ArticleMolecular and cellular biology2008
Hbo1 Links p53-dependent stress signaling to DNA replication licensing.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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.
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.
Who cites it
38 citing papers in PubMed, 69 citations in OpenAlex.
- ATR-dependent phosphorylation of the histone acetyltransferase HBO1 suppresses chromatin binding and promotes replication stress responses.The Journal of biological chemistry · 2026Article
- Histone acetyltransferase HBO1 in cancer biology: Essential mechanisms and implications for targeted therapeutics.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- Multifunctional acyltransferase HBO1: a key regulatory factor for cellular functions.Cellular & molecular biology letters · 2024Review
- BRPF1-KAT6A/KAT6B Complex: Molecular Structure, Biological Function and Human Disease.Cancers · 2022Review
- Histone modification and histone modification-targeted anti-cancer drugs in breast cancer: Fundamentals and beyond.Frontiers in pharmacology · 2022Review
- ProtCID: a data resource for structural information on protein interactions.Nature communications · 2020Article
- Deciphering structure, function and mechanism of lysine acetyltransferase HBO1 in protein acetylation, transcription regulation, DNA replication and its oncogenic properties in cancer.Cellular and molecular life sciences : CMLS · 2020Review
- Biological Functions of the ING Proteins.Cancers · 2019Review
- The essential role of tumor suppressor geneBioscience reports · 2019Review
- Myst2/Kat7 histone acetyltransferase interaction proteomics reveals tumour-suppressor Niam as a novel binding partner in embryonic stem cells.Scientific reports · 2017Article
- INGs are potential drug targets for cancer.Journal of cancer research and clinical oncology · 2017Review
- Intrinsic ubiquitin E3 ligase activity of histone acetyltransferase Hbo1 for estrogen receptor α.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2017Article
- DNA replication origins-where do we begin?Genes & development · 2016Review
- Human T-cell leukemia virus type-1-encoded protein HBZ represses p53 function by inhibiting the acetyltransferase activity of p300/CBP and HBO1.Oncotarget · 2016Article
- DNA sequence templates adjacent nucleosome and ORC sites at gene amplification origins in Drosophila.Nucleic acids research · 2015Article
- Population analysis of microsatellite genotypes reveals a signature associated with ovarian cancer.Oncotarget · 2015Article
- The miR-193a-3p-regulated ING5 gene activates the DNA damage response pathway and inhibits multi-chemoresistance in bladder cancer.Oncotarget · 2015Article
- Histone acetyltransferase Hbo1 destabilizes estrogen receptor α by ubiquitination and modulates proliferation of breast cancers.Cancer science · 2013Article
- Exchange of associated factors directs a switch in HBO1 acetyltransferase histone tail specificity.Genes & development · 2013Article
- Activation of a human chromosomal replication origin by protein tethering.Nucleic acids research · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Hbo1 is a histone acetyltransferase (HAT) that is required for global histone H4 acetylation, steroid-dependent transcription, and chromatin loading of MCM2-7 during DNA replication licensing. It is the catalytic subunit of protein complexes that include ING and JADE proteins, growth regulatory factors and candidate tumor suppressors. These complexes are thought to act via tumor suppressor p53, but the molecular mechanisms and links between stress signaling and chromatin, are currently unknown. Here, we show that p53 physically interacts with Hbo1 and negatively regulates its HAT activity in vitro and in cells. Two physiological stresses that stabilize p53, hyperosmotic shock and DNA replication fork arrest, also inhibit Hbo1 HAT activity in a p53-dependent manner. Hyperosmotic stress during G(1) phase specifically inhibits the loading of the MCM2-7 complex, providing an example of the chromatin output of this pathway. These results reveal a direct regulatory connection between p53-responsive stress signaling and Hbo1-dependent chromatin pathways.
Indexed as
Identifiers
What OpenQuestion holds
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.