome Trust (Wellcome) 214283/Z/18/ZWellcome Trust (Wellcome) 215477/Z/19/Z
6 · The paper itself

Abstract

Glutarate is an intermediate of amino acid catabolism and an important metabolite for reprogramming T cell immunity. Glutarate exerts its effects either by directly inhibiting metabolite-dependent enzymes or through conjugation to substrates. Intriguingly, glutarylation can occur on protein and nonprotein substrates, but our understanding of these distinct glutaryl modifications is in its infancy. Here we uncover ABHD11 as a noncanonical deglutarylating enzyme critical for maintaining the tricarboxylic acid (TCA) cycle. Mechanistically, we find ABHD11 removes glutaryl adducts from lipoate-an essential fatty acid modification required for the TCA cycle. Loss of ABHD11 results in the accumulation of glutaryl-lipoyl adducts that drive an adaptive program, involving 2-oxoglutarate accumulation, that rewires mitochondrial metabolism. Functionally, this role of ABHD11 influences the metabolic programming of human CD8

Indexed as

CD8-Positive T-LymphocytesMitochondriaT-LymphocytesCitric Acid CycleGlutaratesHumansKetoglutaric AcidsLipoylationGlutaratesKetoglutaric Acids

Identifiers

PMID40664791
PMCPMC12643935

What OpenQuestion holds

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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.