ArticleProceedings of the National Academy of Sciences of the United States of America2014
Binding of the histone chaperone ASF1 to the CBP bromodomain promotes histone acetylation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 66 citations in OpenAlex.
- Post‑translational modifications in atherosclerosis: Roles, mechanisms and therapeutic potential (Review).International journal of molecular medicine · 2026Review
- Lactylation: a metabolic-epigenetic driver in atherosclerosis pathogenesis and therapeutic targeting.Frontiers in cardiovascular medicine · 2026Review
- Epigenetic Activation of the CMTM6-IGF2BP1-EP300 Positive Feedback Loop Drives Gemcitabine Resistance in Pancreatic Ductal Adenocarcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
- CREB-binding protein/P300 bromodomain inhibition reduces neutrophil accumulation and activates antitumor immunity in triple-negative breast cancer.JCI insight · 2024Article
- ASF1A-dependent P300-mediated histone H3 lysine 18 lactylation promotes atherosclerosis by regulating EndMT.Acta pharmaceutica Sinica. B · 2024Article
- CBP/P300 BRD Inhibition Reduces Neutrophil Accumulation and Activates Antitumor Immunity in TNBC.bioRxiv : the preprint server for biology · 2024Article
- Stiffness assisted cell-matrix remodeling trigger 3D mechanotransduction regulatory programs.Biomaterials · 2024Article
- Epigenetic underpinnings of tumor-immune dynamics in prostate cancer immune suppression.Trends in cancer · 2024Review
- Marine natural compounds as potential CBP bromodomain inhibitors for treating cancer: an in-silico approach using molecular docking, ADMET, molecular dynamics simulations and MM-PBSA binding free energy calculations.In silico pharmacology · 2024Article
- Systematic proteomics profiling of lysine crotonylation of the lung at Pseudoglandular and Canalicular phases in human fetus.Proteome science · 2023Article
- Development of an interfering peptide M1-20 with potent anti-cancer effects by targeting FOXM1.Cell death & disease · 2023Article
- The Role of CREBBP/EP300 and Its Therapeutic Implications in Hematological Malignancies.Cancers · 2023Review
- The protective role of EP300 in monocrotaline-induced pulmonary hypertension.Frontiers in cardiovascular medicine · 2023Article
- Nicotinic acid supplementation contributes to the amelioration of Alzheimer's disease in mouse models.Annals of translational medicine · 2022Article
- Identification of early and intermediate biomarkers for ARDS mortality by multi-omic approaches.Scientific reports · 2021Observational
- Epigenetic Deregulation of Apoptosis in Cancers.Cancers · 2021Review
- Review
- In silico investigation of the viroporin E as a vaccine target against SARS-CoV-2.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- A novel miRNA inhibits metastasis of prostate cancer via decreasing CREBBP-mediated histone acetylation.Journal of cancer research and clinical oncology · 2021Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The multifunctional Creb-binding protein (CBP) protein plays a pivotal role in many critical cellular processes. Here we demonstrate that the bromodomain of CBP binds to histone H3 acetylated on lysine 56 (K56Ac) with higher affinity than to its other monoacetylated binding partners. We show that autoacetylation of CBP is critical for the bromodomain-H3 K56Ac interaction, and we propose that this interaction occurs via autoacetylation-induced conformation changes in CBP. Unexpectedly, the bromodomain promotes acetylation of H3 K56 on free histones. The CBP bromodomain also interacts with the histone chaperone anti-silencing function 1 (ASF1) via a nearby but distinct interface. This interaction is necessary for ASF1 to promote acetylation of H3 K56 by CBP, indicating that the ASF1-bromodomain interaction physically delivers the histones to the histone acetyl transferase domain of CBP. A CBP bromodomain mutation manifested in Rubinstein-Taybi syndrome has compromised binding to both H3 K56Ac and ASF1, suggesting that these interactions are important for the normal function of CBP.
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Registered trials
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.