EP300
Histone acetyltransferase p300
Also known as: EP300_HUMAN, KAT3B, p300
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q09472
- Gene
- EP300
- Ensembl
- ENSG00000100393
- Chromosome
- 22
- Canonical length
- 2414 aa
- Protein class
- Cancer-related genes, Disease related genes, Enzymes, Human disease related genes, Metabolic proteins, Potential drug targets, Predicted intracellular proteins
- Subcellular location
- Nucleoplasm
OverviewNCBI Gene
This gene encodes the adenovirus E1A-associated cellular p300 transcriptional co-activator protein. It functions as histone acetyltransferase that regulates transcription via chromatin remodeling and is important in the processes of cell proliferation and differentiation. It mediates cAMP-gene regulation by binding specifically to phosphorylated CREB protein. This gene has also been identified as a co-activator of HIF1A (hypoxia-inducible factor 1 alpha), and thus plays a role in the stimulation of hypoxia-induced genes such as VEGF. Defects in this gene are a cause of Rubinstein-Taybi syndrome and may also play a role in epithelial cancer. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
2414 residues, UniProt reviewed canonical sequence.
>Q09472|EP300
1 MAENVVEPGP PSAKRPKLSS PALSASASDG TDFGSLFDLE HDLPDELINS TELGLTNGGD
61 INQLQTSLGM VQDAASKHKQ LSELLRSGSS PNLNMGVGGP GQVMASQAQQ SSPGLGLINS
121 MVKSPMTQAG LTSPNMGMGT SGPNQGPTQS TGMMNSPVNQ PAMGMNTGMN AGMNPGMLAA
181 GNGQGIMPNQ VMNGSIGAGR GRQNMQYPNP GMGSAGNLLT EPLQQGSPQM GGQTGLRGPQ
241 PLKMGMMNNP NPYGSPYTQN PGQQIGASGL GLQIQTKTVL SNNLSPFAMD KKAVPGGGMP
301 NMGQQPAPQV QQPGLVTPVA QGMGSGAHTA DPEKRKLIQQ QLVLLLHAHK CQRREQANGE
361 VRQCNLPHCR TMKNVLNHMT HCQSGKSCQV AHCASSRQII SHWKNCTRHD CPVCLPLKNA
421 GDKRNQQPIL TGAPVGLGNP SSLGVGQQSA PNLSTVSQID PSSIERAYAA LGLPYQVNQM
481 PTQPQVQAKN QQNQQPGQSP QGMRPMSNMS ASPMGVNGGV GVQTPSLLSD SMLHSAINSQ
541 NPMMSENASV PSLGPMPTAA QPSTTGIRKQ WHEDITQDLR NHLVHKLVQA IFPTPDPAAL
601 KDRRMENLVA YARKVEGDMY ESANNRAEYY HLLAEKIYKI QKELEEKRRT RLQKQNMLPN
661 AAGMVPVSMN PGPNMGQPQP GMTSNGPLPD PSMIRGSVPN QMMPRITPQS GLNQFGQMSM
721 AQPPIVPRQT PPLQHHGQLA QPGALNPPMG YGPRMQQPSN QGQFLPQTQF PSQGMNVTNI
781 PLAPSSGQAP VSQAQMSSSS CPVNSPIMPP GSQGSHIHCP QLPQPALHQN SPSPVPSRTP
841 TPHHTPPSIG AQQPPATTIP APVPTPPAMP PGPQSQALHP PPRQTPTPPT TQLPQQVQPS
901 LPAAPSADQP QQQPRSQQST AASVPTPTAP LLPPQPATPL SQPAVSIEGQ VSNPPSTSST
961 EVNSQAIAEK QPSQEVKMEA KMEVDQPEPA DTQPEDISES KVEDCKMEST ETEERSTELK
1021 TEIKEEEDQP STSATQSSPA PGQSKKKIFK PEELRQALMP TLEALYRQDP ESLPFRQPVD
1081 PQLLGIPDYF DIVKSPMDLS TIKRKLDTGQ YQEPWQYVDD IWLMFNNAWL YNRKTSRVYK
1141 YCSKLSEVFE QEIDPVMQSL GYCCGRKLEF SPQTLCCYGK QLCTIPRDAT YYSYQNRYHF
1201 CEKCFNEIQG ESVSLGDDPS QPQTTINKEQ FSKRKNDTLD PELFVECTEC GRKMHQICVL
1261 HHEIIWPAGF VCDGCLKKSA RTRKENKFSA KRLPSTRLGT FLENRVNDFL RRQNHPESGE
1321 VTVRVVHASD KTVEVKPGMK ARFVDSGEMA ESFPYRTKAL FAFEEIDGVD LCFFGMHVQE
1381 YGSDCPPPNQ RRVYISYLDS VHFFRPKCLR TAVYHEILIG YLEYVKKLGY TTGHIWACPP
1441 SEGDDYIFHC HPPDQKIPKP KRLQEWYKKM LDKAVSERIV HDYKDIFKQA TEDRLTSAKE
1501 LPYFEGDFWP NVLEESIKEL EQEEEERKRE ENTSNESTDV TKGDSKNAKK KNNKKTSKNK
1561 SSLSRGNKKK PGMPNVSNDL SQKLYATMEK HKEVFFVIRL IAGPAANSLP PIVDPDPLIP
1621 CDLMDGRDAF LTLARDKHLE FSSLRRAQWS TMCMLVELHT QSQDRFVYTC NECKHHVETR
1681 WHCTVCEDYD LCITCYNTKN HDHKMEKLGL GLDDESNNQQ AAATQSPGDS RRLSIQRCIQ
1741 SLVHACQCRN ANCSLPSCQK MKRVVQHTKG CKRKTNGGCP ICKQLIALCC YHAKHCQENK
1801 CPVPFCLNIK QKLRQQQLQH RLQQAQMLRR RMASMQRTGV VGQQQGLPSP TPATPTTPTG
1861 QQPTTPQTPQ PTSQPQPTPP NSMPPYLPRT QAAGPVSQGK AAGQVTPPTP PQTAQPPLPG
1921 PPPAAVEMAM QIQRAAETQR QMAHVQIFQR PIQHQMPPMT PMAPMGMNPP PMTRGPSGHL
1981 EPGMGPTGMQ QQPPWSQGGL PQPQQLQSGM PRPAMMSVAQ HGQPLNMAPQ PGLGQVGISP
2041 LKPGTVSQQA LQNLLRTLRS PSSPLQQQQV LSILHANPQL LAAFIKQRAA KYANSNPQPI
2101 PGQPGMPQGQ PGLQPPTMPG QQGVHSNPAM QNMNPMQAGV QRAGLPQQQP QQQLQPPMGG
2161 MSPQAQQMNM NHNTMPSQFR DILRRQQMMQ QQQQQGAGPG IGPGMANHNQ FQQPQGVGYP
2221 PQQQQRMQHH MQQMQQGNMG QIGQLPQALG AEAGASLQAY QQRLLQQQMG SPVQPNPMSP
2281 QQHMLPNQAQ SPHLQGQQIP NSLSNQVRSP QPVPSPRPQS QPPHSSPSPR MQPQPSPHHV
2341 SPQTSSPHPG LVAAQANPME QGHFASPDQN SMLSQLASNP GMANLHGASA TDLGLSTDNS
2401 DLNSNLSQST LDIHLocalizationUniProt · AlphaFold · HPA
Whether an antibody against EP300 can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Intracellular
- Secreted
- No
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.53
- Highest tissue expression
- 61 nTPM
Expression across tissuesHPA
Tissue
- bone marrow: 61 nTPM
- thymus: 25 nTPM
- cerebellum: 23 nTPM
- parathyroid gland: 22 nTPM
- tongue: 22 nTPM
- skeletal muscle: 22 nTPM
Single-cell type
- neutrophils: 861 nCPM
- neutrophil progenitors: 448 nCPM
- sertoli cells: 275 nCPM
- microglia: 218 nCPM
- monocytes: 206 nCPM
- thymocytes: 186 nCPM
Immune cell
- neutrophil: 2.4 nTPM
- basophil: 1.3 nTPM
- memory B-cell: 1 nTPM
- NK-cell: 1 nTPM
- plasmacytoid DC: 0.9 nTPM
- classical monocyte: 0.7 nTPM
Brain region
- cerebellum: 68 nTPM
- cerebral cortex: 57 nTPM
- medulla oblongata: 51 nTPM
- white matter: 49 nTPM
- hypothalamus: 47 nTPM
- thalamus: 46 nTPM
DiseaseUniProt · ClinVar · IEDB · PubMed
Four sources answering four different questions about EP300.
Disease | AllUniProt
Conditions EP300 is implicated in, by any mechanism.
- Rubinstein-Taybi syndrome 2 (RSTS2) MIM:613684
- Menke-Hennekam syndrome 2 (MKHK2) MIM:618333
Disease | GeneticClinVar
278 pathogenic / likely-pathogenic of 2,404 ClinVar records.
Conditions with pathogenic or likely-pathogenic variants.
- Rubinstein-Taybi syndrome due to EP300 haploinsufficiency
- Inborn genetic diseases
- EP300-related disorder
- Menke-Hennekam syndrome 2
- Rubinstein-Taybi syndrome due to CREBBP mutations
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 0.1
- gnomAD pLI
- 1
- gnomAD missense Z
- 2.03
- DepMap mean gene effect
- -0.31
- DepMap dependency class
- selective
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 4% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- animal organ morphogenesis
- apoptotic process
- B cell differentiation
- canonical NF-kappaB signal transduction
- canonical Wnt signaling pathway
- cellular response to L-leucine
- cellular response to nutrient levels
- cellular response to UV
- circadian rhythm
- DNA repair-dependent chromatin remodeling
- face morphogenesis
- fat cell differentiation
- heart development
- host-mediated activation of viral transcription
- internal peptidyl-lysine acetylation
- internal protein amino acid acetylation
- intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator
- learning or memory
- lung development
- megakaryocyte development
- multicellular organism growth
- N-terminal peptidyl-lysine acetylation
- negative regulation of autophagy
- negative regulation of brown fat cell differentiation
- negative regulation of chromosome condensation
- negative regulation of gluconeogenesis
- negative regulation of protein-containing complex assembly
- negative regulation of transcription by RNA polymerase II
- nervous system development
- platelet formation
- positive regulation of DNA-binding transcription factor activity
- positive regulation of DNA-templated transcription
- positive regulation of neuron projection development
- positive regulation of protein import into nucleus
- positive regulation of receptor signaling pathway via JAK-STAT
- positive regulation of T-helper 17 cell lineage commitment
- positive regulation of TORC1 signaling
- positive regulation of TORC2 signaling
- positive regulation of transcription by RNA polymerase II
- positive regulation of transforming growth factor beta receptor signaling pathway
- protein acetylation
- protein destabilization
- protein stabilization
- regulation of androgen receptor signaling pathway
- regulation of autophagy
- regulation of cellular response to heat
- regulation of glycolytic process
- regulation of mitochondrion organization
- regulation of signal transduction by p53 class mediator
- response to estrogen
- response to hypoxia
- skeletal muscle tissue development
- somitogenesis
- stimulatory C-type lectin receptor signaling pathway
- thigmotaxis
- transcription initiation-coupled chromatin remodeling
- behavioral defense response
- negative regulation of protein oligomerization
- peptidyl-lysine butyrylation
- peptidyl-lysine crotonylation
- peptidyl-lysine propionylation
- regulation of tubulin deacetylation
- swimming
Molecular functions
- acetylation-dependent protein binding
- acetyltransferase activity
- acyltransferase activity
- beta-catenin binding
- chromatin binding
- chromatin DNA binding
- damaged DNA binding
- DNA binding
- DNA-binding transcription factor binding
- histone acetyltransferase activity
- histone H2B acetyltransferase activity
- histone H3 acetyltransferase activity
- histone H3K18 acetyltransferase activity
- histone H3K27 acetyltransferase activity
- histone H4 acetyltransferase activity
- L-lysine N-acetyltransferase activity, acting on acetyl phosphate as donor
- NF-kappaB binding
- nuclear androgen receptor binding
- nuclear receptor binding
- p53 binding
- peptide 2-hydroxyisobutyryltransferase activity
- peptide butyryltransferase activity
- pre-mRNA intronic binding
- protein propionyltransferase activity
- protein-lysine-acetyltransferase activity
- RNA polymerase II-specific DNA-binding transcription factor binding
- STAT family protein binding
- tau protein binding
- transcription coactivator activity
- transcription coactivator binding
- transcription coregulator binding
- zinc ion binding
- histone butyryltransferase activity
- histone crotonyltransferase activity
- histone H1K75 acetyltransferase activity
- histone H3K122 acetyltransferase activity
- histone isonicotinyltransferase activity
- histone lactyltransferase (CoA-dependent) activity
Cellular components
Protein domainsUniProt · Pfam · InterPro
- Zinc finger, TAZ-type
- Zinc finger, ZZ-type
- Bromodomain
- Coactivator CBP, KIX domain
- Nuclear receptor coactivator, interlocking
- CREB-binding protein/p300, atypical RING domain
- Zinc finger, RING/FYVE/PHD-type
- Histone acetyltransferase Rtt109/CBP
- Nuclear receptor coactivator, CREB-bp-like, interlocking
- Bromodomain, conserved site
- CBP/p300-type histone acetyltransferase domain
- TAZ domain superfamily
- Bromodomain-like superfamily
- Coactivator CBP, KIX domain superfamily
- Nuclear receptor coactivator, CREB-bp-like, interlocking domain superfamily
- CBP/p300, atypical RING domain superfamily
- Zinc finger, ZZ-type superfamily
- Histone acetyltransferase p300/CREBBP, PHD domain
- Bromodomain
- Zinc finger, ZZ type
- TAZ zinc finger
- KIX domain
- CREB-binding protein/p300, atypical RING domain
- Histone acetylation protein
- Creb binding
- Histone acetyltransferase p300-like, PHD domain
KeywordsUniProt
- Acetylation
- Acyltransferase
- Biological rhythms
- Bromodomain
- Cell cycle
- Chromosomal rearrangement
- Chromosome
- Citrullination
- Cytoplasm
- Host-virus interaction
- Intellectual disability
- Isopeptide bond
- Metal-binding
- Methylation
- Nucleus
- Phosphoprotein
- Repeat
- Transcription
- Transcription regulation
- Transferase
- Ubl conjugation
- Zinc
- Zinc-finger
InteractionsUniProt · HPA
Protein binding partners of EP300 in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads EP300 as an antibody target. Whether an autoantibody or antibody against EP300 could matter depends on whether native EP300 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
EP300 is annotated as predominantly intracellular. Intracellular proteins are common autoantibody markers, becoming visible to the immune system after cell injury or altered processing, but are usually markers of disease rather than direct drivers.
Annotation status
The present source text does not explicitly label EP300 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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