Evidence map›Paper›PMID 40319015›Full record

ArticleNature communications2025

The ESCRT protein CHMP5 promotes T cell leukemia by enabling BRD4-p300-dependent transcription.

Katharine Umphred-Wilson, Shashikala Ratnayake, Qianzi Tang, Rui Wang, Sneha Ghosh Chaudhary, Devaiah N Ballachanda, Josephine Trichka, Jan Wisniewski, Lan Zhou, Qingrong Chen and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 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. ESCRT-III function in membrane fission and repair.Nature reviews. Molecular cell biology · 2026
    Review
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors.

Katharine Umphred-WilsonExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Shashikala Ratnayake *Computational Genomics and Bioinformatics Branch, Center for Biomedical Informatics & Information Technology, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20850, USA.
Qianzi Tang *College of Animal Science and Technology, Sichuan Agricultural University, 611130, Chengdu, China.ORCID http://orcid.org/0000-0003-3235-3372
Rui Wang *College of Animal Science and Technology, Sichuan Agricultural University, 611130, Chengdu, China.ORCID http://orcid.org/0000-0002-6842-119X
Sneha Ghosh ChaudharyExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Devaiah N BallachandaExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Josephine TrichkaExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Jan WisniewskiExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Lan ZhouDepartment of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, TX, 77030, USA.
Qingrong ChenComputational Genomics and Bioinformatics Branch, Center for Biomedical Informatics & Information Technology, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20850, USA.
Daoud MeerzamanComputational Genomics and Bioinformatics Branch, Center for Biomedical Informatics & Information Technology, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20850, USA.
Dinah S SingerExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Stanley AdoroExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA. stanley.adoro@nih.gov.ORCID http://orcid.org/0000-0001-9092-5960

Funding

GRADUATE TRAINING IN CELLULAR AND MOLECULAR BIOLOGYT32GM008056 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI DIEHL, JOHN ALAN, SNIDER, MARTIN D · 1985 to 2019
$7.1M
Targeting Notch2 in Hematopoietic Cell Therapy.R01HL103827 · NHLBI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI ZHOU, LAN · 2012 to 2022
$4.3M
Mechanisms of JAG1-mediated immune suppression in the pancreatic cancer microenvironmentR01CA294584 · NCI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI Lan Zhou · 2024 to 2026
$3.3M
Mechanisms of tunable posttranslational control of T-cell homeostasis and toleranceR01AI143992 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI XIAO, TSAN SAM · 2019 to 2023
$2.2M
Hes1-loss promotes dysregulation of epithelial homeostasis and inflammation in a serrated adenocarcinoma modelR01CA222064 · NCI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI ZHOU, LAN · 2018 to 2022
$2.0M
Probing the role of the IRE1alpha-XBP1 pathway in normal and malignant hematopoiesisK22CA218467 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI ADORO, STANLEY · 2017 to 2018
$385k
American Cancer Society (American Cancer Society, Inc.) RSG-19-025-01-DDCNCI NIH HHS K22 CA218467NCI NIH HHS R01 CA222064NCI NIH HHS R01 CA294584NHLBI NIH HHS R01 HL103827NIAID NIH HHS R01 AI143992NIGMS NIH HHS T32 GM008056U.S. Department of Defense (United States Department of Defense) CA180768-W81XWH1910306U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) CA218467U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) CA222064U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) HL103827U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) AI143992U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) GM008056
6 · The paper itself

Abstract

Addiction to oncogene-rewired transcriptional networks is a therapeutic vulnerability in cancer cells, underscoring a need to better understand mechanisms that relay oncogene signals to the transcriptional machinery. Here, using human and mouse T cell acute lymphoblastic leukemia (T-ALL) models, we identify an essential requirement for the endosomal sorting complex required for transport protein CHMP5 in T-ALL epigenetic and transcriptional programming. CHMP5 is highly expressed in T-ALL cells where it mediates recruitment of the coactivator BRD4 and the histone acetyl transferase p300 to enhancers and super-enhancers that enable transcription of T-ALL genes. Consequently, CHMP5 depletion causes severe downregulation of critical T-ALL genes, mitigates chemoresistance and impairs T-ALL initiation by oncogenic NOTCH1 in vivo. Altogether, our findings uncover a non-oncogene dependency on CHMP5 that enables T-ALL initiation and maintenance.

Indexed as

Cell Cycle ProteinsE1A-Associated p300 ProteinEndosomal Sorting Complexes Required for TransportLeukemia, T-Cellp300-CBP Transcription FactorsPrecursor T-Cell Lymphoblastic Leukemia-LymphomaTranscription FactorsAnimalsBromodomain Containing ProteinsCell Line, TumorGene Expression Regulation, LeukemicHumansMiceNuclear ProteinsReceptor, Notch1Transcription, GeneticBRD4 protein, humanBrd4 protein, mouseBromodomain Containing ProteinsCell Cycle ProteinsE1A-Associated p300 ProteinEndosomal Sorting Complexes Required for TransportEP300 protein, humanNuclear Proteinsp300-CBP Transcription FactorsReceptor, Notch1Transcription Factors

Identifiers

PMID40319015
PMCPMC12049546

What Socratic holds

Textmetadata
LicenceCC BY
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.