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Showing CREBBP — CBP is a alias.

CREBBP

CREB-binding protein · UniProt Q92793

Length
2442 aa
Mass
265.4 kDa
Annotated
2026-06-09
100 papers in source corpus 35 papers cited in narrative 35 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CREBBP encodes a lysine acetyltransferase and transcriptional coactivator that integrates multiprotein regulatory complexes to deposit enhancer histone acetylation and acetylate non-histone substrates across diverse signaling pathways (PMID:9177780, PMID:27733359). Through its HAT domain, CREBBP maintains H3K27 acetylation at enhancers and super-enhancers that drive B-cell receptor and CD40 signaling, germinal-center/plasma-cell development, and MHC class II antigen presentation; loss of function permits unopposed deacetylation by the BCL6/SMRT/HDAC3 repressor complex, and HDAC3 inhibition restores these enhancers and suppresses CREBBP-mutant lymphoma (PMID:27733359, PMID:28069569). CREBBP physically partners with KMT2D on select enhancers and directly acetylates KMT2D to sustain H3K4me1, with combined Crebbp/Kmt2d haploinsufficiency synergistically driving abnormal germinal-center expansion and immune evasion through CD8+ T-cell exhaustion (PMID:36893259, PMID:38570506). As a haploinsufficient tumor suppressor, CREBBP loss reduces MHCII surface expression to enable immune escape, derepresses MYC, and partially overlaps with EP300, with which it has a synthetic-lethal relationship in mutant DLBCL (PMID:28831000, PMID:28288979, PMID:31519498). Its acetyltransferase activity extends beyond chromatin to direct substrates—p53 in the DNA-damage response, KRAS in RAS/MAPK signaling, RB1CC1/FIP200 in autophagy, and OGG1/DNA pol β/PCNA in base excision repair—linking CREBBP to genome maintenance, growth signaling, and cellular homeostasis (PMID:28825697, PMID:27979926, PMID:36394358, PMID:31504229). Beyond cancer, CREBBP coactivates lineage transcription factors (SREBPs, C/EBPs, PPARs, STATs, PHOX2B, GATA1) governing energy metabolism, neuronal differentiation, and neuroendocrine programs (PMID:11818964, PMID:19191321, PMID:20207472). Germline CREBBP dysfunction underlies Rubinstein-Taybi syndrome, with CH1-domain and HAT-impairing mutations producing neurobehavioral deficits and impaired base excision repair (PMID:26730956, PMID:31504229).

Mechanistic history

Synthesis pass · year-by-year structured walk · 19 steps
  1. 1997 Medium

    Establishing CREBBP's genomic identity and disease relevance answered where the gene lay and why it mattered, defining it as a transcriptional integrator disrupted in Rubinstein-Taybi syndrome and t(8;16) AML.

    Evidence Cosmid contig construction, FISH mapping, and full cDNA sequencing of the chromosome 16p13.3 locus

    PMID:9177780

    Open questions at the time
    • Did not define catalytic mechanism or specific substrates
    • No enhancer-level functional data
  2. 2002 High

    Crebbp haploinsufficiency phenotyping showed CBP coordinates whole-body energy balance, establishing it as a coactivator of metabolic transcription factors rather than solely a chromatin enzyme.

    Evidence Metabolic phenotyping of Crebbp+/- mice (body composition, glucose/insulin/leptin sensitivity, high-fat challenge)

    PMID:11818964

    Open questions at the time
    • Direct acetylation of named metabolic TFs not biochemically demonstrated here
    • Tissue-autonomous mechanism not dissected
  3. 2009 Medium

    Domain-mapped interaction with PHOX2B answered how CBP achieves transcription-factor-specific coactivation and how disease mutants subvert it.

    Evidence Co-IP domain mapping and cotransfection reporter assays with PHOX2B mutants

    PMID:19191321

    Open questions at the time
    • Single-system reporter context
    • No genome-wide PHOX2B target validation
  4. 2010 Medium

    Deletion-construct analysis in neuronal progenitors linked specific CBP domains to proliferation-versus-differentiation control through HAT activity and TF-complex promoter binding.

    Evidence CREBBP deletion-construct transfection in NT2 cells with HAT assays, ChIP-PCR, Co-IP, and cell-cycle profiling

    PMID:20207472

    Open questions at the time
    • Overexpressed deletion constructs may not reflect endogenous regulation
    • Pathway gene effects not validated in vivo
  5. 2011 High

    Sequencing relapsed ALL pinpointed HAT-domain mutations as recurrent and functionally impairing, establishing loss of acetyltransferase activity as a driver of altered target-gene regulation including glucocorticoid response.

    Evidence Resequencing of matched diagnosis/relapse ALL with HAT-activity and target-gene functional assays

    PMID:21390130

    Open questions at the time
    • Did not resolve enhancer-level consequences
    • Non-histone substrate contributions unaddressed
  6. 2011 Medium

    Microenvironmental analysis showed CBP haploinsufficiency acts non-cell-autonomously in bone marrow, altering niche factors that govern stem/progenitor maintenance versus myeloproliferation.

    Evidence Crebbp+/- BM microenvironment analysis with histomorphometry, CFU-F assays, and MMP9/KITL/ESAM1/CDH5 expression

    PMID:21555743

    Open questions at the time
    • Direct transcriptional targets in niche cells not mapped
    • Single-lab phenotype
  7. 2012 Medium

    Identifying SRCAP as a CBP coactivator extended the partner network and linked it to Floating-Harbor syndrome via an intact CBP-binding domain.

    Evidence Whole-exome sequencing and protein domain analysis in Floating-Harbor syndrome

    PMID:22265015

    Open questions at the time
    • No direct biochemical reconstitution of the SRCAP-CBP complex
    • Functional cooperativity inferred from domain integrity
  8. 2016 High

    Defining the BCL6/SMRT/HDAC3 counter-regulatory axis answered the mechanism of enhancer dysfunction in CREBBP-mutant B cells and revealed HDAC3 inhibition as a corrective strategy.

    Evidence Conditional KO, H3K27ac ChIP-seq, Co-IP, and in vitro/in vivo HDAC3 loss-of-function rescue

    PMID:27733359

    Open questions at the time
    • Direct CREBBP enhancer recruitment mechanism not fully resolved
    • Generality beyond GC B cells untested here
  9. 2016 Medium

    Demonstrating direct KRAS acetylation and H3K18ac loss connected CREBBP to RAS/MAPK signaling and MEK-inhibitor sensitivity in ALL.

    Evidence RNAi knockdown in ALL lines and primagrafts with direct KRAS acetylation assay and pathway/MEK-inhibitor readouts

    PMID:27979926

    Open questions at the time
    • KRAS acetylation site and stoichiometry not defined
    • Single-lab finding
  10. 2016 Medium

    CH1-domain knock-in mice established that this domain is required for CBP's role in cognition, social behavior, and synaptic plasticity, modeling Rubinstein-Taybi neurobehavior.

    Evidence CH1-deletion knock-in mouse with behavioral battery and synaptic electrophysiology

    PMID:26730956

    Open questions at the time
    • Molecular targets underlying behavior not identified
    • Single mutant allele
  11. 2016 Medium

    ZNF384 fusion analysis showed that fusion of CREBBP/EP300 produces dominant-negative loss of HAT activity, linking global acetylation loss to aberrant hematopoietic differentiation and transformation.

    Evidence Transcriptome sequencing, luciferase reporters, global acetylation measurement, and HSPC differentiation/transformation assays

    PMID:27903646

    Open questions at the time
    • Specific deregulated loci not pinpointed
    • In vitro transformation only
  12. 2017 High

    Multiple complementary studies established CREBBP as a haploinsufficient tumor suppressor in germinal-center B cells, governing enhancer networks for BCR/CD40 signaling, MHCII-dependent immune surveillance, MYC repression, and p53-dependent DNA-damage response.

    Evidence GC-specific conditional KO mice, ChIP-seq, B-cell functional assays, CRISPR knock-in, xenograft/transplant with CD4+ depletion, p53 acetylation assays, and BCL2-cooperation lymphoma models

    PMID:28069569 PMID:28288979 PMID:28825697 PMID:28831000

    Open questions at the time
    • Relative contribution of each program to malignant transformation unresolved
    • Stage-dependence of premalignant clone selection only partly mapped
  13. 2018 Medium

    Bromodomain-dependent and substrate-specific studies broadened the mechanistic picture: bromodomains sustain GATA1/MYC and AR enhancer programs, while neuroendocrine CREBBP loss silences Cdh1 to drive SCLC, and FL cells fail to upregulate PRDM1 via aberrant BCL6 retention.

    Evidence Bromodomain inhibitor CBP30, ChIP-seq, autochthonous SCLC mouse with Cdh1 ChIP and HDAC-inhibitor rescue, and BCL6 ChIP-qPCR with vorinostat rescue

    PMID:29884215 PMID:30181244 PMID:30348636 PMID:30606771

    Open questions at the time
    • Distinct bromodomain versus HAT contributions context-dependent and not unified
    • Several mechanisms from single labs
  14. 2019 High

    Dual Crebbp/Ep300 deletion modeling resolved their overlap-and-divergence, revealing partial compensation through common targets and a synthetic-lethal dependency exploitable in CREBBP-mutant DLBCL.

    Evidence Individual and combined GC-directed conditional deletions with in vivo GC assays and selective CREBBP/EP300 inhibitors

    PMID:31519498

    Open questions at the time
    • Molecular basis of distinct versus shared targets not fully defined
    • Therapeutic window in patients untested
  15. 2020 Medium

    A cluster of substrate and dependency studies extended CREBBP into base excision repair (OGG1/pol β/PCNA), autophagy precursors, NCOA-binding evolution, and lineage-dependent vulnerabilities in TNBC (FOXM1), CARM1 synthetic lethality, and breast-cancer FOXA1 enhancers.

    Evidence RSTS lymphoblast BER assays with complementation, cross-species NCBD:CID biophysics, functional genomics screens, CARM1 inhibition, and CPI-1612 with FOXA1/H3K27ac ChIP-seq

    PMID:31504229 PMID:32329110 PMID:32576962 PMID:33509944 PMID:35353838

    Open questions at the time
    • Several substrate roles from single labs without reciprocal validation
    • Acetylation sites not always mapped
  16. 2021 Medium

    Refinements detailed how CREBBP HAT activity controls homologous recombination/radiosensitivity (with a hyperacetylation gain-of-function on BRCA1), macrophage polarization via FBXW7/NOTCH, profibrotic enhancers (ACTA2/COL1A1, collagen VI), E2F3a-CASP8AP2 leukemic proliferation, and a CRISPR-validated CREBBP dependency under EP300 truncation.

    Evidence In vivo shRNA radiation screen and HAT inhibitors, CREBBP/EP300 knockdown with NOTCH/CCL2/CSF1 readouts, SGC-CBP30 with ChIP/proteomics, Co-IP/ChIP for E2F3a, and whole-genome CRISPR screens

    PMID:32759223 PMID:32945392 PMID:33431788 PMID:33911074 PMID:34732714

    Open questions at the time
    • Gain-of-function hyperacetylation mechanism needs broader confirmation
    • Many axes are single-lab
  17. 2022 High

    Direct acetylation of RB1CC1/FIP200 at K276 established acetylation-ubiquitination crosstalk stabilizing an autophagy regulator, extending CREBBP's non-histone substrate scope.

    Evidence Mass spectrometry, acetyltransferase assays, K276 mutagenesis, ubiquitination assays, and autophagy readouts in breast cancer cells

    PMID:36394358

    Open questions at the time
    • Physiological contexts beyond breast cancer untested
    • Single-lab finding
  18. 2023 High

    Identifying direct KMT2D acetylation by CREBBP and their enhancer co-complex unified two GC tumor suppressors mechanistically, linking acetylation to H3K4me1 maintenance and synergistic lymphomagenesis.

    Evidence Co-IP, direct acetylation assay, H3K27ac/H3K4me1 ChIP-seq, and conditional double-KO mouse model

    PMID:36893259

    Open questions at the time
    • KMT2D acetylation site(s) and effect on its catalytic activity not fully resolved
    • Generality beyond GC B cells untested
  19. 2024 High

    Compound haploinsufficiency studies showed CREBBP and KMT2D bind chromatin mutually dependently, jointly enabling immune-synapse super-enhancers, with combined loss driving severe immune evasion via CD8+ T-cell exhaustion.

    Evidence Compound Crebbp/Kmt2d haploinsufficient mouse with CREBBP/KMT2D ChIP-seq, immune phenotyping, and immune-synapse gene expression; plus A-485 in MLL-r AML with multi-omics

    PMID:38570506 PMID:38693103

    Open questions at the time
    • Mechanism of mutually dependent recruitment not structurally resolved
    • Clinical translatability of dual-targeting unestablished

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CREBBP selects between its many histone and non-histone substrates and is targeted to specific enhancers in each cell type remains unresolved, as does whether gain-of-function hyperacetylation states are a generalizable feature of mutant alleles.
  • No unifying model of enhancer/substrate selection
  • Structural basis of CREBBP-KMT2D mutual recruitment unknown
  • Gain-of-function versus loss-of-function balance across mutation classes undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 5 GO:0140096 catalytic activity, acting on a protein 5 GO:0140110 transcription regulator activity 4 GO:0042393 histone binding 3 GO:0060090 molecular adaptor activity 2
Localization
GO:0005634 nucleus 4 GO:0000228 nuclear chromosome 3
Pathway
R-HSA-1640170 Cell Cycle 4 R-HSA-4839726 Chromatin organization 4 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-1643685 Disease 3 R-HSA-168256 Immune System 3 R-HSA-73894 DNA Repair 3 R-HSA-1430728 Metabolism 1 R-HSA-9612973 Autophagy 1
Partners
BCL6E2F3AEP300HDAC3KMT2DNCOAPHOX2BSRCAP
Complex memberships
BCL6/SMRT/HDAC3 repressor complex (counter-regulatory)CREBBP/KMT2D enhancer complex

Evidence

Reading pass · 35 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2011 CREBBP mutations in relapsed ALL cluster in the histone acetyltransferase (HAT) domain, resulting in truncated alleles or deleterious substitutions that impair histone acetylation and transcriptional regulation of CREBBP target genes, including glucocorticoid-responsive genes. Resequencing of 300 genes in matched diagnosis/relapse ALL samples, functional assays of HAT activity and glucocorticoid target gene expression in mutant cells Nature High 21390130
2016 CREBBP loss-of-function causes focal depletion of enhancer H3K27 acetylation in germinal center B cells. CREBBP-regulated enhancers are counter-regulated by the BCL6/SMRT/HDAC3 repressor complex; loss of CREBBP enables unopposed deacetylation by this complex at enhancers of B-cell signaling and MHC class II genes. HDAC3 loss-of-function rescues these enhancers and suppresses CREBBP-mutant lymphomas. Conditional mouse knockout, ChIP-seq for H3K27ac, Co-IP demonstrating BCL6/SMRT/HDAC3 complex binding at MHC class II loci, in vitro and in vivo HDAC3 loss-of-function rescue experiments Cancer discovery High 27733359
2017 CREBBP acts as a haploinsufficient tumor suppressor in germinal center B cells by regulating enhancer/super-enhancer networks controlling B-cell receptor and CD40 receptor signaling, transcriptional control of GC/plasma cell development, and antigen presentation; Crebbp-deficient B cells show enhanced mitogenic response and perturbed plasma cell differentiation. Conditional GC-specific Crebbp knockout mice, ChIP-seq for enhancer acetylation, B-cell functional assays (mitogenic response, plasma cell differentiation), compound Crebbp-haploinsufficient/BCL2-transgenic mouse lymphoma model Cancer discovery High 28069569
2017 CREBBP inactivation in germinal center B cells reduces MHCII surface expression and promotes immune evasion; MHCII deficiency phenocopies the lymphomagenesis-promoting effects of CREBBP loss, and CD4+ T cell depletion facilitates lymphoma engraftment, demonstrating that CREBBP-mediated MHCII expression is required for tumor immune control. CRISPR-introduced patient mutation in DLBCL cell line, conditional Crebbp/Ep300 mouse knockout, xenograft and serial transplantation models, CD4+ T cell depletion experiments Proceedings of the National Academy of Sciences of the United States of America High 28831000
2017 CREBBP inactivation leads to high expression of MYC and altered histone acetylation at intragenic regions enriched for MYC DNA-binding motifs, showing MYC binding; this is associated with Crebbp loss cooperating with Bcl2 overexpression to promote B-cell lymphoma. Transgenic mouse models with Crebbp deletion, transcriptional and epigenetic profiling (histone acetylation ChIP), Myc binding analysis Blood Medium 28288979
2017 Loss of Crebbp in hematopoietic stem and progenitor cells leads to accumulation of hyperproliferative lymphoid progenitors with a defective DNA damage response due to failure to acetylate p53; this identifies a premalignant lymphoma stem cell population with decreased H3K27ac that undergoes transcriptional and genetic evolution leading to lymphomagenesis. Loss of Crebbp later in lymphopoiesis attenuates these effects. Murine Crebbp conditional KO at different hematopoietic stages, p53 acetylation assays, H3K27ac ChIP, functional DNA damage response assays Nature cell biology High 28825697
2019 CREBBP and EP300 modulate common as well as distinct transcriptional programs in germinal center B cells. EP300 but not CREBBP deletion impairs GC B cell fitness in vivo. Combined loss of Crebbp and Ep300 completely abrogates GC formation, demonstrating partial functional compensation through common transcriptional targets and a synthetic lethal interaction retained in CREBBP-mutant DLBCL cells. Conditional GC-directed mouse deletion models for Crebbp and Ep300 individually and combined; in vivo GC formation assays; pharmacological targeting with selective CREBBP/EP300 inhibitors in DLBCL cells Immunity High 31519498
2002 Crebbp haploinsufficiency in mice causes marked reduction of white adipose tissue (lipodystrophy) but increased insulin sensitivity, increased leptin sensitivity, and increased serum adiponectin, demonstrating that CBP functions as a 'master-switch' between energy storage and expenditure by co-activating transcription factors including SREBPs, C/EBPs, PPARs, and STATs via histone acetylation. Analysis of Crebbp+/- mice: body composition, glucose tolerance tests, insulin sensitivity, leptin sensitivity, adiponectin measurement; high-fat diet challenge Nature genetics High 11818964
2012 SRCAP, an SNF2-related chromatin-remodeling factor, serves as a coactivator for CREBBP (CBP). SRCAP mutations causing Floating-Harbor syndrome cluster in a region predicted to abolish AT-hook DNA-binding motifs while leaving the CBP-binding and ATPase domains intact, establishing a functional coactivator relationship between SRCAP and CREBBP. Whole-exome sequencing identifying SRCAP mutations in Floating-Harbor syndrome; protein domain analysis confirming intact CBP-binding domain in mutants American journal of human genetics Medium 22265015
2021 CREBBP/EP300 mutation or knockdown inhibits H3K27 acetylation, downregulates FBXW7 expression, activates the NOTCH pathway and downstream CCL2/CSF1 expression, resulting in tumor-associated macrophage polarization to M2 phenotype in DLBCL. In vitro knockdown and mutation of CREBBP/EP300 in B-lymphoma cells with measurement of H3K27ac, FBXW7, NOTCH pathway activation, CCL2/CSF1 expression; in vivo murine xenograft models with macrophage phenotyping Signal transduction and targeted therapy Medium 33431788
2018 Crebbp loss in mouse neuroendocrine cells results in reduced expression of tight junction and cell adhesion genes including Cdh1 (E-cadherin) with reduced histone acetylation at these loci; suppression of Cdh1 promotes transformation in SCLC. HDAC inhibitor Pracinostat restores histone acetylation and CDH1 expression in Crebbp-deficient SCLC. Autochthonous mouse SCLC model with Crebbp inactivation, gene expression analysis, ChIP for histone acetylation at Cdh1 locus, Cdh1 suppression functional studies, in vivo HDAC inhibitor treatment Cancer discovery High 30181244
2021 CREBBP acetyltransferase activity controls H3K27 acetylation at the profibrotic genes ACTA2 and COL1A1 in myofibroblasts; CREBBP/EP300 inhibition with SGC-CBP30 reduces H3K27ac at profibrotic enhancers and identifies collagen VI as a prominent downstream regulator of myofibroblast contractility, ECM production, chemotaxis, and wound healing. Epigenetic inhibitor screen in Dupuytren's disease fibroblasts; ChIP for H3K27ac; transcriptomic and proteomic profiling after SGC-CBP30 treatment; targeted Col VI knockdown with functional assays Proceedings of the National Academy of Sciences of the United States of America High 32759223
2018 CREBBP/EP300 bromodomains are required to sustain the GATA1/MYC regulatory axis in leukemia and lymphoma cell proliferation; bromodomain inhibitor CBP30 displaces CREBBP and EP300 from GATA1 and MYC binding sites at enhancers, reducing H3K27ac levels at these sites and causing G0/G1 cell cycle arrest. Bromodomain inhibitor treatment of K562 and lymphoma cell lines; ChIP-seq for EP300, GATA1, MYC occupancy; H3K27ac ChIP; cell cycle analysis Epigenetics & chromatin Medium 29884215
2020 CARM1 inhibition reduces histone acetyltransferase activity of CBP genome-wide and downregulates CBP-target genes in DLBCL, creating a synthetic lethality with CREBBP/EP300 mutations; CREBBP/EP300 mutations are monoallelic and require residual WT expression for cell survival, making mutant cells selectively sensitive to CARM1 inhibition. In vitro and in vivo CARM1 inhibition studies in DLBCL models; genome-wide HAT activity assessment; CBP-target gene expression analysis; correlation with CREBBP/EP300 mutation load Leukemia Medium 32576962
2022 CREBBP directly acetylates RB1CC1/FIP200 at lysine K276 in an intrinsically disordered region; this acetylation reduces ubiquitination of RB1CC1 at K276, thereby inhibiting its ubiquitin-dependent degradation. Both K276 acetylation and the N-terminal IDR are required for canonical autophagy function of RB1CC1 in breast cancer cells. Mass spectrometry identification of acetylation/ubiquitination sites; acetyltransferase assays; mutational analysis of K276; ubiquitination assays; autophagy functional readouts in breast cancer cells Autophagy High 36394358
2016 CREBBP knockdown in ALL cells reduces acetylation of histone H3 at lysine 18 (H3K18ac) and directly acetylates KRAS; CREBBP knockdown enhances signaling through the RAS/RAF/MEK/ERK pathway in Ras pathway-mutated ALL cells, which remain sensitive to MEK inhibitors. RNA interference knockdown of CREBBP in ALL cell lines and primagraft ALL cells; measurement of H3K18ac; direct KRAS acetylation assay; RAS/RAF/MEK/ERK pathway signaling assessment; MEK inhibitor sensitivity assays Haematologica Medium 27979926
2011 The bone marrow microenvironment of Crebbp+/- mice fails to maintain immature stem and progenitor cell pools, instead stimulating myeloid differentiation and myeloproliferation. Haploinsufficiency of Crebbp in the microenvironment decreases matrix metallopeptidase-9 (MMP9) and kit ligand (KITL), increases osteoclastogenesis, and alters expression of endothelial cell adhesion molecules ESAM1 and CDH5. Analysis of Crebbp+/- mouse BM microenvironment; bone histomorphometry; CFU-F assays; molecular analysis of MMP9, KITL, ESAM1, CDH5 expression in BM microenvironment cells Blood Medium 21555743
2009 CREBBP (CBP) physically interacts with the transcription factor PHOX2B using specific domains of each protein; CBP acts as a coactivator to mediate synergistic transcriptional activation with PHOX2B. Disease-associated PHOX2B mutants interact with different CBP domains than wild-type PHOX2B, impairing synergistic activation and exerting dominant-interfering effects. Co-immunoprecipitation and domain mapping of PHOX2B-CBP interaction; transient cotransfection reporter assays with PHOX2B mutants and CBP Human mutation Medium 19191321
2016 EP300-ZNF384 and CREBBP-ZNF384 fusion proteins result in loss of histone lysine acetyltransferase activity in a dominant-negative fashion, with concomitant global reduction of histone acetylation; ectopic expression alters differentiation of mouse hematopoietic stem and progenitor cells and potentiates oncogenic transformation in vitro. Whole-transcriptome sequencing identifying ZNF384 fusions; luciferase reporter assays for ZNF384 fusion transcriptional activity; measurement of global histone acetylation in fusion-expressing cells; mouse HSPC differentiation assays; in vitro transformation assays Genome research Medium 27903646
2023 CREBBP directly acetylates KMT2D in germinal center B cells; CREBBP inactivation by FL/DLBCL-associated mutations abrogates KMT2D acetylation, leading to reduced H3K4me1 levels. CREBBP and KMT2D form a biochemical complex on select enhancers/super-enhancers critical for immune signaling in the GC light zone, and dual Crebbp/Kmt2d haploinsufficiency synergistically promotes abnormal GC expansion. Co-IP demonstrating CREBBP-KMT2D complex on enhancers; direct acetylation assay of KMT2D by CREBBP; ChIP-seq for H3K27ac and H3K4me1; conditional double-KO mouse model; analysis of FL/DLBCL-associated mutations Proceedings of the National Academy of Sciences of the United States of America High 36893259
2024 Combined haploinsufficiency of Crebbp and Kmt2d induces more severe lymphoma phenotype and immune evasion (CD8+ T-cell exhaustion) than either alone; CREBBP and KMT2D show mutually dependent binding and function on chromatin, with combined deficiency preferentially impairing activation of immune synapse-responsive super-enhancers. Compound Crebbp/Kmt2d haploinsufficient mouse model; ChIP-seq for CREBBP and KMT2D occupancy; immune phenotyping of tumor microenvironment; gene expression analysis of immune synapse genes Nature communications High 38570506
2021 CREBBP HAT inhibition (but not bromodomain inhibition) radiosensitizes CREBBP/EP300-mutant tumors by repressing homologous recombination following DNA damage. Selected CREBBP mutations lead to a hyperacetylated state that increases CBP and BRCA1 acetylation, representing a gain-of-function targeted by HAT inhibition. In vivo shRNA screen for radiation response; in vitro and in vivo HAT inhibitor studies in cognate mutant tumors; homologous recombination assays; measurement of CBP and BRCA1 acetylation levels Nature communications Medium 34732714
2020 CREBBP acetyltransferase activity is required for acetylation of OGG1 DNA glycosylase, DNA polymerase β, and PCNA in base excision repair; mutations in CREBBP that affect protein levels or KAT activity cause reduced OGG1 acetylation and impaired BER initiation in Rubinstein-Taybi syndrome patient-derived lymphoblastoid cell lines, with increased sensitivity to oxidative DNA damage. BER functional assays in RSTS patient lymphoblastoid cell lines; OGG1, DNA pol β, and PCNA acetylation level measurements; complementation with CBP or p300 expression Carcinogenesis Medium 31504229
2010 CREBBP deletion constructs lacking the CREB, bromo, and HAT domains (CB-HAT) cause hyperproliferation and limited neuronal differentiation, while deletion of the HAT and C-terminal domain (HAT-CT) causes proliferation deficiency and rapid but insufficient neurogenesis; these effects correlate with altered HAT activity, altered binding of CREBBP-transcription factor complexes to promoters of Notch, SHH, Wnt, and retinoid pathway genes, and aberrant transcription of differentiation genes. CREBBP deletion construct transfection into NT2 neuronal progenitor cells; HAT activity assays; ChIP-PCR; Co-IP; cell cycle profiling; gene expression analysis Differentiation; research in biological diversity Medium 20207472
2021 CREBBP CRISPR-dependent screening identifies CREBBP dependency in a DLBCL cell line bearing a truncated EP300 lacking the HAT domain; the synthetic lethal interaction between CREBBP and EP300 was validated across published CRISPR screens and inhibitor assays, confirming that residual WT allele expression is required for survival in cells with EP300 truncation. Whole-genome CRISPR-Cas9 knockout screen; transcriptome sequencing; validation in published CRISPR screens; HAT inhibitor assays Cell death & disease Medium 33911074
2016 CREBBP mutation in the CH1 domain of CBP in mice (CBPΔCH1/ΔCH1) causes Rubinstein-Taybi syndrome-like phenotype including autism-relevant repetitive behaviors, hyperactivity, social interaction deficits, motor dysfunction, impaired recognition memory, and abnormal synaptic plasticity, establishing that the CH1 (TAZ1) domain is required for normal CBP function in motor control, cognition, and social behavior. Knock-in mouse model with CH1 domain deletion; behavioral tests (open field, rotarod, novel object recognition, social interaction, marble burying); electrophysiology for synaptic plasticity PloS one Medium 26730956
2020 CREBBP interacts with the NCOA protein through its NCBD domain binding the NCOA CID domain; this high-affinity interaction evolved specifically in vertebrates, as non-vertebrate deuterostome (sea urchin) NCBD:CID interactions show much lower affinity similar to proposed ancestral domains. Expression and affinity measurement of NCBD and CID domains from multiple species using biophysical binding assays Protein science Medium 32329110
2022 CREBBP acetyltransferase inhibition (CPI-1612) suppresses ER-dependent transcription in ER+ breast cancer by targeting lineage-specific enhancers defined by the pioneer transcription factor FOXA1, reducing H3K27ac at FOXA1-bound enhancers. CREBBP/EP300 acetyltransferase inhibitor CPI-1612 treatment; ChIP-seq for H3K27ac and FOXA1 occupancy; in vitro and in vivo breast cancer growth assays PloS one Medium 35353838
2020 ZFP36 directly binds to CREBBP mRNA via its AU-rich element-binding domain, destabilizing CREBBP mRNA; ZFP36 deficiency upregulates CREBBP and enhances I/R-induced lung injury, apoptosis, and fibrosis via the CREBBP/p53/p21/Bax pathway. RNA immunoprecipitation (RIP) and pulldown assays confirming ZFP36-CREBBP mRNA interaction; in vivo ZFP36-knockdown mouse model; Western blotting and IHC for CREBBP/p53/p21/Bax pathway components Cell death & disease Medium 34238924
2020 CREBBP loss in triple-negative breast cancer upregulates and creates dependency on a FOXM1 proliferative program; CREBBP-altered TNBC cells are selectively sensitive to CDK4/6 inhibitors that indirectly target FOXM1-driven proliferation. 3D spheroid functional genomics screen of 200 frequently mutated breast cancer genes; CREBBP KO/knockdown with FOXM1 pathway analysis; CDK4/6 inhibitor sensitivity in cell line xenografts and patient-derived models Cancer research Medium 33509944
2024 EP300 and CREBBP are core epigenetic regulators in MLL-rearranged AML; EP300/CREBBP inhibitor A-485 selectively depresses MLL-r cell proliferation by downregulating the CDK4/RB/E2F axis and blocking MLL-r-BET complex binding to H3K27ac at critical gene loci, distinct from global histone acetylation effects. ATAC-seq; RNA-seq; CUT&TAG for H3K27ac; EP300/CREBBP knockout and A-485 inhibitor treatment in MLL-r vs. MLL-WT AML cells Cell death discovery Medium 38693103
2018 CREBBP/EP300 bromodomain inhibition in ER-negative AR-expressing breast cancer (MDA-MB-453) downregulates AR-dependent gene expression and reduces H3K27ac levels at AR-binding sites; super-enhancer-associated gene expression is selectively downregulated by CREBBP/EP300 bromodomain inhibitors. Genetic (siRNA) and chemical (CREBBP/EP300 bromodomain inhibitor) approaches; transcriptome analysis; H3K27ac ChIP at AR-binding sites; AR occupancy analysis Molecular cancer research : MCR Medium 30606771
2021 CREBBP interacts with E2F3a transcription factor (Co-IP, co-localization by immunofluorescence) and regulates E2F3a protein levels; CREBBP binds to the promoter of CASP8AP2 (a downstream E2F3a target) by ChIP assay. CREBBP downregulation inhibits leukemia cell proliferation, arrests cells in G0/G1 phase, decreases E2F3a and CASP8AP2 expression, and increases daunorubicin resistance. RNA interference knockdown and overexpression of CREBBP; Co-IP demonstrating CREBBP-E2F3a interaction; immunofluorescence co-localization; ChIP assay for CREBBP at CASP8AP2 promoter; cell cycle analysis; IC50 measurements Molecular medicine reports Medium 32945392
2018 CREBBP-mutated follicular lymphoma cells fail to upregulate PRDM1 in response to IL21 due to abnormal enrichment of BCL6 repressor protein at the PRDM1 gene; pan-HDAC inhibitor vorinostat restores PRDM1 response to IL21 by lowering BCL6 bound to PRDM1 promoter. ChIP-qPCR for BCL6 at PRDM1 locus in CREBBP-mutated vs. wild-type FL cells; IL21 stimulation assays; vorinostat treatment; flow cytometry; transcriptome analysis in patient samples Clinical cancer research Medium 30348636
1997 The human CREBBP gene was cloned, physically mapped to chromosome 16p13.3 within a 100-kb region where all tested Rubinstein-Taybi syndrome and t(8;16)-associated AML breakpoints disrupt a single gene; the full cDNA was sequenced and CREBBP was characterized as an integrator in the assembly of multiprotein regulatory complexes necessary for transcription in multiple signaling pathways. Cosmid contig construction; FISH mapping; Southern blot; full cDNA sequencing Genomics Medium 9177780

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 CREBBP mutations in relapsed acute lymphoblastic leukaemia. Nature 498 21390130
2016 CREBBP Inactivation Promotes the Development of HDAC3-Dependent Lymphomas. Cancer discovery 215 27733359
2017 The CREBBP Acetyltransferase Is a Haploinsufficient Tumor Suppressor in B-cell Lymphoma. Cancer discovery 190 28069569
2021 CREBBP/EP300 mutations promoted tumor progression in diffuse large B-cell lymphoma through altering tumor-associated macrophage polarization via FBXW7-NOTCH-CCL2/CSF1 axis. Signal transduction and targeted therapy 189 33431788
2017 Exploitation of EP300 and CREBBP Lysine Acetyltransferases by Cancer. Cold Spring Harbor perspectives in medicine 175 27881443
2018 Crebbp Loss Drives Small Cell Lung Cancer and Increases Sensitivity to HDAC Inhibition. Cancer discovery 148 30181244
2012 Mutations in SRCAP, encoding SNF2-related CREBBP activator protein, cause Floating-Harbor syndrome. American journal of human genetics 142 22265015
2002 Increased insulin sensitivity despite lipodystrophy in Crebbp heterozygous mice. Nature genetics 140 11818964
2019 Unique and Shared Epigenetic Programs of the CREBBP and EP300 Acetyltransferases in Germinal Center B Cells Reveal Targetable Dependencies in Lymphoma. Immunity 116 31519498
2016 Whole-transcriptome sequencing identifies a distinct subtype of acute lymphoblastic leukemia with predominant genomic abnormalities of EP300 and CREBBP. Genome research 107 27903646
2015 KRAS and CREBBP mutations: a relapse-linked malicious liaison in childhood high hyperdiploid acute lymphoblastic leukemia. Leukemia 99 25917266
2005 DNA sequencing of CREBBP demonstrates mutations in 56% of patients with Rubinstein-Taybi syndrome (RSTS) and in another patient with incomplete RSTS. Human genetics 98 16021471
2017 Inactivation of CREBBP expands the germinal center B cell compartment, down-regulates MHCII expression and promotes DLBCL growth. Proceedings of the National Academy of Sciences of the United States of America 87 28831000
2017 CREBBP and p300 lysine acetyl transferases in the DNA damage response. Cellular and molecular life sciences : CMLS 85 29170789
2017 Crebbp loss cooperates with Bcl2 overexpression to promote lymphoma in mice. Blood 74 28288979
2020 Identifying collagen VI as a target of fibrotic diseases regulated by CREBBP/EP300. Proceedings of the National Academy of Sciences of the United States of America 73 32759223
2023 The Role of CREBBP/EP300 and Its Therapeutic Implications in Hematological Malignancies. Cancers 71 36831561
2012 CREBBP HAT domain mutations prevail in relapse cases of high hyperdiploid childhood acute lymphoblastic leukemia. Leukemia 71 22388726
1997 Construction of a 1.2-Mb contig surrounding, and molecular analysis of, the human CREB-binding protein (CBP/CREBBP) gene on chromosome 16p13.3. Genomics 66 9177780
2021 A Novel Intronic Circular RNA Antagonizes Influenza Virus by Absorbing a microRNA That Degrades CREBBP and Accelerating IFN-β Production. mBio 63 34281396
2006 Rubinstein-Taybi Syndrome: spectrum of CREBBP mutations in Italian patients. BMC medical genetics 63 17052327
2017 Early loss of Crebbp confers malignant stem cell properties on lymphoid progenitors. Nature cell biology 57 28825697
2016 Expanding the molecular signature of ossifying fibromyxoid tumors with two novel gene fusions: CREBBP-BCORL1 and KDM2A-WWTR1. Genes, chromosomes & cancer 57 27537276
2014 Insights into genotype-phenotype correlations from CREBBP point mutation screening in a cohort of 46 Rubinstein-Taybi syndrome patients. Clinical genetics 56 25388907
2016 CREBBP mutations in individuals without Rubinstein-Taybi syndrome phenotype. American journal of medical genetics. Part A 55 27311832
2017 The mutational landscape of ocular marginal zone lymphoma identifies frequent alterations in TNFAIP3 followed by mutations in TBL1XR1 and CREBBP. Oncotarget 52 28152507
2019 Solid-type adenoid cystic carcinoma of the breast, a distinct molecular entity enriched in NOTCH and CREBBP mutations. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 50 31857685
2018 CREBBP/EP300 bromodomains are critical to sustain the GATA1/MYC regulatory axis in proliferation. Epigenetics & chromatin 50 29884215
2018 JUNB, DUSP2, SGK1, SOCS1 and CREBBP are frequently mutated in T-cell/histiocyte-rich large B-cell lymphoma. Haematologica 49 30213827
2012 Acute myeloid leukemia with translocation (8;16)(p11;p13) and MYST3-CREBBP rearrangement harbors a distinctive microRNA signature targeting RET proto-oncogene. Leukemia 46 23022987
2018 Structural dynamics and quantum mechanical aspects of shikonin derivatives as CREBBP bromodomain inhibitors. Journal of molecular graphics & modelling 45 29758466
2007 Spectrum of CREBBP gene dosage anomalies in Rubinstein-Taybi syndrome patients. European journal of human genetics : EJHG 43 17473832
2020 CREBBP and STAT6 co-mutation and 16p13 and 1p36 loss define the t(14;18)-negative diffuse variant of follicular lymphoma. Blood cancer journal 42 32555149
2011 Crebbp haploinsufficiency in mice alters the bone marrow microenvironment, leading to loss of stem cells and excessive myelopoiesis. Blood 42 21555743
2015 Characterization of 14 novel deletions underlying Rubinstein-Taybi syndrome: an update of the CREBBP deletion repertoire. Human genetics 39 25805166
2007 High frequency of mosaic CREBBP deletions in Rubinstein-Taybi syndrome patients and mapping of somatic and germ-line breakpoints. Genomics 39 17855048
2020 CARM1 inhibition reduces histone acetyltransferase activity causing synthetic lethality in CREBBP/EP300-mutated lymphomas. Leukemia 38 32576962
2021 ZFP36 protects lungs from intestinal I/R-induced injury and fibrosis through the CREBBP/p53/p21/Bax pathway. Cell death & disease 35 34238924
2004 Analysis of CBP (CREBBP) gene deletions in Rubinstein-Taybi syndrome patients using real-time quantitative PCR. Human mutation 35 14974086
2012 Somatic mutations of the CREBBP and EP300 genes affect response to histone deacetylase inhibition in malignant DLBCL clones. Leukemia research reports 32 24371765
2021 Inhibition of histone acetyltransferase function radiosensitizes CREBBP/EP300 mutants via repression of homologous recombination, potentially targeting a gain of function. Nature communications 31 34732714
2019 CREBBP/EP300 Bromodomain Inhibition Affects the Proliferation of AR-Positive Breast Cancer Cell Lines. Molecular cancer research : MCR 31 30606771
2021 Genome-wide CRISPR screens reveal synthetic lethal interaction between CREBBP and EP300 in diffuse large B-cell lymphoma. Cell death & disease 30 33911074
2015 CREBBP and EP300 mutational spectrum and clinical presentations in a cohort of Swedish patients with Rubinstein-Taybi syndrome. Molecular genetics & genomic medicine 29 26788536
2022 Regulation of RB1CC1/FIP200 stability and autophagy function by CREBBP-mediated acetylation in an intrinsically disordered region. Autophagy 28 36394358
2021 Circular RNA CREBBP Suppresses Hepatic Fibrosis Via Targeting the hsa-miR-1291/LEFTY2 Axis. Frontiers in pharmacology 28 34887753
2012 Duplication 16p13.3 and the CREBBP gene: confirmation of the phenotype. European journal of medical genetics 28 23063576
2003 Analysis of genetic stability at the EP300 and CREBBP loci in a panel of cancer cell lines. Genes, chromosomes & cancer 27 12696060
2019 LINC01857 as an oncogene regulates CREB1 activation by interacting with CREBBP in breast cancer. Journal of cellular physiology 26 30628071
2019 New insights into genetic variant spectrum and genotype-phenotype correlations of Rubinstein-Taybi syndrome in 39 CREBBP-positive patients. Molecular genetics & genomic medicine 26 31566936
2016 CREBBP knockdown enhances RAS/RAF/MEK/ERK signaling in Ras pathway mutated acute lymphoblastic leukemia but does not modulate chemotherapeutic response. Haematologica 26 27979926
2024 Loss of CREBBP and KMT2D cooperate to accelerate lymphomagenesis and shape the lymphoma immune microenvironment. Nature communications 24 38570506
2021 Enabling chemical protein (semi)synthesis via reducible solubilizing tags (RSTs). Chemical science 24 35222920
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
2013 Novel cAMP binding protein-BP (CREBBP) mutation in a girl with Rubinstein-Taybi syndrome, GH deficiency, Arnold Chiari malformation and pituitary hypoplasia. BMC medical genetics 24 23432975
2020 Fusions involving BCOR and CREBBP are rare events in infiltrating glioma. Acta neuropathologica communications 23 32493417
2022 Analysis and therapeutic targeting of the EP300 and CREBBP acetyltransferases in anaplastic large cell lymphoma and Hodgkin lymphoma. Leukemia 22 36456744
2021 Controlling Intramolecular Interactions in the Design of Selective, High-Affinity Ligands for the CREBBP Bromodomain. Journal of medicinal chemistry 22 34255515
2021 CREBBP cooperates with the cell cycle machinery to attenuate chidamide sensitivity in relapsed/refractory diffuse large B-cell lymphoma. Cancer letters 22 34481935
2012 Case-control association study of 14 variants of CREB1, CREBBP and CREM on diagnosis and treatment outcome in major depressive disorder and bipolar disorder. Psychiatry research 22 22386572
2006 Exclusion of mutations in the PRNP, JPH3, TBP, ATN1, CREBBP, POU3F2 and FTL genes as a cause of disease in Portuguese patients with a Huntington-like phenotype. Journal of human genetics 22 16858508
2018 iPSC-derived neurons of CREBBP- and EP300-mutated Rubinstein-Taybi syndrome patients show morphological alterations and hypoexcitability. Stem cell research 20 29883886
2016 Mutation of the CH1 Domain in the Histone Acetyltransferase CREBBP Results in Autism-Relevant Behaviors in Mice. PloS one 19 26730956
2022 BMSC-EV-derived lncRNA NORAD Facilitates Migration, Invasion, and Angiogenesis in Osteosarcoma Cells by Regulating CREBBP via Delivery of miR-877-3p. Oxidative medicine and cellular longevity 18 35281474
2022 Circ-CREBBP inhibits sperm apoptosis via the PI3K-Akt signaling pathway by sponging miR-10384 and miR-143-3p. Communications biology 18 36476986
2016 CREBBP is a target of epigenetic, but not genetic, modification in juvenile myelomonocytic leukemia. Clinical epigenetics 18 27158276
2010 Spectrum of CREBBP mutations in Indian patients with Rubinstein-Taybi syndrome. Journal of biosciences 18 20689175
2022 CREBBP/EP300 acetyltransferase inhibition disrupts FOXA1-bound enhancers to inhibit the proliferation of ER+ breast cancer cells. PloS one 17 35353838
2021 3D Functional Genomics Screens Identify CREBBP as a Targetable Driver in Aggressive Triple-Negative Breast Cancer. Cancer research 17 33509944
2014 Comparison between karyotyping-FISH-reverse transcription PCR and RNA-sequencing-fusion gene identification programs in the detection of KAT6A-CREBBP in acute myeloid leukemia. PloS one 17 24798186
2009 Interaction between PHOX2B and CREBBP mediates synergistic activation: mechanistic implications of PHOX2B mutants. Human mutation 17 19191321
2022 Circular RNA CREBBP modulates cartilage degradation by activating the Smad1/5 pathway through the TGFβ2/ALK1 axis. Experimental & molecular medicine 16 36224344
2020 Selective Fragments for the CREBBP Bromodomain Identified from an Encoded Self-assembly Chemical Library. ChemMedChem 16 32686307
2023 KMT2D acetylation by CREBBP reveals a cooperative functional interaction at enhancers in normal and malignant germinal center B cells. Proceedings of the National Academy of Sciences of the United States of America 15 36893259
2023 Comparative Analysis of Drug-like EP300/CREBBP Acetyltransferase Inhibitors. ACS chemical biology 15 37737090
2020 Screening of a large Rubinstein-Taybi cohort identified many novel variants and emphasizes the importance of the CREBBP histone acetyltransferase domain. American journal of medical genetics. Part A 15 32827181
2010 CREBBP re-arrangements affect protein function and lead to aberrant neuronal differentiation. Differentiation; research in biological diversity 15 20207472
2020 Mutations in CREBBP and EP300 genes affect DNA repair of oxidative damage in Rubinstein-Taybi syndrome cells. Carcinogenesis 14 31504229
2017 Low CREBBP expression is associated with adverse long-term outcomes in paediatric acute lymphoblastic leukaemia. European journal of haematology 14 28452416
2020 A novel miRNA inhibits metastasis of prostate cancer via decreasing CREBBP-mediated histone acetylation. Journal of cancer research and clinical oncology 13 33221996
2019 Clinical exome sequencing identifies novel CREBBP variants in 18 Chinese Rubinstein-Taybi Syndrome kids with high frequency of polydactyly. Molecular genetics & genomic medicine 13 31637876
2011 Multilocus association of genetic variants in MLL, CREBBP, EP300, and TOP2A with childhood acute lymphoblastic leukemia in Hispanics from Texas. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 13 21493871
2011 A polymorphism of the CREB binding protein (CREBBP) gene is a risk factor for addiction. Brain research 13 21752352
2006 Screening for partial deletions in the CREBBP gene in Rubinstein-Taybi syndrome patients using multiplex PCR/liquid chromatography. Genetic testing 13 17253932
2022 LINC00665 sponges miR-641 to promote the progression of breast cancer by targeting the SNF2-related CREBBP activator protein (SRCAP). Bioengineered 12 35152838
2022 Diffusely infiltrating glioma with CREBBP-BCORL1 fusion showing overexpression of not only BCORL1 but BCOR: A case report. Brain tumor pathology 12 35596897
2021 Circ-CREBBP promotes cell tumorigenesis and glutamine catabolism in glioma by regulating miR-375/glutaminase axis. Brain research 12 34813772
2020 Downregulating CREBBP inhibits proliferation and cell cycle progression and induces daunorubicin resistance in leukemia cells. Molecular medicine reports 12 32945392
2019 Fetal phenotype of Rubinstein-Taybi syndrome caused by CREBBP mutations. Clinical genetics 12 30633342
2019 Preferential sensitivity to HDAC inhibitors in tumors with CREBBP mutation. Cancer gene therapy 12 31068675
2019 Genetic polymorphism and transcriptional regulation of CREBBP gene in patient with diffuse large B-cell lymphoma. Bioscience reports 12 31366566
2010 High frequency of copy number imbalances in Rubinstein-Taybi patients negative to CREBBP mutational analysis. European journal of human genetics : EJHG 12 20125191
2008 Malignant pleural mesothelioma-targeted CREBBP/EP300 inhibitory protein 1 promoter system for gene therapy and virotherapy. Cancer research 12 18757427
1995 Localization of human CREBBP (CREB binding protein) to 16p13.3 by fluorescence in situ hybridization. Cytogenetics and cell genetics 12 7606928
2021 The novel and recurrent variants in exon 31 of CREBBP in Japanese patients with Menke-Hennekam syndrome. American journal of medical genetics. Part A 11 34652060
2023 RNF6 promotes gastric cancer progression by regulating CCNA1/CREBBP transcription. Cell cycle (Georgetown, Tex.) 10 37904524
2021 CREBBP knockdown suppressed proliferation and promoted chemo-sensitivity via PERK-mediated unfolded protein response in ovarian cancer. Journal of Cancer 10 34149923
2024 The epigenetic regulators EP300/CREBBP represent promising therapeutic targets in MLL-rearranged acute myeloid leukemia. Cell death discovery 9 38693103
2020 High affinity between CREBBP/p300 and NCOA evolved in vertebrates. Protein science : a publication of the Protein Society 9 32329110
2016 Identification of the MYST3-CREBBP fusion gene in infants with acute myeloid leukemia and hemophagocytosis. Revista brasileira de hematologia e hemoterapia 9 27863755

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