ArticleOncogene2000
The adenovirus E1A binding protein BS69 is a corepressor of transcription through recruitment of N-CoR.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 79 citations in OpenAlex.
- Bromodomain-Driven Regulation of Stem Cells: A Potential Target for Cancer Therapeutic Intervention.Stem cell reviews and reports · 2026Review
- Novel intermolecular zinc fingers and redox-driven conformational changes dictate tumor suppressor ZMYND11's role in cooperative recognition of diverse targets.Nucleic acids research · 2026Article
- Epigenetic reader ZMYND11 noncanonical function restricts HNRNPA1-mediated stress granule formation and oncogenic activity.Signal transduction and targeted therapy · 2024Article
- Zinc finger myeloid Nervy DEAF-1 type (ZMYND) domain containing proteins exert molecular interactions to implicate in carcinogenesis.Discover oncology · 2022Review
- Identification of bromodomain-containing proteins prognostic value and expression significance based on a genomic landscape analysis of ovarian serous cystadenocarcinoma.Frontiers in oncology · 2022Article
- ZMYND11-MBTD1 induces leukemogenesis through hijacking NuA4/TIP60 acetyltransferase complex and a PWWP-mediated chromatin association mechanism.Nature communications · 2021Article
- MicroRNA-196a promotes renal cancer cell migration and invasion by targeting BRAM1 to regulate SMAD and MAPK signaling pathways.International journal of biological sciences · 2021Article
- Bromodomain and BET family proteins as epigenetic targets in cancer therapy: their degradation, present drugs, and possible PROTACs.RSC advances · 2020Review
- PDCD2 functions as an evolutionarily conserved chaperone dedicated for the 40S ribosomal protein uS5 (RPS2).Nucleic acids research · 2020Article
- The Transcriptional Repressor BS69 is a Conserved Target of the E1A Proteins from Several Human Adenovirus Species.Viruses · 2018Article
- The Histone Variant H3.3 in Transcriptional Regulation and Human Disease.Journal of molecular biology · 2017Review
- Mouse myofibers lacking the SMYD1 methyltransferase are susceptible to atrophy, internalization of nuclei and myofibrillar disarray.Disease models & mechanisms · 2016Article
- BS69/ZMYND11 C-Terminal Domains Bind and Inhibit EBNA2.PLoS pathogens · 2016Article
- Histone H3.3 and cancer: A potential reader connection.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Smyd1 facilitates heart development by antagonizing oxidative and ER stress responses.PloS one · 2015Article
- Refining analyses of copy number variation identifies specific genes associated with developmental delay.Nature genetics · 2014Article
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- Hepatoma-derived growth factor represses SET and MYND domain containing 1 gene expression through interaction with C-terminal binding protein.Journal of molecular biology · 2009Article
- BS69 is involved in cellular senescence through the p53-p21Cip1 pathway.EMBO reports · 2007Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BS69 was first identified as a protein that interacts directly with the transactivation domain (conserved region 3) of the 289R adenovirus type 5 E1A protein. We show here that BS69 is a potent repressor of transcription. BS69 mediates repression, at least in part, through interaction with the co-repressor N-CoR. BS69 interacts with N-CoR through a MYND domain in its carboxyl terminus. A recently cloned splice variant of BS69, designated BRAM1, is also capable of interacting with N-CoR and E1A, but unlike BS69, is not able to repress transcription, indicating that N-CoR interaction is necessary but not sufficient for BS69 repression. Expression of E1A inhibits repression mediated by BS69. Our data suggest that BS69 participates in transcriptional repressor complexes and that E1A can modulate these complexes through interaction with BS69.
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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.