ArticleMolecular cell2011
JNK1 phosphorylation of Cdt1 inhibits recruitment of HBO1 histone acetylase and blocks replication licensing in response to stress.
Article in Molecular cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 47 citations in OpenAlex.
- 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
- Non-canonical functions of enhancers: regulation of RNA polymerase III transcription, DNA replication, and V(D)J recombination.Trends in genetics : TIG · 2024Article
- Review
- A first-in-class HBO1 inhibitor WM-3835 inhibits castration-resistant prostate cancer cell growth in vitro and in vivo.Cell death & disease · 2023Article
- HBO1 induces histone acetylation and is important for non-small cell lung cancer cell growth.International journal of biological sciences · 2022Article
- Article
- Histone H3 N-terminal mimicry drives a novel network of methyl-effector interactions.The Biochemical journal · 2021Article
- Regulation of DNA Replication Licensing and Re-Replication by Cdt1.International journal of molecular sciences · 2021Review
- The histone acetyltransferase HBO1 functions as a novel oncogenic gene in osteosarcoma.Theranostics · 2021Article
- Distinct and sequential re-replication barriers ensure precise genome duplication.PLoS genetics · 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
- HBO1 (KAT7) Does Not Have an Essential Role in Cell Proliferation, DNA Replication, or Histone 4 Acetylation in Human Cells.Molecular and cellular biology · 2020Article
- The Protective Effect of HBO1 on Cigarette Smoke Extract-Induced Apoptosis in Airway Epithelial Cells.International journal of chronic obstructive pulmonary disease · 2020Article
- Order from clutter: selective interactions at mammalian replication origins.Nature reviews. Genetics · 2017Review
- Regulation and Function of Cdt1; A Key Factor in Cell Proliferation and Genome Stability.Genes · 2016Review
- JNK Signaling: Regulation and Functions Based on Complex Protein-Protein Partnerships.Microbiology and molecular biology reviews : MMBR · 2016Review
- A replicator-specific binding protein essential for site-specific initiation of DNA replication in mammalian cells.Nature communications · 2016Article
- CDK1-dependent inhibition of the E3 ubiquitin ligase CRL4CDT2 ensures robust transition from S Phase to Mitosis.The Journal of biological chemistry · 2015Article
- Mitotic UV irradiation induces a DNA replication-licensing defect that potentiates G1 arrest response.PloS one · 2015Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
In response to environmental stresses, cells activate stress-response genes and inhibit DNA replication. HBO1 histone acetylase is a coactivator both for AP-1 transcription factors responding to stress-activated JNK kinases and also for the Cdt1 licensing factor that ensures that DNA is replicated exactly once per cell cycle. In response to nongenotoxic stress, JNK phosphorylates Jun, an AP-1 transcription factor, leading to increased recruitment of HBO1 and increased transcription of target genes. In addition, JNK phosphorylates Cdt1 on threonine 29, leading to rapid dissociation of HBO1 from replication origins, thereby blocking initiation of DNA replication. Upon relief of stress, HBO1 reassociates with replication origins. Thus, regulated and reciprocal recruitment of the HBO1 coactivator to target genes and replication origins via JNK-mediated phosphorylation of the recruiting transcription and replication licensing factors coordinates the transcriptional and DNA replication response to cellular stress.
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