Evidence map›Paper›PMID 41851123›Full record

ArticleNature communications2026

Chromatin reorganization drives overexpression of a Btaf1 variant underpinning hematopoietic aging.

Le Zong, Bongsoo Park, Yaqiang Cao, Fei Ma, Ferda Tekin-Turhan, Wakako Kuribayashi, Keji Zhao, Isabel Beerman

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 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. 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

8 authors.

Le Zong *Epigenetics and Stem Cell Unit, Translational Gerontology Branch, National Institute on Aging, NIH, Baltimore, MD, USA.
Bongsoo Park *Epigenetics and Stem Cell Unit, Translational Gerontology Branch, National Institute on Aging, NIH, Baltimore, MD, USA.
Yaqiang CaoLaboratory of Epigenome Biology, Systems Biology Center, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD, USA.ORCID http://orcid.org/0000-0002-4665-1517
Fei MaLaboratory of Molecular Biology and Immunology, National Institute on Aging, NIH, Baltimore, MD, USA.ORCID http://orcid.org/0000-0003-0401-0954
Ferda Tekin-TurhanEpigenetics and Stem Cell Unit, Translational Gerontology Branch, National Institute on Aging, NIH, Baltimore, MD, USA.ORCID http://orcid.org/0000-0002-6749-9219
Wakako KuribayashiEpigenetics and Stem Cell Unit, Translational Gerontology Branch, National Institute on Aging, NIH, Baltimore, MD, USA.
Keji ZhaoLaboratory of Epigenome Biology, Systems Biology Center, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD, USA.ORCID http://orcid.org/0000-0001-5559-6233
Isabel BeermanEpigenetics and Stem Cell Unit, Translational Gerontology Branch, National Institute on Aging, NIH, Baltimore, MD, USA. isabel.beerman@nih.gov.ORCID http://orcid.org/0000-0002-7758-8231

Funding

U.S. Department of Health & Human Services | National Institutes of Health (NIH) AG000992
6 · The paper itself

Abstract

Age-associated hematopoietic stem cell (HSC) dysfunction is accompanied by dramatic transcription changes, but it remains unclear whether specific transcripts could orchestrate these HSC aging phenotypes. Here, we perform epigenetic profiling in male mice to investigate the regulatory mechanisms underlying the HSC aging transcriptome and screen for potential aging driver genes. We identify a looping structure formed between part of the Btaf1 gene and the whole Ide gene in old HSCs which is accompanied by overexpression of a shorter variant of Btaf1 (nBtaf1). Mechanistically, elevated expression of nBtaf1 drives the aging-associated overexpression of HSC and megakaryocyte progenitor (MkP) signature genes via regulating TBP binding at their promoters, which contributes to HSC expansion and elevated MkP production in aged mice. ShRNA-mediated knockdown of nBtaf1 restores a younger HSC transcriptome and specifically represses aging-associated HSC expansion and elevated MkP production. In summary, our data provide high resolution analysis of a dysregulated HSC aging epigenome and reveal a Btaf1 variant that drives HSC aging phenotypes in mice.

Indexed as

AgingCellular SenescenceChromatin Assembly and DisassemblyHematopoietic Stem CellsRepressor ProteinsTumor Suppressor ProteinsAnimalsChromatinEpigenesis, GeneticMaleMiceMice, Inbred C57BLPromoter Regions, GeneticTranscriptomeChromatinRepressor ProteinsTumor Suppressor Proteins

Identifiers

PMID41851123
PMCPMC13149550

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.