Affinage

CREBBP

CREB-binding protein · UniProt Q92793

Round 2 corrected
Length
2442 aa
Mass
265.4 kDa
Annotated
2026-04-28
130 papers in source corpus 65 papers cited in narrative 64 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CREBBP (CBP) is a lysine acetyltransferase and transcriptional coactivator that integrates diverse signal transduction pathways by bridging phosphorylation-dependent transcription factors—including CREB, p53, NF-κB, STATs, Smads, and nuclear receptors—to the basal transcription machinery and to chromatin (PMID:8413673, PMID:9194564, PMID:9096323, PMID:8616895). CBP acetylates histones H3K18, H3K27, and H2B within nucleosomes, reading pre-existing H4 tail acetylation via its bromodomain and transcribing that mark to H2A–H2B dimers to destabilize nucleosomes, while also acetylating non-histone substrates such as p53, RelA, DOT1L, and GAPDH to regulate their stability or transcriptional activity (PMID:21131905, PMID:37460559, PMID:18485870, PMID:12456660, PMID:32042335). Its activity is tuned by phosphorylation (CaMKIV at Ser301, IKKα at Ser1382/1386, aPKC at Ser436), by enhancer RNAs that directly stimulate HAT activity, and by inhibitory interactions with proteins such as HOX family members and USP12 (PMID:11970865, PMID:17434128, PMID:28086087, PMID:11585930, PMID:31899788). Heterozygous loss-of-function mutations in CREBBP cause Rubinstein–Taybi syndrome and are recurrently found in follicular and diffuse large B-cell lymphoma, where impaired acetylation of BCL6 and p53 drives lymphomagenesis (PMID:7630403, PMID:21390126, PMID:28069569).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1993 High

    Identification of CBP as a phosphorylation-dependent coactivator resolved how PKA-phosphorylated CREB activates cAMP-responsive genes, establishing the coactivator paradigm for signal-dependent transcription.

    Evidence Co-immunoprecipitation and fusion-protein transcriptional activation assay showing CBP binds phospho-CREB but not unphosphorylated CREB

    PMID:8413673

    Open questions at the time
    • Enzymatic activity of CBP unknown at this stage
    • Mechanism of transcriptional activation beyond scaffolding undefined
  2. 1994 High

    Demonstration that CBP contacts basal factor TFIIB and is required for multiple signaling pathways (cAMP, AP-1) established CBP as a general integrative coactivator rather than a CREB-specific adapter.

    Evidence Fluorescence anisotropy binding to TFIIB, microinjection of anti-CBP antibody blocking CRE and AP-1-driven transcription

    PMID:7913207 PMID:8028671

    Open questions at the time
    • Whether CBP possesses intrinsic enzymatic activity not yet tested
    • Number and identity of additional signal-dependent partners unknown
  3. 1995 High

    Positional cloning of CREBBP mutations in Rubinstein–Taybi syndrome patients established CBP haploinsufficiency as the molecular basis of a developmental disorder, demonstrating dosage sensitivity of its coactivator function in vivo.

    Evidence Germline mutation analysis in RTS families

    PMID:7630403

    Open questions at the time
    • Which CBP-dependent transcriptional programs drive RTS phenotypes not defined
    • Functional consequence of individual mutations not characterized
  4. 1996 High

    Mapping of CBP interactions with nuclear receptors, p160 coactivators, and STATs, together with evidence for competitive binding by NF-κB/AP-1, established the model of CBP as a limiting integrator whose availability arbitrates between competing signaling pathways.

    Evidence In vitro binding assays, co-IP, and transcriptional competition experiments; MOZ–CBP translocation cloning in AML

    PMID:8616895 PMID:8782817 PMID:8848048

    Open questions at the time
    • Whether CBP acetylates non-histone substrates not yet explored
    • Structural basis for multi-partner binding unresolved
  5. 1997 High

    Discovery that CBP directly binds and coactivates p53 and NF-κB p65, and that RNA helicase A bridges CBP to RNA Pol II, defined the molecular architecture of CBP-nucleated transcriptional complexes at multiple classes of promoters.

    Evidence Reciprocal co-IP, GST pulldowns, mutagenesis of p53 transactivation domain, RHA helicase-dead mutant analysis

    PMID:9096323 PMID:9194564 PMID:9194565 PMID:9323138

    Open questions at the time
    • HAT substrate specificity of CBP not yet mapped
    • Relative contribution of scaffolding versus catalytic activity unclear
  6. 2001 High

    Sequestration and inhibition of CBP by polyglutamine-expanded huntingtin provided a mechanistic link between CBP acetyltransferase loss and neurodegenerative transcriptional dysregulation, and showed that HDAC inhibitors can rescue polyglutamine toxicity.

    Evidence In vitro HAT inhibition, immunofluorescence in HD brain, neuronal rescue by CBP overexpression and HDAC inhibitors in Drosophila

    PMID:11264541 PMID:11607033

    Open questions at the time
    • Whether CBP sequestration is primary pathogenic event or bystander effect debated
    • Specific gene targets affected by CBP depletion in neurons uncharacterized
  7. 2002 High

    Identification of CaMKIV phosphorylation of CBP Ser301 and phosphorylation-dependent p65 switching between CBP and HDAC-1 established that CBP itself is a regulated enzyme whose partner selectivity and activity are modulated by post-translational modifications.

    Evidence In vitro kinase assay, Ser301 mutagenesis in neurons; phospho-p65 co-IP switching between CBP and HDAC-1

    PMID:11931769 PMID:11970865 PMID:12456660

    Open questions at the time
    • Full phosphorylation map of CBP not established
    • Whether other kinases similarly modulate CBP partner switching unknown
  8. 2007 High

    IKKα phosphorylation of CBP at Ser1382/1386 was shown to switch CBP's binding preference from p53 to NF-κB, providing a direct mechanism by which inflammatory kinase signaling suppresses tumor suppression and promotes growth.

    Evidence In vitro kinase assay, mutagenesis, co-IP switch, correlation with IKKα activation in human lung tumors

    PMID:17434128

    Open questions at the time
    • Whether this switch operates in all cell types not established
    • Phosphatase(s) reversing this modification unidentified
  9. 2010 High

    Genetic deletion of CBP/p300 revealed that these enzymes are uniquely responsible for H3K18ac and H3K27ac genome-wide and are essential for ligand-induced Pol II recruitment at nuclear receptor targets, distinguishing them from GCN5/PCAF.

    Evidence Genetic deletion, mass spectrometry of histone acetylation, ChIP

    PMID:21131905

    Open questions at the time
    • Whether CBP and p300 have fully redundant or partially distinct histone substrate preferences unclear
    • Genome-wide maps of CBP versus p300 occupancy not yet available
  10. 2011 High

    Sequencing of follicular and diffuse large B-cell lymphomas uncovered frequent inactivating CREBBP mutations that impair BCL6 acetylation-mediated inactivation and p53 activation, establishing CREBBP as a haploinsufficient tumor suppressor in germinal center-derived lymphomas.

    Evidence Genomic sequencing of large lymphoma cohorts, acetylation assays, functional reporter assays

    PMID:21390126

    Open questions at the time
    • Whether restoration of CBP HAT activity can reverse lymphomagenesis not shown
    • Contribution of non-HAT CBP functions to lymphoma suppression unclear
  11. 2017 High

    Discovery that enhancer RNAs directly bind CBP's HAT domain and stimulate its acetyltransferase activity at active enhancers provided a feed-forward mechanism linking transcription from enhancers to increased H3K27ac and target gene activation.

    Evidence RNA immunoprecipitation, in vitro HAT stimulation assay, ChIP-seq, RNA knockdown

    PMID:28086087

    Open questions at the time
    • Structural basis of eRNA–HAT domain interaction unresolved
    • Selectivity rules for which eRNAs stimulate CBP unknown
  12. 2019 High

    Domain-selective chemical probes demonstrated that the CBP/p300 bromodomain and HAT domain perform distinct functions: bromodomain inhibition facilitates cellular reprogramming by removing somatic gene expression, whereas HAT inhibition blocks iPSC formation entirely.

    Evidence Selective bromodomain versus HAT inhibitors, ATAC-seq, ChIP, iPSC reprogramming assay

    PMID:30962627

    Open questions at the time
    • Which bromodomain-read marks are critical for somatic identity maintenance not fully mapped
    • Relevance of these findings beyond reprogramming context uncertain
  13. 2023 High

    Cryo-EM structures revealed that CBP/p300 reads H4 tail acetylation via its bromodomain and writes acetylation onto H2B within the same nucleosome, promoting H2A–H2B dimer dissociation and nucleosome destabilization — providing the first structural mechanism for CBP-driven chromatin opening.

    Evidence Cryo-EM at near-atomic resolution, in vitro HAT assay with defined nucleosome substrates, histone dissociation assay

    PMID:37460559

    Open questions at the time
    • Whether this read-write mechanism operates at all CBP-occupied genomic loci unknown
    • How eRNA stimulation integrates with the structural mechanism not addressed
  14. 2024 High

    Combined Crebbp and Kmt2d haploinsufficiency revealed mutual chromatin-binding dependency and cooperative regulation of immune-synapse super-enhancers, demonstrating that CREBBP loss shapes both tumor-intrinsic transcription and the immune microenvironment.

    Evidence Compound knockout mouse model, ChIP-seq for CREBBP/KMT2D and H3K27ac, tumor microenvironment flow cytometry

    PMID:38570506

    Open questions at the time
    • Whether immune evasion in CREBBP-mutant lymphomas is reversible by HAT restoration not tested
    • Molecular basis of mutual KMT2D–CREBBP chromatin dependency unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis for eRNA-mediated HAT stimulation, whether CBP and p300 have genuinely non-redundant genomic targets in vivo, and whether pharmacological HAT restoration can reverse CREBBP-mutant lymphomagenesis in patients.
  • Full structural model of eRNA–CBP HAT domain interaction lacking
  • In vivo non-redundancy of CBP versus p300 at specific loci not systematically resolved
  • Clinical validation of CBP-targeted therapies in CREBBP-mutant cancers ongoing

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 9 GO:0140110 transcription regulator activity 7 GO:0016740 transferase activity 5 GO:0042393 histone binding 3 GO:0003723 RNA binding 1
Localization
GO:0005634 nucleus 4 GO:0005654 nucleoplasm 2
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-1643685 Disease 4 R-HSA-168256 Immune System 4 R-HSA-4839726 Chromatin organization 4 R-HSA-5357801 Programmed Cell Death 3 R-HSA-1266738 Developmental Biology 2
Partners
CREB1DHX9KAT2BKMT2DNCOA1NCOA3RELATP53
Complex memberships
CREB–CBP–RNA helicase A–Pol II complexNuclear receptor coactivator complex (with p160/SRC-1/ACTR/P/CAF)

Evidence

Reading pass · 64 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1993 CREB-binding protein (CBP/CREBBP), a 265 kDa nuclear protein, was identified as a binding partner that specifically interacts with PKA-phosphorylated CREB but not unphosphorylated CREB; fusion of a heterologous DNA-binding domain to CBP enabled it to function as a PKA-regulated transcriptional activator, establishing CBP as a phosphorylation-dependent coactivator in cAMP-regulated gene expression. Co-immunoprecipitation, fusion protein transcriptional activation assay in cells Nature High 8413673
1994 CBP functions as a transcriptional coactivator: it activates transcription through a domain in its carboxy terminus, and this activation domain interacts directly with the basal transcription factor TFIIB through a region conserved in the yeast coactivator ADA-1; fluorescence anisotropy defined equilibrium binding parameters of the phosphoCREB:CBP interaction. Fluorescence anisotropy binding assay, transcriptional activation assay, in vitro interaction with TFIIB Nature High 7913207
1994 Microinjection of anti-CBP antiserum into fibroblasts inhibits transcription from cAMP-responsive promoters; CBP also cooperates with upstream activators such as c-Jun for mitogen-responsive transcription, establishing CBP as a common nuclear factor required by multiple signaling pathways. Microinjection of neutralizing antibody, reporter gene assay Nature High 8028671
1995 Germline mutations (gross chromosomal rearrangements and point mutations) in the CBP gene cause Rubinstein-Taybi syndrome (RTS); patients are heterozygous for CBP mutations, establishing haploinsufficiency of CREBBP as the molecular basis of RTS and its associated developmental abnormalities. Positional cloning, mutation analysis in RTS patients Nature High 7630403
1996 CBP directly interacts with the ligand-binding domain of multiple nuclear receptors and with p160 nuclear receptor coactivators (SRC-1 variants); CBP is required in addition to distinct coactivators for nuclear receptor function; competition between NF-κB/AP-1 and nuclear receptors for limiting CBP/p300 provides a mechanism for AP-1 inhibition by nuclear receptors. In vitro binding assays, transient transfection, co-immunoprecipitation Cell High 8616895
1996 The adenoviral oncoprotein E1A blocks interferon-alpha responses by inhibiting p300/CBP function; specifically, the first cysteine-histidine-rich region of CBP/p300 binds the carboxy-terminal segment of Stat2, and this interaction is required for IFN-alpha-activated transcription through ISGF3. Co-immunoprecipitation, transient transfection reporter assay, domain mapping Nature High 8848048
1996 The t(8;16)(p11;p13) translocation in acute myeloid leukemia fuses MOZ (a putative acetyltransferase with zinc fingers) to CBP, producing an in-frame MOZ-CBP fusion transcript; the fusion retains MOZ finger motifs and acetyltransferase domain combined with largely intact CBP, suggesting aberrant chromatin acetylation drives leukemogenesis. Positional cloning, breakpoint mapping, fusion transcript characterization Nature genetics High 8782817
1997 CBP directly binds the amino-terminal activation domain of p53 both in vitro and in vivo; p300 and p53 colocalize in the nucleus and exist in a stable DNA-binding complex; E1A, by binding p300/CBP, disrupts p53-mediated activation of p21 and bax promoters and suppresses p53-induced cell-cycle arrest and apoptosis. Co-immunoprecipitation, colocalization, transcriptional reporter assays, cell-cycle analysis Nature High 9194565
1997 CBP acts as a p53 coactivator: the amino-terminal activation domain of p53 interacts with the carboxy-terminal portion of CBP both in vitro and in vivo; a double point mutation abolishing p53 transactivation also abolishes CBP binding; CBP and p53 synergistically activate mdm-2 and Gal4-responsive reporter genes. GST pulldown, co-IP, transient transfection in SaoS-2 cells, point mutagenesis Nature High 9194564
1997 RNA helicase A (RHA) mediates association of CBP with RNA polymerase II; complex formation between CBP and Pol II requires RHA; RHA cooperates with CBP in mediating CREB-dependent target gene activation; an RHA mutation compromising helicase activity reduces CREB-dependent transcription, indicating RHA-induced chromatin changes promote transcriptional apparatus engagement. Co-immunoprecipitation, transient transfection, helicase-dead mutant analysis Cell High 9323138
1997 ACTR (nuclear receptor coactivator) directly binds nuclear receptors and recruits both CBP and P/CAF to form a multisubunit coactivator complex; this complex contains at least three classes of histone acetyltransferases acting cooperatively in hormonal gene activation. Co-immunoprecipitation, in vitro HAT assay, transcriptional activation assay Cell High 9267036
1997 The LXXLL motif in CBP (and SRC-1, RIP-140) is necessary and sufficient to mediate binding to liganded nuclear receptors; integrity of LXXLL motifs and key hydrophobic residues in helix 12 of the estrogen receptor are required for ligand-induced activation. Mutagenesis, GST pulldown, transcriptional activation assay Nature High 9192902
1997 p/CIP forms a complex with CBP in cells and is required for transcriptional activity of nuclear receptors and other CBP/p300-dependent transcription factors; p/CIP, NCoA-1, and CBP all contain related leucine-rich charged helical interaction motifs required for receptor-specific gene activation. Co-immunoprecipitation, transcriptional reporter assay, domain mapping Nature High 9192892
1997 CBP and p300 are transcriptional coactivators of the NF-κB p65 (RelA) subunit; both proteins physically interact with p65 via their N- and C-terminal domains; overexpression of CBP/p300 potentiates p65-activated transcription of E-selectin and VCAM-1 reporters; E1A inhibits p65-dependent gene expression by binding CBP/p300. GST pulldown, co-immunoprecipitation, transcriptional reporter assay, two-hybrid assay Proceedings of the National Academy of Sciences of the United States of America High 9096323
1998 Akt/PKB phosphorylates CREB at Ser-133, promoting recruitment of CBP and subsequent target gene expression; Akt/PKB-induced CREB activity requires the phosphatidylinositol 3-kinase pathway, establishing CBP recruitment as a downstream effector of Akt-mediated cell survival signaling. Phosphorylation assay, transcriptional reporter assay, kinase inhibitor experiments The Journal of biological chemistry High 9829964
1998 Following Sendai virus infection, IRF-3 associates with CBP coactivator via C-terminal domains of both proteins; this interaction requires phosphorylation of IRF-3 at Ser-396/Ser-398; virus-induced phosphorylation triggers nuclear translocation and CBP-dependent transcriptional activation of IFN-α/β genes. Co-immunoprecipitation, mutagenesis, transcriptional reporter assay Molecular and cellular biology High 9566918
1999 ACT (LIM-only protein) stimulates CREB and CREM transcriptional activity independently of the classical CBP coactivator pathway; ACT bypasses the requirement for phosphorylation of CREM Ser117 and interaction with CBP, defining a CBP-independent route for CREM/CREB activation in testis. Two-hybrid screen, transcriptional reporter assay in yeast and mammalian cells Nature High 10086359
1999 CBP physically interacts with Smad1 both in vitro and in vivo; the C-terminal half of Smad1 harbors two interaction domains binding the same C-terminal region of CBP; phosphorylation of Smad1 enhances its binding to CBP and further stimulates Smad1-dependent transcription, providing a mechanism for BMP signaling via CBP. GST pulldown, co-immunoprecipitation, transcriptional reporter assay Biochimica et biophysica acta Medium 10673036
1999 p300 but not CBP contributes to ionizing radiation sensitivity and IR-induced apoptosis; cells deficient in p300, but not CBP-deficient cells, show impaired apoptotic response to DNA damage, demonstrating functional non-redundancy between the two paralogs in the DNA damage response. Stable cell lines deficient in p300 or CBP, IR sensitivity assay, apoptosis assay Oncogene Medium 10523850
1999 CBP cooperates with Stat6 to activate IL-4-induced gene transcription; the C-terminal region of Stat6 is required for cooperation with CBP/p300; E1A inhibits CBP/p300-mediated Stat6 coactivation; cooperation does not depend on acetylation of Stat6. Transcriptional reporter assay, co-immunoprecipitation, E1A inhibition Journal of interferon & cytokine research Medium 10454341
2000 BRCA1 physically associates with CBP and p300 in a phosphorylation-independent manner; BRCA1 interacts with the CREB domain of p300/CBP via both its amino and carboxyl termini; p300/CBP enhances BRCA1-mediated transactivation; E1A suppresses this effect; BRCA1 and p300 associate in a cell cycle-dependent manner by immunocolocalization. Co-immunoprecipitation (endogenous and overexpressed), transcriptional reporter assay, immunolocalization Proceedings of the National Academy of Sciences of the United States of America Medium 10655477
2000 CBP is recruited to and acetylates UBF (upstream binding factor) both in vitro and in vivo, activating RNA polymerase I transcription through its acetyltransferase domain; CBP activation and Rb-mediated suppression of ribosomal transcription via UBF are mutually exclusive, constituting an acetylation-deacetylation flip-flop regulating PolI transcription. In vitro acetylation assay, in vivo CBP recruitment, reporter assay, reconstituted PolI transcription Molecular cell High 11106745
2001 CBP and RSK2 form a complex in quiescent cells where both RSK2 kinase activity and CBP acetyltransferase activity are inhibited; upon mitogenic stimulation, phosphorylation of RSK2 at Ser227 causes complex dissociation and stimulates both kinase and HAT activities, allowing coordinated phosphorylation and acetylation of specific substrates for gene activation. Co-immunoprecipitation, in vitro HAT assay, kinase assay, phosphorylation-site mutagenesis Molecular and cellular biology High 11564891
2001 Each of 14 HOX proteins (from 11 paralog groups) binds CBP or p300 via the homeodomain; HOX proteins are not substrates for CBP HAT but instead inhibit CBP HAT activity in vitro and in vivo; CBP prevents HOX protein binding to DNA; these mutually inhibitory interactions prevent CBP from potentiating HOX-driven transcription. Co-immunoprecipitation, in vitro HAT assay, DNA binding assay, transcriptional reporter assay Molecular and cellular biology High 11585930
2001 Expanded polyglutamine repeats (huntingtin, atrophin-1) interfere with CBP-mediated gene transcription; CBP is depleted from its normal nuclear location and sequestered in polyglutamine aggregates in HD cell culture, transgenic mice, and human HD brain; overexpression of CBP rescues polyglutamine-induced neuronal toxicity. Immunofluorescence, co-immunoprecipitation, transcriptional reporter assay, neuronal rescue experiment Science High 11264541
2001 The polyglutamine-containing domain of huntingtin directly binds the acetyltransferase domains of CBP and P/CAF in cell-free assays; Httex1p inhibits acetyltransferase activity of CBP, p300, and P/CAF; expression of Httex1p in cells reduces acetylated histones H3 and H4; HDAC inhibitors reverse this reduction and arrest neuronal degeneration in Drosophila polyglutamine models. In vitro acetyltransferase assay, cell-based histone acetylation assay, Drosophila genetic model Nature High 11607033
2001 Huntingtin protein interacts with CBP and mSin3a in vitro; expanded httex1p represses transcription from p53-regulated promoters (p21WAF1/CIP1, MDR-1) and sequesters CBP in neuronal intranuclear inclusions in HD transgenic mouse brain. In vitro binding assay, transcriptional reporter assay, immunohistochemistry in transgenic mice Proceedings of the National Academy of Sciences of the United States of America High 10823891
2002 In the absence of Ca2+, DREAM binds the LCD motif in the kinase-inducible domain of CREB, impairing recruitment of CBP by phospho-CREB and blocking CBP-mediated transactivation at CRE sites; Ca2+ binding to DREAM relieves this inhibition, establishing Ca2+-dependent DREAM-CREB interaction as a cross-talk point between cAMP and Ca2+ signaling. Co-immunoprecipitation, transcriptional reporter assay, domain mapping The EMBO journal Medium 12198160
2002 Phosphorylation of NF-κB p65 determines whether it associates with CBP (leading to transcriptional activation) or HDAC-1 (leading to repression); phosphorylated p65 displaces p50-HDAC-1 complexes from DNA and recruits CBP. Co-immunoprecipitation, chromatin-based binding assay, transcriptional reporter assay Molecular cell High 11931769
2002 p300 and CBP acetyltransferases acetylate RelA at specific lysines (218, 221, 310); acetylation at K221 enhances DNA binding and impairs IκBα assembly; acetylation at K310 is required for full transcriptional activity; site-specific acetylation by CBP/p300 thus differentially regulates distinct NF-κB biological activities. In vivo acetylation assay, lysine-to-arginine mutagenesis, dominant-negative p300 co-expression, DNA-binding assay The EMBO journal High 12456660
2002 Phosphorylation of CBP at Ser301 by CaM kinase IV (CaMKIV) mediates transcriptional activation in response to neuronal activity and NMDA; NMDA activates CREB-responsive genes with ERK responsible for CREB phosphorylation and CaMKIV responsible for CBP phosphorylation; mutation of Ser301 impairs NMDA- and CaMKIV-stimulated transcription. In vitro and in vivo phosphorylation assay, site-directed mutagenesis, CaM kinase inhibitors, neuronal transcription reporter Neuron High 11970865
2003 Early B-cell factor (EBF) binds the HAT/CH3 domain of p300/CBP via two EBF domains; EBF inhibits the HAT activity of p300/CBP in vivo and in vitro; EBF cannot bind p300/CBP and DNA simultaneously; this inhibitory property is shared only with E1A, Twist, Pu.1, and HOX proteins. Co-immunoprecipitation, in vitro HAT assay, DNA binding assay, transcriptional reporter assay Molecular and cellular biology Medium 12748286
2004 CBP inactivation in mouse thymocytes leads to T-cell lymphoma; CBP-null tumors show reduced p27Kip1 and increased cyclin E and Skp2; introduction of a p27Kip1-null allele accelerates lymphomagenesis, establishing that CBP loss mediates oncogenesis cooperatively with p27Kip1 reduction rather than through p53 pathway loss. Conditional knockout mouse model, genetic epistasis (CBP KO × p27Kip1 KO), western blot, tumor analysis Cancer cell High 14998493
2005 The MLL-CBP fusion protein selectively expands granulocyte/macrophage progenitors (GMP) and enhances their self-renewal; it upregulates a subset of genes including HoxA9; RNA interference against HoxA9 demonstrates MLL-CBP requires HoxA9 for enhanced cell expansion; after mutagenic exposure, MLL-CBP mice develop myeloproliferative disorders mirroring human therapy-related leukemia. Conditional knockin mouse model, gene expression analysis, RNA interference, mutagenic treatment model The EMBO journal High 15635450
2005 Mutant huntingtin selectively binds and degrades CBP (but not p300) via the proteasome pathway; soluble mutant huntingtin represses CBP transcriptional activity at early time points; HAT activity of CBP is gradually diminished; this selective CBP degradation is absent in SCA3, indicating specificity. Co-immunoprecipitation, proteasome inhibitor experiments, transcriptional reporter assay, western blot Molecular and cellular neurosciences Medium 15994095 16456924
2006 CBP interacts with nuclear transport proteins CAS and Importin-α (Impα); CAS binds the SRC1-interaction domain of CBP via a leucine-rich motif; CBP and Impα form a complex; HDAC inhibitor treatment sequesters Impα in the nuclear envelope and increases CBP-containing PML bodies, linking CBP to nuclear transport regulation. Co-immunoprecipitation, immunofluorescence localization, HDAC inhibitor treatment Cell cycle Medium 16969114
2007 IKKα phosphorylates CBP at serine 1382 and serine 1386, enhancing CBP's HAT and transcriptional activities; this phosphorylation switches CBP's binding preference from p53 to NF-κB, promoting NF-κB-mediated gene expression while suppressing p53-mediated expression and promoting cell growth; CBP phosphorylation correlates with constitutive IKKα activation in human lung tumors. In vitro kinase assay, site-directed mutagenesis, co-immunoprecipitation, transcriptional reporter assay, tumor tissue analysis Molecular cell High 17434128
2007 CBP is phosphorylated by ATM and ATR in response to DNA damage, as identified by large-scale phosphoproteomic analysis of over 900 regulated phosphorylation sites on >700 proteins, placing CBP within the DNA damage response network. Large-scale mass spectrometry phosphoproteomics with ATM/ATR substrate motif enrichment Science Medium 17525332
2008 Nuclear GAPDH (S-nitrosylated by NO) is acetylated at Lys160 by CBP/p300 through direct protein interaction; this acetylation in turn stimulates CBP/p300 acetyltransferase activity; consequently, downstream CBP/p300 targets including p53 are activated, mediating apoptosis; GAPDH-K160R dominant-negative mutant prevents CBP/p300 activation and reduces apoptotic gene induction. Co-immunoprecipitation, in vitro acetyltransferase assay, mutagenesis (K160R), apoptosis assay Nature cell biology High 18552833
2008 p53 acetylation by CBP/p300 (and P/CAF) is indispensable for p53 activation; unacetylated p53 retains ability to induce the p53-Mdm2 feedback loop but loss of acetylation completely abolishes p53-dependent growth arrest and apoptosis; acetylation abrogates Mdm2-mediated repression by blocking Mdm2 recruitment to p53-responsive promoters. Acetylation site mapping, lysine-to-arginine mutagenesis, chromatin immunoprecipitation, cell-cycle and apoptosis assays Cell High 18485870
2009 IL-4 activates androgen receptor (AR) through CBP/p300: IL-4 increases CBP/p300 protein expression and enhances AR-CBP/p300 interaction; CBP/p300 is recruited to androgen-responsive elements; CBP/p300 siRNA abolishes IL-4-mediated AR activation and AR acetylation, establishing CBP/p300 HAT activity as required for IL-4-driven AR activation in prostate cancer. Co-immunoprecipitation, ChIP assay, siRNA knockdown, AR acetylation assay The Prostate Medium 18819102
2010 CBP/p300 specifically and dramatically reduce H3K18 and H3K27 acetylation (H3K18/27ac) when deleted in cells; CBP/p300 and their HAT activities are essential for ligand-induced RNA Pol II recruitment and activation of nuclear receptor target genes; this is distinct from GCN5/PCAF which controls H3K9ac and is dispensable for NR target gene activation. Genetic deletion of CBP/p300, ChIP, H3K18/K27 acetylation mass spectrometry, transcriptional reporter assay The EMBO journal High 21131905
2011 CREBBP and EP300 are frequently mutated (inactivating mutations in HAT domain, deletions) in follicular lymphoma (~41%) and diffuse large B-cell lymphoma (~39%); CREBBP mutations cause specific defects in acetylation-mediated inactivation of BCL6 oncoprotein and impaired activation of p53 tumor suppressor, establishing CREBBP/EP300 mutations as a major pathogenetic mechanism in B-cell lymphoma. Genomic sequencing, deletion mapping, acetylation assays, functional reporter assays in lymphoma cells Nature High 21390126
2013 CBP drives β-adrenoceptor/cAMP/PKA-mediated apoptosis by transcriptionally inducing the pro-apoptotic BH3-only protein Bim; CBP associates with c-Myc and this association alters histone acetylation and methylation patterns at the Bim promoter; catecholamine-mediated apoptosis in thymus and heart is abrogated by Bim loss. Co-immunoprecipitation, ChIP, genetic knockouts (Bim KO), reporter assay Cell death and differentiation Medium 23579242
2015 Ku80 interacts with CBP; CBP acetylates Ku80 to co-regulate COX-2 promoter activation; overexpression of CBP increases Ku80 acetylation, promoting COX-2 expression and cell growth; CBP-specific inhibition or siRNA reduces COX-2 expression and tumor cell growth. Streptavidin pulldown/proteomics, co-immunoprecipitation, acetylation assay, siRNA knockdown, xenograft model Oncotarget Medium 25797267
2015 Ajuba (LIM protein) recruits CBP/p300 via its LIM domain and facilitates CBP/p300 binding to PPARγ; Ajuba, PPARγ, and CBP/p300 cooperatively occupy PPARγ target promoters and increase histone acetylation, promoting adipogenic differentiation; depletion of Ajuba decreases PPARγ target gene expression and delays adipogenesis. Co-immunoprecipitation, ChIP, siRNA knockdown, overexpression in 3T3-L1 cells Cell death and differentiation Medium 26113042
2016 Salicylate inhibits CBP and p300 lysine acetyltransferase activity in vitro by direct competition with acetyl-CoA at the catalytic site; diflunisal inhibits p300 more potently; at plasma-attainable concentrations, both drugs block acetylation of histone and non-histone proteins in cells; diflunisal suppresses growth of p300-dependent AML1-ETO leukemia cells in vitro and in vivo. In vitro acetyltransferase competition assay, cell-based acetylation assay, xenograft tumor model eLife High 27244239
2017 CBP directly binds RNAs in vivo and in vitro, including a large number of enhancer RNAs (eRNAs); an RNA-binding region in the HAT domain of CBP (unique to CBP/p300) allows RNA to stimulate CBP's HAT activity; at active enhancers, CBP-eRNA interaction increases H3K27ac and corresponding target gene expression. RNA immunoprecipitation (in vivo and in vitro), steady-state HAT assay, ChIP-seq, RNA knockdown Cell High 28086087
2017 CREBBP regulates enhancer/super-enhancer networks controlling GC/post-GC B-cell fate, including B-cell receptor, CD40 signaling, and transcriptional control of GC and plasma cell development genes; Crebbp-deficient B cells show enhanced mitogenic responses and perturbed plasma cell differentiation; Crebbp haploinsufficiency combined with BCL2 transgene drives clonal lymphomas in mice. Conditional knockout mouse model, ChIP-seq, BCL2-transgenic compound mouse model, B-cell functional assays Cancer discovery High 28069569
2017 Loss of Crebbp in hematopoietic stem and progenitor cells (HSPCs) leads to accumulation of hyperproliferative lymphoid progenitors with defective DNA damage response due to failure to acetylate p53; early loss of Crebbp confers malignant stem cell properties; when Crebbp is lost later in lymphopoiesis, these abnormalities and tumor generation are attenuated. Conditional knockout mouse model, DNA damage response assays, ChIP for histone acetylation (H3K27ac), p53 acetylation assay Nature cell biology High 28825697
2017 The aPKC (atypical protein kinase C) phosphorylates CBP at Ser436; disruption of this aPKC-CBP pathway in CbpS436A knockin mice increases reprogramming efficiency of ischemia-activated pericytes to neural precursors after stroke, and impairs vascular remodeling and functional recovery, establishing aPKC-CBP as a pathway modulating post-stroke neurovascular remodeling. Knockin mouse model (CbpS436A), focal ischemic stroke model, cell reprogramming assay, vascular analysis Stem cell reports High 29173896
2018 Crebbp inactivation accelerates SCLC in an autochthonous mouse model; Crebbp loss results in reduced expression of tight junction and cell adhesion genes including Cdh1 with reduced histone acetylation; suppression of Cdh1 promotes transformation; HDAC inhibitor Pracinostat restores CDH1 expression and histone acetylation; CREBBP-mutant SCLCs show exceptional responses to Pracinostat in vivo. Autochthonous mouse model, gene expression profiling, ChIP for histone acetylation, HDAC inhibitor treatment in vivo Cancer discovery High 30181244
2018 COASY (CoA synthase) and CBP regulate mitotic fidelity through a coordinated acetylation mechanism; CBP transiently acetylates TPX2 during early mitosis, stabilizing TPX2 and activating Aurora A; COASY recruitment inhibits CBP-mediated TPX2 acetylation, promoting TPX2 degradation for mitotic exit; pharmacological and genetic CBP inactivation rescues mitotic defects caused by COASY knockdown. Acetylome mass spectrometry, co-immunoprecipitation, Aurora A kinase assay, genetic and pharmacological CBP inhibition, mitosis phenotyping Nature communications High 29531224
2018 DYRK1A interacts with CBP and p300 as identified by proteomics; DYRK1A overexpression causes hyperphosphorylation of CBP and p300; DYRK1A co-localizes with CBP at enhancers genome-wide by ChIP-seq; DYRK1A knockdown reduces H3K27ac at these enhancers, suggesting DYRK1A modulates CBP activity at enhancers. Affinity purification mass spectrometry, co-immunoprecipitation, ChIP-seq, shRNA knockdown Nucleic acids research Medium 30137413
2019 CBP/EP300 bromodomain inhibition decreases somatic-specific gene expression, H3K27ac, and chromatin accessibility at target promoters and enhancers, enabling cellular reprogramming; in contrast, catalytic (HAT) inhibition of CBP/EP300 prevents iPSC formation, demonstrating distinct functions for the bromodomain versus the catalytic domain in reprogramming; PRRX1 is identified as a functionally important CBP/EP300 bromodomain target. Chemical probe inhibitors (bromodomain vs. HAT), ATAC-seq, ChIP, iPSC reprogramming assay Nature chemical biology High 30962627
2019 CBP and SRF co-regulate neuronal dendritic growth and synaptic maturation; mice with CBP ablation in newborn neurons show perinatal death, defective diaphragm innervation, impaired adult-born neuron growth, and deficient activity-dependent synaptic remodeling; increasing SRF activity in a CBP-independent manner ameliorates transcriptional, synaptic, and growth defects caused by CBP loss. Conditional knockout mouse model, inducible adult neurogenesis KO, in vitro neuron culture, genetic rescue via SRF overactivation Cell death and differentiation High 30850733
2020 CBP mediates DOT1L acetylation at K358 in colon cancer cells, stabilizing DOT1L by preventing RNF8-mediated ubiquitination and proteasomal degradation without affecting DOT1L enzyme activity; stabilized DOT1L catalyzes H3K79 methylation at EMT genes (SNAIL, ZEB1), promoting cancer metastasis. Affinity purification/mass spectrometry, co-immunoprecipitation, acetylation assay, ubiquitination assay, in vivo metastasis imaging Theranostics High 32042335
2020 CARM1 inhibition further reduces CBP HAT activity genome-wide in DLBCL cells with CREBBP/EP300 mutations and downregulates CBP target genes, resulting in synthetic lethality; CARM1 inhibition synergizes with CBP/p300 inhibitor in DLBCL without CREBBP/EP300 mutations. In vitro/in vivo DLBCL models, ChIP-seq for H3K27ac, CARM1 inhibitor treatment, genetic CREBBP mutation analysis Leukemia Medium 32576962
2020 USP12 interacts with the HAT domain of CBP and inhibits CBP acetyltransferase activity; upon IFN signaling, USP12 translocates from cytoplasm to nucleus; decreased cytoplasmic USP12 facilitates CBP-induced acetylation and activation of IFN signaling proteins; nuclear USP12 accumulation blocks CBP-induced acetylation of phospho-STAT1, inhibiting TCPTP-mediated dephosphorylation and maintaining IFN antiviral efficacy. Co-immunoprecipitation, in vitro acetyltransferase assay, subcellular fractionation, USP12 knockdown PLoS pathogens High 31899788
2021 Targeted degradation of CBP and p300 by the PROTAC dCBP-1 (leveraging the E3 ligase cereblon) is exceptionally potent at killing multiple myeloma cells and abolishes the enhancer driving MYC oncogene expression; dCBP-1 designed using in silico modeling of ternary complex formation. PROTAC degrader design, western blot for protein degradation, viability assay, ChIP for enhancer activity Cell chemical biology High 33400925
2021 CCS1477, a novel small-molecule inhibitor of the p300/CBP conserved bromodomain, inhibits cell proliferation in prostate cancer lines, decreases AR- and C-MYC-regulated gene expression, and has antitumor activity in AR splice variant-driven models by regulating AR and C-MYC signaling. Bromodomain inhibitor cell proliferation assay, gene expression profiling, in vivo xenograft models, clinical biopsy biomarker analysis Cancer discovery High 33431496
2023 Cryo-EM structures reveal p300/CBP as a monomer that reads H4 N-terminal tail acetylation (H4NTac) via the bromodomain and simultaneously acetylates non-H4 histone tails within the same nucleosome; the primary write target upon reading H4NTac is H2B N-terminal tail; H2BNTac promotes H2A-H2B dissociation from the nucleosome; p300/CBP thus replicates H3-H4 tetramer acetylation and transcribes it to H2B-H2A dimers to activate transcription through nucleosome destabilization. Cryo-EM structure determination, in vitro HAT assay, histone dissociation assay, mutagenesis Nature communications High 37460559
2023 CCS1477 (inobrodib), a potent EP300/CBP bromodomain inhibitor, in myeloid leukemia cells promotes rapid eviction of EP300/CBP from MYB-occupied, high-H3K27ac enhancers with downregulation of the oncogenic network; in myeloma, it evicts EP300/CBP from FGFR3 and IRF4-occupied sites while redistributing to TCF3/E2A sites; early-phase clinical activity includes differentiation responses in AML and objective responses in myeloma. ChIP-seq for EP300/CBP occupancy, H3K27ac profiling, cell-cycle and differentiation assays, clinical trial biomarker analysis Cancer cell High 37995682
2024 Combined haploinsufficiency of Crebbp and Kmt2d induces more severe mouse lymphoma and unexpectedly confers immune-evasive microenvironment (CD8+ T-cell exhaustion, reduced infiltration); CREBBP and KMT2D show mutual binding dependency on chromatin; their combined deficiency preferentially impairs activation of immune synapse-responsive super-enhancers, revealing functional cooperation of these co-activators at specialized regulatory elements. Compound knockout mouse model, ChIP-seq for CREBBP/KMT2D occupancy and H3K27ac, flow cytometry of tumor microenvironment Nature communications High 38570506

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2007 ATM and ATR substrate analysis reveals extensive protein networks responsive to DNA damage. Science (New York, N.Y.) 2519 17525332
1996 A CBP integrator complex mediates transcriptional activation and AP-1 inhibition by nuclear receptors. Cell 1894 8616895
1993 Phosphorylated CREB binds specifically to the nuclear protein CBP. Nature 1793 8413673
1997 A signature motif in transcriptional co-activators mediates binding to nuclear receptors. Nature 1735 9192902
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
1996 A p300/CBP-associated factor that competes with the adenoviral oncoprotein E1A. Nature 1299 8684459
1994 Nuclear protein CBP is a coactivator for the transcription factor CREB. Nature 1298 7913207
2006 Substrate and functional diversity of lysine acetylation revealed by a proteomics survey. Molecular cell 1260 16916647
1997 Nuclear receptor coactivator ACTR is a novel histone acetyltransferase and forms a multimeric activation complex with P/CAF and CBP/p300. Cell 1255 9267036
2015 The BioPlex Network: A Systematic Exploration of the Human Interactome. Cell 1118 26186194
1997 The transcriptional co-activator p/CIP binds CBP and mediates nuclear-receptor function. Nature 1099 9192892
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
1999 Dominant negative mutations in human PPARgamma associated with severe insulin resistance, diabetes mellitus and hypertension. Nature 1045 10622252
2001 Histone deacetylase inhibitors arrest polyglutamine-dependent neurodegeneration in Drosophila. Nature 958 11607033
1995 Rubinstein-Taybi syndrome caused by mutations in the transcriptional co-activator CBP. Nature 955 7630403
2005 Toll-like receptor-mediated cytokine production is differentially regulated by glycogen synthase kinase 3. Nature immunology 938 16007092
2001 p300/CBP proteins: HATs for transcriptional bridges and scaffolds. Journal of cell science 894 11559745
2012 Intestinal tumorigenesis initiated by dedifferentiation and acquisition of stem-cell-like properties. Cell 873 23273993
2001 Interference by huntingtin and atrophin-1 with cbp-mediated transcription leading to cellular toxicity. Science (New York, N.Y.) 861 11264541
2000 The Huntington's disease protein interacts with p53 and CREB-binding protein and represses transcription. Proceedings of the National Academy of Sciences of the United States of America 839 10823891
2018 VIRMA mediates preferential m6A mRNA methylation in 3'UTR and near stop codon and associates with alternative polyadenylation. Cell discovery 829 29507755
1998 CREB is a regulatory target for the protein kinase Akt/PKB. The Journal of biological chemistry 829 9829964
1996 Role of CBP/P300 in nuclear receptor signalling. Nature 823 8779723
2002 The phosphorylation status of nuclear NF-kappa B determines its association with CBP/p300 or HDAC-1. Molecular cell 795 11931769
1998 Virus-dependent phosphorylation of the IRF-3 transcription factor regulates nuclear translocation, transactivation potential, and proteasome-mediated degradation. Molecular and cellular biology 781 9566918
2011 Inactivating mutations of acetyltransferase genes in B-cell lymphoma. Nature 742 21390126
2017 Roles of tau protein in health and disease. Acta neuropathologica 716 28386764
1997 A preliminary evaluation of a recombinant circumsporozoite protein vaccine against Plasmodium falciparum malaria. RTS,S Malaria Vaccine Evaluation Group. The New England journal of medicine 712 8988885
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
1997 CREB-binding protein/p300 are transcriptional coactivators of p65. Proceedings of the National Academy of Sciences of the United States of America 705 9096323
2008 Acetylation is indispensable for p53 activation. Cell 697 18485870
2002 Acetylation of RelA at discrete sites regulates distinct nuclear functions of NF-kappaB. The EMBO journal 695 12456660
1994 Activation of cAMP and mitogen responsive genes relies on a common nuclear factor. Nature 694 8028671
2010 Distinct roles of GCN5/PCAF-mediated H3K9ac and CBP/p300-mediated H3K18/27ac in nuclear receptor transactivation. The EMBO journal 666 21131905
1996 The translocation t(8;16)(p11;p13) of acute myeloid leukaemia fuses a putative acetyltransferase to the CREB-binding protein. Nature genetics 657 8782817
1997 Binding and modulation of p53 by p300/CBP coactivators. Nature 619 9194565
1997 Synergistic activation of transcription by CBP and p53. Nature 530 9194564
2004 p300/CBP and cancer. Oncogene 519 15156177
1997 RNA helicase A mediates association of CBP with RNA polymerase II. Cell 471 9323138
1996 Cooperation of Stat2 and p300/CBP in signalling induced by interferon-alpha. Nature 428 8848048
2008 Nitric oxide-induced nuclear GAPDH activates p300/CBP and mediates apoptosis. Nature cell biology 345 18552833
1998 Conjunction dysfunction: CBP/p300 in human disease. Trends in genetics : TIG 343 9613201
2015 Genetic Diversity and Protective Efficacy of the RTS,S/AS01 Malaria Vaccine. The New England journal of medicine 325 26488565
2017 RNA Binding to CBP Stimulates Histone Acetylation and Transcription. Cell 297 28086087
2002 Phosphorylation of CBP mediates transcriptional activation by neural activity and CaM kinase IV. Neuron 286 11970865
1999 p300 and CBP: partners for life and death. Journal of cellular physiology 240 10497301
2021 Targeting the p300/CBP Axis in Lethal Prostate Cancer. Cancer discovery 231 33431496
2017 Systems analysis of protective immune responses to RTS,S malaria vaccination in humans. Proceedings of the National Academy of Sciences of the United States of America 219 28193898
2007 Phosphorylation of CBP by IKKalpha promotes cell growth by switching the binding preference of CBP from p53 to NF-kappaB. Molecular cell 205 17434128
2001 p300/CBP/p53 interaction and regulation of the p53 response. European journal of biochemistry 203 11358491
2022 Histone acetyltransferases CBP/p300 in tumorigenesis and CBP/p300 inhibitors as promising novel anticancer agents. Theranostics 192 35836809
2010 From the circumsporozoite protein to the RTS, S/AS candidate vaccine. Human vaccines 190 19806009
1999 CBP-independent activation of CREM and CREB by the LIM-only protein ACT. Nature 190 10086359
2017 The CREBBP Acetyltransferase Is a Haploinsufficient Tumor Suppressor in B-cell Lymphoma. Cancer discovery 186 28069569
2000 CBP/p300 interact with and function as transcriptional coactivators of BRCA1. Proceedings of the National Academy of Sciences of the United States of America 179 10655477
2017 Exploitation of EP300 and CREBBP Lysine Acetyltransferases by Cancer. Cold Spring Harbor perspectives in medicine 174 27881443
1997 The multifunctional role of the co-activator CBP in transcriptional regulation. Recent progress in hormone research 165 9238849
2005 Towards an RTS,S-based, multi-stage, multi-antigen vaccine against falciparum malaria: progress at the Walter Reed Army Institute of Research. Vaccine 152 15755604
2018 Crebbp Loss Drives Small Cell Lung Cancer and Increases Sensitivity to HDAC Inhibition. Cancer discovery 141 30181244
1999 Potent induction of focused Th1-type cellular and humoral immune responses by RTS,S/SBAS2, a recombinant Plasmodium falciparum malaria vaccine. The Journal of infectious diseases 136 10515829
2021 Targeted degradation of the enhancer lysine acetyltransferases CBP and p300. Cell chemical biology 132 33400925
2007 Expression of HDAC1 and CBP/p300 in human colorectal carcinomas. Journal of clinical pathology 124 17720775
2000 Competitive recruitment of CBP and Rb-HDAC regulates UBF acetylation and ribosomal transcription. Molecular cell 114 11106745
2001 Mitogen-regulated RSK2-CBP interaction controls their kinase and acetylase activities. Molecular and cellular biology 106 11564891
1996 p300 and CBP as transcriptional regulators and targets of oncogenic events. Biological chemistry 101 8960368
2001 CBP, a transcriptional coactivator and acetyltransferase. Biochemistry and cell biology = Biochimie et biologie cellulaire 98 11467739
2004 Targeting CREB-binding protein (CBP) loss of function as a therapeutic strategy in neurological disorders. Biochemical pharmacology 97 15313413
2001 The HOX homeodomain proteins block CBP histone acetyltransferase activity. Molecular and cellular biology 96 11585930
2002 Ca2+-dependent block of CREB-CBP transcription by repressor DREAM. The EMBO journal 94 12198160
2004 Loss of CBP causes T cell lymphomagenesis in synergy with p27Kip1 insufficiency. Cancer cell 92 14998493
2003 Development of RTS,S/AS02: a purified subunit-based malaria vaccine candidate formulated with a novel adjuvant. Expert review of vaccines 92 12899574
2005 Conditional MLL-CBP targets GMP and models therapy-related myeloproliferative disease. The EMBO journal 89 15635450
2023 Therapeutic targeting of EP300/CBP by bromodomain inhibition in hematologic malignancies. Cancer cell 88 37995682
2012 Genomic occupancy of the transcriptional co-activators p300 and CBP. Transcription 87 23131664
2017 CREBBP and p300 lysine acetyl transferases in the DNA damage response. Cellular and molecular life sciences : CMLS 82 29170789
2005 Mutations and deletions of the CBP gene in human lung cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 80 15701835
2019 Bromodomain inhibition of the coactivators CBP/EP300 facilitate cellular reprogramming. Nature chemical biology 76 30962627
2023 The Role of CREBBP/EP300 and Its Therapeutic Implications in Hematological Malignancies. Cancers 70 36831561
2005 Mutant huntingtin represses CBP, but not p300, by binding and protein degradation. Molecular and cellular neurosciences 69 15994095
2015 RTS,S: Toward a first landmark on the Malaria Vaccine Technology Roadmap. Vaccine 66 26431982
2001 Functional interaction between coactivators CBP/p300, PCAF, and transcription factor FKLF2. The Journal of biological chemistry 64 11748222
2021 A Novel Intronic Circular RNA Antagonizes Influenza Virus by Absorbing a microRNA That Degrades CREBBP and Accelerating IFN-β Production. mBio 63 34281396
2004 Cellular immunity induced by the recombinant Plasmodium falciparum malaria vaccine, RTS,S/AS02, in semi-immune adults in The Gambia. Clinical and experimental immunology 63 14738458
2001 Interactions between CBP, NF-kappaB, and CREB in the lungs after hemorrhage and endotoxemia. American journal of physiology. Lung cellular and molecular physiology 62 11435217
1999 Cooperation of the transcriptional coactivators CBP and p300 with Stat6. Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research 59 10454341
2020 Differential contribution of p300 and CBP to regulatory element acetylation in mESCs. BMC molecular and cell biology 57 32690000
2016 Salicylate, diflunisal and their metabolites inhibit CBP/p300 and exhibit anticancer activity. eLife 57 27244239
2023 Epigenetic mechanisms to propagate histone acetylation by p300/CBP. Nature communications 56 37460559
2018 Modulating the masters: chemical tools to dissect CBP and p300 function. Current opinion in chemical biology 55 30025258
2017 Early loss of Crebbp confers malignant stem cell properties on lymphoid progenitors. Nature cell biology 53 28825697
1999 Function for p300 and not CBP in the apoptotic response to DNA damage. Oncogene 52 10523850
1999 Activation of Smad1-mediated transcription by p300/CBP. Biochimica et biophysica acta 50 10673036
2016 Development of Selective CBP/P300 Benzoxazepine Bromodomain Inhibitors. Journal of medicinal chemistry 48 27673482
2003 Rapid translation system (RTS): a promising alternative for recombinant protein production. Current protein & peptide science 48 12570786
2015 Ku80 cooperates with CBP to promote COX-2 expression and tumor growth. Oncotarget 47 25797267
2020 CBP mediated DOT1L acetylation confers DOT1L stability and promotes cancer metastasis. Theranostics 44 32042335
2007 Spectrum of CREBBP gene dosage anomalies in Rubinstein-Taybi syndrome patients. European journal of human genetics : EJHG 43 17473832
2005 Mutant huntingtin represses CBP, but not p300, by binding and protein degradation. Molecular and cellular neurosciences 43 16456924
2022 Mosquirix™ RTS, S/AS01 Vaccine Development, Immunogenicity, and Efficacy. Vaccines 41 35632469
2021 Towards Eradication of Malaria: Is the WHO's RTS,S/AS01 Vaccination Effective Enough? Risk management and healthcare policy 41 33737844
2013 CREB-binding protein (CBP) regulates β-adrenoceptor (β-AR)-mediated apoptosis. Cell death and differentiation 41 23579242
2003 Inhibition of p300/CBP by early B-cell factor. Molecular and cellular biology 41 12748286
2023 Discovery of Exceptionally Potent, Selective, and Efficacious PROTAC Degraders of CBP and p300 Proteins. Journal of medicinal chemistry 39 37276143
2020 CARM1 inhibition reduces histone acetyltransferase activity causing synthetic lethality in CREBBP/EP300-mutated lymphomas. Leukemia 38 32576962
2002 Acetyltransferase machinery conserved in p300/CBP-family proteins. Oncogene 38 11948408
2000 Viral replication and the coactivators p300 and CBP. Trends in microbiology 38 11115752
2018 CoA synthase regulates mitotic fidelity via CBP-mediated acetylation. Nature communications 37 29531224
2017 Characterization of T-cell immune responses in clinical trials of the candidate RTS,S malaria vaccine. Human vaccines & immunotherapeutics 36 28934066
2006 Csk-binding protein (Cbp) negatively regulates epidermal growth factor-induced cell transformation by controlling Src activation. Oncogene 36 16636672
2004 Analysis of CBP (CREBBP) gene deletions in Rubinstein-Taybi syndrome patients using real-time quantitative PCR. Human mutation 35 14974086
2019 CBP/p300 in brain development and plasticity: disentangling the KAT's cradle. Current opinion in neurobiology 32 30856481
2018 DYRK1A interacts with histone acetyl transferase p300 and CBP and localizes to enhancers. Nucleic acids research 32 30137413
2015 The LIM protein Ajuba promotes adipogenesis by enhancing PPARγ and p300/CBP interaction. Cell death and differentiation 30 26113042
2017 The aPKC-CBP Pathway Regulates Post-stroke Neurovascular Remodeling and Functional Recovery. Stem cell reports 29 29173896
2008 CBP/p300-interacting protein CITED1 modulates parathyroid hormone regulation of osteoblastic differentiation. Endocrinology 29 18187554
2019 CBP and SRF co-regulate dendritic growth and synaptic maturation. Cell death and differentiation 28 30850733
1999 The coactivators p300 and CBP have different functions during the differentiation of F9 cells. Journal of molecular medicine (Berlin, Germany) 28 10475063
2021 Circular RNA CREBBP Suppresses Hepatic Fibrosis Via Targeting the hsa-miR-1291/LEFTY2 Axis. Frontiers in pharmacology 27 34887753
2006 Functional interaction of CREB binding protein (CBP) with nuclear transport proteins and modulation by HDAC inhibitors. Cell cycle (Georgetown, Tex.) 26 16969114
2021 Delayed fractional dosing with RTS,S/AS01 improves humoral immunity to malaria via a balance of polyfunctional NANP6- and Pf16-specific antibodies. Med (New York, N.Y.) 25 35590199
2016 CBP/p300 acetyltransferases regulate the expression of NKG2D ligands on tumor cells. Oncogene 25 27477692
2009 Spatiotemporal expression of histone acetyltransferases, p300 and CBP, in developing embryonic hearts. Journal of biomedical science 25 19272189
2019 Gene activation by dCas9-CBP and the SAM system differ in target preference. Scientific reports 24 31792240
2018 Pan-HDAC Inhibitors Restore PRDM1 Response to IL21 in CREBBP-Mutated Follicular Lymphoma. Clinical cancer research : an official journal of the American Association for Cancer Research 24 30348636
2009 Interleukin-4 activates androgen receptor through CBP/p300. The Prostate 24 18819102
2024 Loss of CREBBP and KMT2D cooperate to accelerate lymphomagenesis and shape the lymphoma immune microenvironment. Nature communications 23 38570506
2022 Induction, decay, and determinants of functional antibodies following vaccination with the RTS,S malaria vaccine in young children. BMC medicine 23 36002841
2021 Enabling chemical protein (semi)synthesis via reducible solubilizing tags (RSTs). Chemical science 22 35222920
2020 USP12 translocation maintains interferon antiviral efficacy by inhibiting CBP acetyltransferase activity. PLoS pathogens 22 31899788
2020 Fusions involving BCOR and CREBBP are rare events in infiltrating glioma. Acta neuropathologica communications 22 32493417