Evidence map›Paper›PMID 38503284›Full record

ArticleMolecular cell2024

Anti-apoptotic MCL-1 promotes long-chain fatty acid oxidation through interaction with ACSL1.

Tristen Wright, Meghan E Turnis, Christy R Grace, Xiao Li, Lauren A Brakefield, Yong-Dong Wang, Haiyan Xu, Ewa Kaminska, Leslie K Climer, Tresor O Mukiza and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2024. 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
10.1field-weighted citation impact, top 1% 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, 43 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Review
  6. Article
  7. Regulated cell death programs shaping cancer therapy.Cellular oncology (Dordrecht, Netherlands) · 2026
    Review
  8. Article
  9. Article
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  11. Article
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  15. HFrontiers in cell and developmental biology · 2026
    Review
  16. Article
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  18. Review
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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

13 authors at 1 institution in 1 country.

Tristen WrightDepartment of Cell and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA; Graduate School of Biomedical Sciences, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Meghan E TurnisDepartment of Cell and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Christy R GraceDepartment of Structural Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Xiao LiDepartment of Cell and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Lauren A BrakefieldDepartment of Cell and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA; Integrated Program in Biomedical Sciences, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Yong-Dong WangDepartment of Cell and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Haiyan XuDepartment of Cell and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Ewa KaminskaDepartment of Cell and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Leslie K ClimerDepartment of Cell and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Tresor O MukizaDepartment of Cell and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Chi-Lun ChangDepartment of Cell and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Tudor MoldoveanuDepartment of Structural Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Joseph T OpfermanDepartment of Cell and Molecular Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. Electronic address: joseph.opferman@stjude.org.
St. Jude Children's Research Hospital · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Shondra Michelle Miller · 1985 to 2026
$166.9M
Regulation of Cell Death and Mitochondrial Physiology by Anti-Apoptotic MCL-1R01HL102175 · NHLBI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI OPFERMAN, JOSEPH T. · 2010 to 2014
$2.1M
Pathway Specific Combinational Therapy in Poor Prognosis B-Lineage Acute Lymphoblastic LeukemiaR01CA201069 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI OPFERMAN, JOSEPH T. · 2016 to 2020
$2.0M
Regulation of Cardiac Death and Energy Metabolism by MCL-1R01HL123543 · NHLBI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI OPFERMAN, JOSEPH T. · 2015 to 2018
$1.8M
Elucidating the structural basis of mitochondrial outer membrane permeabilization in apoptosisR01GM129470 · NIGMS · UNIV OF ARKANSAS FOR MED SCIS · PI MOLDOVEANU, TUDOR · 2020 to 2024
$1.7M
Identifying the mechanisms behind non-apoptotic functions of mitochondrial matrix-localized MCL-1F31CA275373 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL GRADUATE SCHOOL OF BIOMEDICAL SCIENCES, LLC · PI WRIGHT, TRISTEN · 2022 to 2024
$104k
NCI NIH HHS F31 CA275373NCI NIH HHS P30 CA008748NCI NIH HHS P30 CA021765NCI NIH HHS R01 CA201069NHLBI NIH HHS R01 HL102175NHLBI NIH HHS R01 HL123543NIGMS NIH HHS R01 GM129470
6 · The paper itself

Abstract

MCL-1 is essential for promoting the survival of many normal cell lineages and confers survival and chemoresistance in cancer. Beyond apoptosis regulation, MCL-1 has been linked to modulating mitochondrial metabolism, but the mechanism(s) by which it does so are unclear. Here, we show in tissues and cells that MCL-1 supports essential steps in long-chain (but not short-chain) fatty acid β-oxidation (FAO) through its binding to specific long-chain acyl-coenzyme A (CoA) synthetases of the ACSL family. ACSL1 binds to the BH3-binding hydrophobic groove of MCL-1 through a non-conventional BH3-domain. Perturbation of this interaction, via genetic loss of Mcl1, mutagenesis, or use of selective BH3-mimetic MCL-1 inhibitors, represses long-chain FAO in cells and in mouse livers and hearts. Our findings reveal how anti-apoptotic MCL-1 facilitates mitochondrial metabolism and indicate that disruption of this function may be associated with unanticipated cardiac toxicities of MCL-1 inhibitors in clinical trials.

Indexed as

Fatty AcidsMitochondriaAnimalsApoptosisCoenzyme A LigasesMiceMyeloid Cell Leukemia Sequence 1 ProteinOxidation-ReductionACSL1 protein, mouseCoenzyme A LigasesFatty AcidsMcl1 protein, mouseMyeloid Cell Leukemia Sequence 1 Proteinacyl-coenzyme A synthetaseapoptosisfatty acidMCL-1metabolismmitochondriaβ-oxidation

Identifiers

PMID38503284
PMCPMC11017322
OpenAlexW4392897821

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.