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Crotonate-activated histone H3K14 crotonylation enhances intestinal regeneration after injury [RNA-seq]

ABSTRACT: Crotonate-activated histone H3K14 crotonylation enhances intestinal regeneration after injury [RNA-seq]

PROVIDER: PRJNA1170273 | ENA |

REPOSITORIES: ENA

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Crotonate-activated histone H3K14 crotonylation enhances intestinal regeneration after injury

Project description:Crotonate-activated histone H3K14 crotonylation enhances intestinal regeneration after injury

| PRJNA1263501 | ENA

Crotonate-activated histone H3K14 crotonylation enhances intestinal regeneration after injury [ChIP-seq]

Project description:Crotonate-activated histone H3K14 crotonylation enhances intestinal regeneration after injury [ChIP-seq]

| PRJNA1169859 | ENA

Crotonate-activated histone H3K14 crotonylation enhances intestinal regeneration after injury [RNA-seq]

Project description:The intestinal epithelium undergoes rapid turnover driven by Lgr5+ intestinal stem cells (ISCs) at the crypt base, and can recover despite ISC loss during damage. However, the role of epigenetic modifications in regulating this regeneration remains unclear. In this study, we report that H3K14 crotonylation (H3K14cr), a vital histone modification mediated by the acyltransferase HBO1, is essential for intestinal regeneration. HBO1 ablation in the intestinal epithelium exacerbates dextran sulfate sodium (DSS)-induced colitis.

2025-08-13 | GSE279059 | GEO

Crotonate-activated histone H3K14 crotonylation enhances intestinal regeneration after injury [ChIP-seq]

2025-08-13 | GSE278970 | GEO

Crotonate-activated histone H3K14 crotonylation enhances intestinal regeneration after injury

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-08-13 | GSE297315 | GEO

Mus musculus

Project description:Crotonate enhances intestinal regeneration after injury via HBO1-mediated H3K14 crotonylation (PRJCA044771)

| PRJDB39371 | ENA

Effect of Crotonylation in the development of glioma

Project description:To investigate the role of Crotonylation in the regulation of tumor progression and development, we treated T98G cell with Crotonate.

2025-07-16 | GSE297117 | GEO

Histone crotonylation promotes endoderm differentiation. [scRNA-Seq]

Project description:In this study we report that histone crotonylation promotes human embryonic stem cell differentiation to endoderm cells. Addition of crotonate, a precursor for crotonyl-CoA and therefore histone crotonylation, dramatically enhanced endoderm cell differentiation from human embryonic stem cells, while incubation of acetate, a precursor of acetyl-CoA and therefore histone acetylation, did not change the efficiency of endoderm differentiation.

2021-02-23 | GSE130341 | GEO

ACSS2-Mediated Lysine Crotonylation Attenuates Senescence and Enhances the Therapeutic Efficacy of Adipose-derived Stem Cells in Inflammatory Bowel Disease [RNA-Seq]

Project description:Background Inflammatory bowel disease (IBD) remains a significant clinical challenge with limited curative options. Adipose-derived mesenchymal stem cells (ADSCs) hold therapeutic promise, but their anti-inflammatory efficacy is often compromised by cellular senescence. This study investigates the role of lysine crotonylation (Kcr) in ADSCs senescence and explores its therapeutic potential. Methods We analyzed Pan-Kcr levels in senescent ADSCs and evaluated the effects of sodium crotonate (NaCr), a crotonyl-CoA precursor, on senescence, proliferation, and anti-inflammatory function. A murine colitis model was used to assess therapeutic efficacy. Molecular mechanisms focusing on ACSS2-mediated Kcr regulation and H3K9 crotonylation (H3K9cr) at the ACSS2 promoter. Results Senescent ADSCs exhibited a marked decline in Pan-Kcr levels. NaCr treatment ameliorated senescence, enhanced proliferation, and improved anti-inflammatory capacity. ACSS2, a key regulator of Kcr, was downregulated in senescent ADSCs. Moreover, the anti-senescence effect of NaCr depended on ACSS2-mediated crotonylation. NaCr promoted H3K9cr modification at the ACSS2 promoter, forming a positive feedback loop that elevated Kcr levels. Mechanistically, ACSS2-mediated Kcr suppressed the NF-κB pathway to delay ADSCs senescence. Conclusion Our findings reveal an epigenetic pathway (ACSS2-Kcr-H3K9cr) regulating ADSCs senescence and propose Kcr modulation as a novel strategy to enhance ADSCs-based therapy for IBD.

2026-02-09 | GSE315663 | GEO

ACSS2-Mediated Lysine Crotonylation Attenuates Senescence and Enhances the Therapeutic Efficacy of Adipose-derived Stem Cells in Inflammatory Bowel Disease [ChIP-Seq]

2026-02-09 | GSE315662 | GEO