ArticleCell cycle (Georgetown, Tex.)2011
Double null cells reveal that CBP and p300 are dispensable for p53 targets p21 and Mdm2 but variably required for target genes of other signaling pathways.
Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Paradoxical cancer cell proliferation after FGFR inhibition through decreased p21 signaling in FGFR1-amplified breast cancer cells.Breast cancer research : BCR · 2024Article
- Article
- The pericentromeric protein shugoshin 2 cooperates with HSF1 in heat shock response and RNA Pol II recruitment.The EMBO journal · 2019Article
- A CRISPR Interference of CBP and p300 Selectively Induced Synthetic Lethality in Bladder Cancer CellsInternational journal of biological sciences · 2019Article
- DYRK1A interacts with histone acetyl transferase p300 and CBP and localizes to enhancers.Nucleic acids research · 2018Article
- Exposure of Rat Neural Stem Cells to Ethanol Affects Cell Numbers and Alters Expression of 28 Proteins.Neurochemical research · 2018Article
- Article
- ID4 regulates transcriptional activity of wild type and mutant p53 via K373 acetylation.Oncotarget · 2017Article
- Emerging Roles of the Mitogen and Stress Activated Kinases MSK1 and MSK2.Frontiers in cell and developmental biology · 2016Review
- p53 dynamics upon response element recognition explored by molecular simulations.Scientific reports · 2015Article
- Vitamin A deficiency impairs spatial learning and memory: the mechanism of abnormal CBP-dependent histone acetylation regulated by retinoic acid receptor alpha.Molecular neurobiology · 2015Article
- ATF1 modulates the heat shock response by regulating the stress-inducible heat shock factor 1 transcription complex.Molecular and cellular biology · 2015Article
- p53 Acetylation: Regulation and Consequences.Cancers · 2014Review
- The high-risk HPV16 E7 oncoprotein mediates interaction between the transcriptional coactivator CBP and the retinoblastoma protein pRb.Journal of molecular biology · 2014Article
- Genome-wide and single-cell analyses reveal a context dependent relationship between CBP recruitment and gene expression.Nucleic acids research · 2014Article
- Article
- Genetic syndromes caused by mutations in epigenetic genes.Human genetics · 2013Review
- p53-dependent growth arrest and induction of p21: a critical role for PCAF-mediated histone acetylation.Cell cycle (Georgetown, Tex.) · 2012Article
- The histone acetyltransferase PCAF regulates p21 transcription through stress-induced acetylation of histone H3.Cell cycle (Georgetown, Tex.) · 2012Article
- Mice heterozygous for CREB binding protein are hypersensitive to γ-radiation and invariably develop myelodysplastic/myeloproliferative neoplasm.Experimental hematology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The histone acetyltransferase coactivators CBP (CREBBP) and p300 (EP300) have more than 400 described protein interaction partners and are implicated in numerous transcriptional pathways. We have shown previously that CBP and p300 double knockout mutations in mouse embryonic fibroblasts (dKO MEFs) result in mixed effects on cAMP-inducible gene expression, with many CREB target genes requiring CBP/p300 for full expression, while others are unaffected or expressed better in their absence. Here we used CBP and p300 dKO MEFs to examine gene expression in response to four other signals: DNA damage (via p53), double-stranded RNA, serum, and retinoic acid. We found that while retinoic acid-inducible gene expression tends to be uniformly dependent on CBP/p300, dsRNA- and serum-inducible genes displayed non-uniform requirements for CBP/p300, with the dsRNA-inducible expression of Ifnb1 (interferon-β) being particularly dependent on CBP/p300. Surprisingly, the p53-dependent genes Cdkn1a (p21/CIP/WAF) and Mdm2 did not require CBP/p300 for their expression. As with cAMP-responsive CREB targets, we propose that the signal-responsive recruitment of CBP and p300 does not necessarily indicate a requirement for these coactivators at a locus. Rather, target gene context (e.g. DNA sequence) influences the extent to which transcription requires CBP/p300 versus other coactivators, which may not be HATs.
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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.