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Information on EC 2.3.1.48 - histone acetyltransferase and Organism(s) Mus musculus and UniProt Accession Q9JHD2
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2.3.1.48 histone acetyltransferaseIUBMB Comments
A group of enzymes acetylating histones. Several of the enzymes can also acetylate lysines in other proteins [3,4].
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Word Map
- 2.3.1.48
- rhythm
-
oscillation
-
suprachiasmatic
- chromatin
-
entrain
-
night
- scn
- sleep
- melatonin
- drosophila
-
diurnal
-
pacemaker
-
locomotor
-
light-dark
- nuclei
- deacetylases
-
pineal
-
morning
-
photoperiodic
- retinal
-
draw
- hypothalamus
- hdacs
-
light-induced
- melanogaster
- photoreceptors
-
noise
-
bayesian
-
nocturnal
-
evening
-
daytime
-
deacetylation
-
coherent
-
co-activator
-
oscillatory
- dementia
-
transactivation
- flies
-
neuropeptide
-
wake
-
schedule
-
24-hour
-
pulses
-
circuit
- medicine
-
lengthen
- molecular biology
-
trichostatin
-
mood
-
verbal
-
neuropsychological
- drug development
- tick
- analysis
- pharmacology
The taxonomic range for the selected organisms is: Mus musculus
The enzyme appears in selected viruses and cellular organisms
The enzyme appears in selected viruses and cellular organisms
Synonyms
clock, histone acetyltransferase, n-acetyltransferase, tip60, histone acetyltransferases, cbp/p300, creb-binding protein, ep300, crebbp, creb binding protein, 
more
topSYNONYM 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
acetyltransferase, histone
-
-
-
-
Cbp
factor acetyltransferase
-
enzyme form A is also able to acetylate nonhistone proteins, mostly transcription factors, overview
FAT
-
when acetylating nonhistone transcription factor proteins, factor specific, overview
Gcn5
HAT
histone acetokinase
-
-
-
-
histone acetylase
-
-
-
-
histone transacetylase
-
-
-
-
lysine acetyltransferase
Mof
NCOAT
nucleosome-histone acetyltransferase
-
-
-
-
p300
PCAF
additional information
NCOAT
nuclear cytoplasmic O-GlcNacase and acetyltransferase, bifunctional enzyme
additional information
-
MOZ is the founding member of the MOZ, Ybf2/Sas2, Tip60 , i.e. MYST family of HATs, characterized by the presence of a conserved MYST domain that comprises both the C2HC nucleosome-binding domain and the putative HAT domain
additional information
-
MOZ, i.e. monocytic leukemia zinc finger protein, is a Myst, i.e. MOZ, Ybf2 (Sas3), Sas2, Tip60, type histone acetyltransferase, HAT
additional information
-
part of the double-histone-acetyltransferase complex ATAC, ADA2A-containing complex
additional information
-
the enzyme belongs to the MYST family histone acetyltransferases which is divided in three sub-families, overview
additional information
-
the enzyme belongs to the MYST family of histone acetyltransferases
REACTION TYPE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
Acyl group transfer
-
-
-
-
SYSTEMATIC NAME
IUBMB Comments
acetyl-CoA:[protein]-L-lysine acetyltransferase
A group of enzymes acetylating histones. Several of the enzymes can also acetylate lysines in other proteins [3,4].
CAS REGISTRY NUMBER
COMMENTARY
9054-51-7
-
SUBSTRATE
PRODUCT
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate)
(Substrate)
LITERATURE
(Substrate)
(Substrate)
COMMENTARY
(Product)
(Product)
LITERATURE
(Product)
(Product)
Reversibility
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
acetyl-CoA + [Geminin]-L-lysine14
CoA + [Geminin]-N6-acetyl-L-lysine14
-
-
-
?
acetyl-CoA + [histone H3]-L-lysine
CoA + [histone H3]-N6-acetyl-L-lysine
-
-
-
?
acetyl-CoA + [histone H3]-L-lysine14
CoA + [histone H3]-N6-acetyl-L-lysine14
-
-
-
?
acetyl-CoA + [histone H4]-L-lysin16
CoA + [histone H4]-N6-acetyl-L-lysine16
-
-
-
?
acetyl-CoA + [histone H4]-L-lysine
CoA + [histone H4]-N6-acetyl-L-lysine
-
-
-
?
acetyl-CoA + [histone H4]-L-lysine16
CoA + [histone H4]-N6-acetyl-L-lysine16
-
-
-
?
acetyl-CoA + [protein]-L-lysine
CoA + [protein]-N6-acetyl-L-lysine
-
-
-
?
acetyl-CoA + [protein]-L-lysine
CoA + [protein]-N6-acetyl-L-lysine
-
-
-
?
acetyl-CoA + [protein]-L-lysine
CoA + [protein]-N6-acetyl-L-lysine
-
-
-
?
acetyl-CoA + [protein]-L-lysine
CoA + [protein]-N6-acetyl-L-lysine
endogenous GCN5 and EGR2 in iNKT cells
-
-
?
acetyl-CoA + c-Myc
CoA + acetylated c-Myc
-
acetylation by Tip60 increases c-Myc protein stability in transfected H-1299 human lung carcinoma cells
-
-
?
acetyl-CoA + histone
CoA + acetylhistone
-
histone H3 is the preferred substrate
-
r
acetyl-CoA + histone
CoA + acetylhistone
the bifunctional enzyme NCOAT, nuclear cytoplasmic O-GlcNacase and acetyltransferase, may be regulated to reduce the state of glycosylation of transcriptional activators while increasing the acetylation of histones to allow for concerted activation of eukaryotic gene transcription
-
-
?
acetyl-CoA + histone H3
CoA + acetylhistone H3
-
Gcn5 protein: preferred substrate, acetylation at Lys14
-
r
acetyl-CoA + histone H3
CoA + acetylhistone H3
-
CBP binds and acetylates histones at neural promoters, and regulates Corpus Callosum development. CBP binds to neuronal and glial promoters and globally promotes histone acetylation in the embryonic cortex, e.g. the beta-actin promoter, overview
-
-
?
acetyl-CoA + histone H3
CoA + acetylhistone H3
-
H4R3 methylation, catalyzed by PRMT1, facilitates beta-globin transcription by regulating histone acetyltransferase binding, and histone H3 and H4 acetylation, overview
-
-
?
acetyl-CoA + histone H3
CoA + acetylhistone H3
-
acetylation of Lys9 and Lys14
-
-
?
acetyl-CoA + histone H3
CoA + acetylhistone H3
-
acetylation of Lys9 and Lys14 by PCAF. PCAF binds to dimethyl-Arg3 at histone H4 tails, dimethyl H4R3 provides a binding surface for PCAF and directly enhances histone H3 and H4 acetylation in vitro
-
-
?
acetyl-CoA + histone H4
CoA + acetylhistone H4
-
H4R3 methylation, catalyzed by PRMT1, facilitates beta-globin transcription by regulating histone acetyltransferase binding, and histone H3 and H4 acetylation, overview
-
-
?
acetyl-CoA + histone H4
CoA + acetylhistone H4
-
Mof is solely responsible for H4K16 acetylation in mouse blastocysts. Tip60 plays essential roles in cell cycle progression in vitro
-
-
?
acetyl-CoA + histone H4
CoA + acetylhistone H4
-
PCAF binds to dimethyl-Arg3 at histone H4 tails, dimethyl H4R3 provides a binding surface for PCAF and directly enhances histone H3 and H4 acetylation in vitro
-
-
?
acetyl-CoA + histone H4
CoA + acetylhistone H4
-
recombinant ATAC2 has a weak HAT activity directed to histone H4
-
-
?
histone H4 + acetyl-CoA
acetyl-histone H4 + CoA
-
acetylation at Lys8, NCOAT has the ability to directly associate with both an acetylated and unacetylated histone H4 tail in vitro without tequiring acetyl-lysine contacts, binding and interaction mechanism, overview
-
-
?
additional information
?
-
-
Gcn5 and PCAF protein are transcription cofactors
-
-
?
additional information
?
-
-
the nuclear cytoplasmic O-GlcNAcase and acetyltransferase, NCOAT, is a bifunctional enzyme with both glycoside hydrolase and alkyltransferase activity and contains a zinc finger-like motif responsible for substrate recognition, via making contacts with the histone tails within nucleosomes, essential for activity, overview
-
-
?
additional information
?
-
-
MOZ specifically interacts and associates with transcription factors such as AML1, PU.1, p53, Runx2 and NF-kappaB, functioning as their transcriptional coactivator and cooperatively activating target gene transcription
-
-
?
additional information
?
-
-
ATAC2 associates with GCN5 and other proteins linked to chromatin metabolism
-
-
?
additional information
?
-
-
specific role of MOZ-driven acetylation in controlling a desirable balance between proliferation and differentiation during hematopoiesis. MOZ also shows activity either as Runx1 coactivator or in the induction of leukemic transformation via transcriptional intermediary factor 2, TIF2, but is not essentially required
-
-
?
additional information
?
-
-
the mammalian complex corresponding to the yeast NuA4 complex contains the MYST HAT Tip60. Myc recruits the Tip60 complex to the chromatin in Rat1 wild-type cells, but not in Rat1 Myc mutant cells. Hbo1 appears to function predominantly in transcriptional repression
-
-
?
additional information
?
-
HBO1 exerts significant acetyltransferase activity on proteins such as ORC2, MCM2, CDC6, and Geminin in in vitro assays
-
-
-
NATURAL SUBSTRATE
NATURAL PRODUCT
REACTION DIAGRAM
ORGANISM
UNIPROT
COMMENTARY
(Substrate)
(Substrate)
LITERATURE
(Substrate)
(Substrate)
COMMENTARY
(Product)
(Product)
LITERATURE
(Product)
(Product)
REVERSIBILITY
r=reversible
ir=irreversible
?=not specified
r=reversible
ir=irreversible
?=not specified
acetyl-CoA + c-Myc
CoA + acetylated c-Myc
-
acetylation by Tip60 increases c-Myc protein stability in transfected H-1299 human lung carcinoma cells
-
-
?
acetyl-CoA + [histone H3]-L-lysine
CoA + [histone H3]-N6-acetyl-L-lysine
-
-
-
?
acetyl-CoA + [histone H3]-L-lysine14
CoA + [histone H3]-N6-acetyl-L-lysine14
-
-
-
?
acetyl-CoA + [histone H4]-L-lysin16
CoA + [histone H4]-N6-acetyl-L-lysine16
-
-
-
?
acetyl-CoA + [histone H4]-L-lysine
CoA + [histone H4]-N6-acetyl-L-lysine
-
-
-
?
acetyl-CoA + [histone H4]-L-lysine16
CoA + [histone H4]-N6-acetyl-L-lysine16
-
-
-
?
acetyl-CoA + [protein]-L-lysine
CoA + [protein]-N6-acetyl-L-lysine
-
-
-
?
acetyl-CoA + [protein]-L-lysine
CoA + [protein]-N6-acetyl-L-lysine
-
-
-
?
acetyl-CoA + [protein]-L-lysine
CoA + [protein]-N6-acetyl-L-lysine
endogenous GCN5 and EGR2 in iNKT cells
-
-
?
acetyl-CoA + histone
CoA + acetylhistone
-
histone H3 is the preferred substrate
-
r
acetyl-CoA + histone
CoA + acetylhistone
the bifunctional enzyme NCOAT, nuclear cytoplasmic O-GlcNacase and acetyltransferase, may be regulated to reduce the state of glycosylation of transcriptional activators while increasing the acetylation of histones to allow for concerted activation of eukaryotic gene transcription
-
-
?
acetyl-CoA + histone H3
CoA + acetylhistone H3
-
CBP binds and acetylates histones at neural promoters, and regulates Corpus Callosum development. CBP binds to neuronal and glial promoters and globally promotes histone acetylation in the embryonic cortex, e.g. the beta-actin promoter, overview
-
-
?
acetyl-CoA + histone H3
CoA + acetylhistone H3
-
H4R3 methylation, catalyzed by PRMT1, facilitates beta-globin transcription by regulating histone acetyltransferase binding, and histone H3 and H4 acetylation, overview
-
-
?
acetyl-CoA + histone H4
CoA + acetylhistone H4
-
H4R3 methylation, catalyzed by PRMT1, facilitates beta-globin transcription by regulating histone acetyltransferase binding, and histone H3 and H4 acetylation, overview
-
-
?
acetyl-CoA + histone H4
CoA + acetylhistone H4
-
Mof is solely responsible for H4K16 acetylation in mouse blastocysts. Tip60 plays essential roles in cell cycle progression in vitro
-
-
?
additional information
?
-
-
MOZ specifically interacts and associates with transcription factors such as AML1, PU.1, p53, Runx2 and NF-kappaB, functioning as their transcriptional coactivator and cooperatively activating target gene transcription
-
-
?
additional information
?
-
-
ATAC2 associates with GCN5 and other proteins linked to chromatin metabolism
-
-
?
additional information
?
-
-
specific role of MOZ-driven acetylation in controlling a desirable balance between proliferation and differentiation during hematopoiesis. MOZ also shows activity either as Runx1 coactivator or in the induction of leukemic transformation via transcriptional intermediary factor 2, TIF2, but is not essentially required
-
-
?
additional information
?
-
-
the mammalian complex corresponding to the yeast NuA4 complex contains the MYST HAT Tip60. Myc recruits the Tip60 complex to the chromatin in Rat1 wild-type cells, but not in Rat1 Myc mutant cells. Hbo1 appears to function predominantly in transcriptional repression
-
-
?
COFACTOR
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
METALS and IONS
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
INHIBITOR
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
garcinol
after induction of hind limb ischemia, blood flow recovery is impaired in both PCAF-/- mice and healthy wild type mice treated with the pharmacological PCAF inhibitor garcinol
N'-(4-fluoro-5-methyl-[1,1'-biphenyl]-3-carbonyl)-benzenesulfonohydrazide
-
N'-(5-chloro-4-fluoro-[1,1'-biphenyl]-3-carbonyl)-benzenesulfonohydrazide
-
Plumbagin
-
RTK1, naturally occurring hydroxynaphthoquinone, isolated from Plumbago rosea roots
protein HBZ
HTLV-1 (basic zipper factor, from a human T cell leukemia virus), interacts with HBO1 during pathogenesis and inhibits its acetylation activity to reduce p53-mediated transcription activation of p21/CDKN1A and Gadd45a, and subsequently delays G2-cell cycle arrest
-
tert-butyl-(3-(2-(naphthalen-2-ylsulfono)hydrazinecarbonyl)-phenyl)carbamate
-
WM-8014
highly potent inhibitor, competitive inhibition with respect to acetyl-CoA
ACTIVATING COMPOUND
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
BRPF2
i.e. BRD1, BRPF2 is a cofactor directing HBO1 binding to the histone and binds to HBO1 in a cervical-loop structure proximity to the MYST domain to facilitate histone binding. BRPF2 binds to HBO1 on the hinge connecting the NTD and MYST domain, thus it is reasonable to develop BRPF2-mimic peptides or molecules for disrupting HBO1-BRPF2 interaction andsubsequently prevent the binding of HBO1 to chromatin
-
dimethyl-arginine 3-histone H4
-
dimethyl H4R3 provides a binding surface for PCAF and directly enhances histone H3 and H4 acetylation in vitro
-
IC50 VALUE [mM]
INHIBITOR
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
IMAGE
0.0071
2'-chloro-N'-(phenylsulfonyl)biphenyl-3-carbohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.00062
2'-fluoro-N'-(phenylsulfonyl)biphenyl-3-carbohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0082
2'-methoxy-N'-(phenylsulfonyl)biphenyl-3-carbohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.125
2-chloro-N'-(naphthalen-2-ylsulfonyl)benzohydrazide
Mus musculus
IC50 above 0.125 mM, in the presence of 0.015 mM acetyl-CoA, pH and temperature not specified in the publication
0.0073
2-cyano-N'-(2-fluorobenzoyl)benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0018
2-fluoro-N'-(phenylsulfonyl)benzohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0044
2-fluoro-N'-[[3-(trifluoromethyl)phenyl]sulfonyl]benzohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.049
2-hydroxy-N'-(naphthalen-2-ylsulfonyl)benzohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.00079
3'-chloro-N'-(phenylsulfonyl)biphenyl-3-carbohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0034
3'-cyano-N'-(phenylsulfonyl)biphenyl-3-carbohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.011
3'-fluoro-N'-(phenylsulfonyl)biphenyl-3-carbohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.009
3'-methoxy-N'-(phenylsulfonyl)biphenyl-3-carbohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.012
3-(2-(2-fluorobenzoyl)hydrazinylsulfono)benzamide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.00049
3-amino-N'-(2-fluorobenzoyl)benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0017
3-chloro-N'-(2-fluorobenzoyl)benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.00052
3-chloro-N'-(naphthalen-2-ylsulfonyl)benzohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.014
3-cyano-N'-(2-fluorobenzoyl)benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0013
3-fluoro-N'-(2-fluorobenzoyl)benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0014
3-methyl-N'-(naphthalen-2-ylsulfonyl)benzohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.004
4'-chloro-N'-(phenylsulfonyl)biphenyl-3-carbohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.041
4'-cyano-N'-(phenylsulfonyl)biphenyl-3-carbohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0095
4'-fluoro-N'-(phenylsulfonyl)biphenyl-3-carbohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0258
4'-methoxy-N'-(phenylsulfonyl)biphenyl-3-carbohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0125
4-amino-N'-(2-fluorobenzoyl)benzenesulfonohydrazide
Mus musculus
IC50 above 0.0125 mM, in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.125
4-butoxy-N'-(naphthalen-2-ylsulfonyl)benzohydrazide
Mus musculus
IC50 above 0.125 mM, in the presence of 0.015 mM acetyl-CoA, pH and temperature not specified in the publication
0.06
4-chloro-N'-(naphthalen-2-ylsulfonyl)benzohydrazide
Mus musculus
in the presence of 0.015 mM acetyl-CoA, pH and temperature not specified in the publication
0.0125
4-cyano-N'-(2-fluorobenzoyl)benzenesulfonohydrazide
Mus musculus
IC50 above 0.0125 mM, in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.03
4-hydroxy-N'-(naphthalen-2-ylsulfonyl)benzohydrazide
Mus musculus
in the presence of 0.015 mM acetyl-CoA, pH and temperature not specified in the publication
0.00027
N'-( 2-fluoro-[1,1'- biphenyl]-3-carbonyl)-benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.00074
N'-(2,3-difluorobenzoyl)benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.00013
N'-(2,3-difluorobenzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0125
N'-(2-dluorobenzoyl)-4-methylbenzenesulfonohydrazide
Mus musculus
IC50 above 0.0125 mM, in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.00039
N'-(2-fluoro-3-(trifluoromethyl)benzoyl)-benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.000077
N'-(2-fluoro-3-(trifluoromethyl)benzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.00049
N'-(2-fluoro-3-methoxybenzoyl)benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.00023
N'-(2-fluoro-3-methylbenzoyl)benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.00012
N'-(2-fluoro-3-methylbenzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.00091
N'-(2-fluoro-5-methylbenzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.017
N'-(2-fluorobenzoyl)-2-methoxybenzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0062
N'-(2-fluorobenzoyl)-2-methylbenzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0011
N'-(2-fluorobenzoyl)-3-methoxybenzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0035
N'-(2-fluorobenzoyl)-3-methylbenzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0125
N'-(2-fluorobenzoyl)-4-methoxybenzenesulfonohydrazide
Mus musculus
IC50 above 0.0125 mM, in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.042
N'-(2-methoxybenzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.019
N'-(2-methylbenzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.019
N'-(2-phenylisonicotinoyl)benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.125
N'-(3-(1H-pyrazol-1-yl)benzoyl)benzenesulfonohydrazide
Mus musculus
IC50 above 0.125 mM, in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0074
N'-(3-(piperazin-1-yl)benzoyl)benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.125
N'-(3-(pyridin-3-yl)benzoyl)benzenesulfonohydrazide
Mus musculus
IC50 above 0.125 mM, in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.029
N'-(3-(pyrimidin-5-yl)benzoyl)benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.00016
N'-(3-(thiophen-2-yl)benzoyl)benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.013
N'-(3-(thiophen-3-yl)benzoyl)benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0028
N'-(3-(trifluoromethoxy)benzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.011
N'-(3-(trifluoromethyl)benzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.125
N'-(3-acetylbenzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
IC50 above 0.125 mM, in the presence of 0.015 mM acetyl-CoA, pH and temperature not specified in the publication
0.019
N'-(3-aminobenzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
in the presence of 0.015 mM acetyl-CoA, pH and temperature not specified in the publication
0.00013
N'-(3-chloro-2-fluorobenzoyl)benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.000043
N'-(3-chloro-2-fluorobenzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.024
N'-(3-cyanobenzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.00058
N'-(3-ethyl-2-fluorobenzoyl)benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.000062
N'-(3-ethyl-2-fluorobenzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0021
N'-(3-fluorobenzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0078
N'-(3-isopropylbenzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.018
N'-(3-methoxylbenzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
in the presence of 0.015 mM acetyl-CoA, pH and temperature not specified in the publication
0.125
N'-(4-(trifluoromethoxy)benzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
IC50 above 0.125 mM, in the presence of 0.015 mM acetyl-CoA, pH and temperature not specified in the publication
0.125
N'-(4-cyanobenzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
IC50 above 0.125 mM, in the presence of 0.015 mM acetyl-CoA, pH and temperature not specified in the publication
0.000008
N'-(4-fluoro-5-methyl-[1,1'-biphenyl]-3-carbonyl)-benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.000017
N'-(4-fluoro-[1,1'-biphenyl]-3-carbonyl)-benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.12
N'-(4-fluorobenzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
in the presence of 0.015 mM acetyl-CoA, pH and temperature not specified in the publication
0.12
N'-(4-methoxybenzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
in the presence of 0.015 mM acetyl-CoA, pH and temperature not specified in the publication
0.03
N'-(4-methylbenzoyl)naphthalene-2-sulfonohydrazide
Mus musculus
in the presence of 0.015 mM acetyl-CoA, pH and temperature not specified in the publication
0.00001
N'-(5-chloro-4-fluoro-[1,1'-biphenyl]-3-carbonyl)-benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.022
N'-(5-phenylnicotinoyl)benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.018
N'-(6-phenylpicolinoyl)benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0042
N'-(naphthalen-2-ylsulfonyl)benzohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.00029
N'-([1,1'-biphenyl]-3-carbonyl)benzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.00088
N'-([1,1'-biphenyl]-3-carbonyl)naphthalene-2-sulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0067
N'-benzoylbenzenesulfonohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.001
N'-[(3-bromophenyl)sulfonyl]-2-fluorobenzohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.019
N'-[(3-ethylphenyl)sulfonyl]-2-fluorobenzohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.00046
N'-[(4-bromophenyl)sulfonyl]-2-fluorobenzohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.071
tert-butyl-(3-(2-(naphthalen-2-ylsulfono)hydrazinecarbonyl)-phenyl)carbamate
Mus musculus
in the presence of 0.015 mM acetyl-CoA, pH and temperature not specified in the publication
additional information
additional information
Mus musculus
-
significant decrease of histone acetylation in plumbagin treated mouse liver in vivo 6 h after intraperitoneal injection of 25 mg plumbagin/kg body mass
-
0.0041
2-fluoro-N'-[(3-fluorophenyl)sulfonyl]benzohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.0057
2-fluoro-N'-[(3-fluorophenyl)sulfonyl]benzohydrazide
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
0.001
CTX-0124143
Mus musculus
in the presence of 0.0004 mM acetyl-CoA, pH and temperature not specified in the publication
pH OPTIMUM
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
TEMPERATURE OPTIMUM
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
ORGANISM
COMMENTARY
LITERATURE
UNIPROT
SEQUENCE DB
SOURCE
SOURCE TISSUE
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
SOURCE
invariant natural killer T (iNKT) cells. Enzyme GCN5 promotes iNKT development during the maturation stage. iNKT cells undergo several well-defined developmental stages in the thymus. Dramatic accumulation of iNKT cells at the stage 0 in thymus of Gcn5 knockout mice
-
the Qkf gene, in addition to being strongly expressed in the developing cerebral cortex and in adult neural stem cells, is also expressed in post-mitotic cells such as neurons
-
cortex, CBP is expressed throughout embryogenesis, enzyme levels are decreasing postnatally
-
in the embryonic cortex, nestin-positive precursors and betaII-tubulin positive neurons from E12-E13 primary cortical precursor cell culture
-
expressed in embryonic lens. The lens-specific chromatin domain contains both promoter localized CBP on the background of locus spread-presence of CBP and p300
-
e.g. GFAP-positive astrocyytes and A2B5-positive oligodendrocyte precursors
additional information
-
the embryonic cortex, nestin-positive precursors and betaII-tubulin positive neurons from E12-E13 primary cortical precursor cell culture
-
the Qkf gene, in addition to being strongly expressed in the developing cerebral cortex and in adult neural stem cells, is also expressed in post-mitotic cells such as neurons
additional information
enzyme GCN5 expression analysis in different tissues from fasted (4 h) and anesthetized mice, overview
additional information
-
Moz gene is expressed throughout the developing embryo and in most adult organs
additional information
-
expression of GCN5 is decreased significantly in the bone tissue sections of ovariectomized mice or aged mice
additional information
colocalization of Foxp3 and PCAF in nuclei of T-regulatory cells (Tregs)
additional information
colocalization of Foxp3 and PCAF in nuclei of T-regulatory cells (Tregs)
LOCALIZATION
ORGANISM
UNIPROT
COMMENTARY
GeneOntology No.
LITERATURE
SOURCE
GENERAL INFORMATION
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
evolution
three main histone/protein acetyltransferase (HAT) families, CBP/p300, GNAT (GCN5/PCAF) and MYST exist. GCN5 belongs to the GNAT family
malfunction
metabolism
two prototypical GNAT family members, GCN5 (general control nonrepressed-protein 5, lysine acetyltransferase (KAT)2a) and p300/CBP-associated factor (p300/CBP-associated factor (PCAF), Kat2b) contribute to Treg functions through partially distinct and partially overlapping mechanisms
physiological function
evolution
malfunction
metabolism
physiological function
additional information
in vitro-expressed full-length HBO1 exerts less acetylation activity compared to that of the separate MYST domain. The N-terminal domain may provide a regulatory switch for HBO1 activity
malfunction
deletion of Gcn5 or PCAF do not affect Treg development or suppressive function in vitro, but do affect inducible Treg (iTreg) development, and in vivo, abrogate Treg-dependent allograft survival. Mice lacking GCN5 show prolonged allograft survival, suggesting this HAT might be a target for epigenetic therapy in allograft recipients. Dual deletion of GCN5 and PCAF leads to decreased Treg stability and numbers in peripheral lymphoid tissues, and mice succumbed to severe autoimmunity by 3-4 weeks of life. Conditional deletion of GCN5 in the Tregs of GCN5flfFoxp3YFP-cre mice have no significant effect on T-cell numbers or their baseline level of immune activation. GCN5 deletion also decreases Teff cell functions in vivo. GCN5 deletion in Foxp3+ Treg cells causes lethal autoimmunity
malfunction
GCN5 loss leads to a modest impairment in T cell development. The generation of iNKT cells, identified by TCRbeta antibody and NK1.1 or CD1d-alphaGalCer tetramer, is largely diminished in the thymus of GCN5 KO mice. This block cannot be compensated in the periphery, as indicated by a profound decrease in iNKT cell frequencies and numbers in the spleen and liver of GCN5 KO mice. Impaired iNKT cell development is unlikely due to elevated cell death, as annexin V-positive populations of iNKT cells in the thymus, spleen, and liver are indistinguishable between wild-type and GCN5 KO mice. Dramatic accumulation of iNKT cells at the stage 0 in thymus of Gcn5 knockout mice. Phenotype, overview. GCN5 knockdown inhibits EGR2 acetylation
malfunction
loss of GCN5 in vivo does not promote metabolic remodeling in mouse skeletal muscle. Skeletal muscle gene expression of metabolic, angiogenic, and mitochondrial genes is not affected by loss of GCN5. Loss of GCN5 does not affect myosin heavy chain (MHC) composition, and markers of skeletal muscle development are unaffected by loss of GCN5. Skeletal muscle maximal respiratory capacity and succinate dehydrogenase (SDH) enzyme activity are not affected by loss of GCN5. Loss of GCN5 does not affect mitochondrial content or adaptations to endurance exercise training
physiological function
histone acetyltransferases (HATs) play critical roles in controlling T-regulation (Treg) development
physiological function
lysine acetyltransferase GCN5 is a regulator of mitochondrial biogenesis via its inhibitory action on peroxisome proliferator activated receptor-gamma coactivator-1alpha (PGC-1alpha). Specific contribution of GCN5 to skeletal muscle metabolism and mitochondrial adaptations to endurance exercise in vivo
physiological function
lysine acetyltransferases GCN5 is a transcription-related histone acetyltransferase. GCN5 is a specific lysine acetyltransferase of EGR2, a transcription factor required for CD1d-restricted invariant natural killer T (iNKT) cell development. The histone acetyltransferase GCN5 is essential for iNKT cell development during the maturation stage. GCN5-mediated acetylation positively regulated EGR2 transcriptional activity, and both genetic and pharmacological GCN5 suppression specifically inhibits the transcription of EGR2 target genes in iNKT cells, including Runx1, PLZF, IL-2Rb, and T-bet. Therefore, GCN5-mediated EGR2 acetylation is a molecular mechanism that regulates iNKT development. GCN5 has been shown to play critical roles in a variety of important biological functions including metabolic regulation, cell growth and survival, DNA damage repair, and embryonic development. Role of GCN5 in T cell immunity, overview. GCN5 is required for the development of iNKT cells in mice. GCN5 regulates the expression of genes driving iNKT development through EGR2
evolution
HBO1 (also known as KAT7, MYST2) is a canonical member of the MYST (MOZ, Ybf1/Sas3, Sas2 and Tip60) acetyltransferase family. HBO1 contains the MYST domain that is a highly conserved acetyltransferase domain shared by the MYST family such as MYST1 (MOF/KAT8), MYST2 (HBO1/KAT7), and MYST3 (MOZ/KAT6A). HBO1 comprises a cervical-loop structure proximity to the MYST domain that mediates the interaction with the N-terminal region (residues 31-80) of BRPF2 (also known as BRD1), for BRPF2 is a cofactor directing HBO1 binding to the histone
evolution
three main histone/protein acetyltransferase (HAT) families, CBP/p300, GNAT (GCN5/PCAF) and MYST exist. PCAF belongs to the GNAT family
malfunction
-
dysfunction is associated with diseases like asthma, cardiovascular disorders, diabetes, and cancer
malfunction
-
MOZ generates fusion genes, such as MOZ-TIF2, MOZ-CBP and MOZ-p300, in acute myeloid leukemia by chromosomal translocation leading to repressed differentiation, hyper-proliferation, and self-renewal of myeloid progenitors through deregulation of MOZ-regulated target gene expression. Roles of MOZ and MOZ fusion genes in normal and malignant hematopoiesis, mechanism, overview
malfunction
-
the haploinsufficient enzyme causes the Rubinstein-Taybi syndrome, a genetic disorder with cognitive dysfunction, by disrupting the control mechanism of neural precursor competency to differentiate
malfunction
-
knockdown of GCN5 inhibits the osteogenic differentiation of and mineralization in mesenchymal stem cells. Impaired osteogenic differentiation by GCN5 knockdown is blocked by inhibition of NF-kappaB
malfunction
PCAF deficiency reduces the in vitro inflammatory response in leukocytes and vascular cells involved in arteriogenesis. PCAF deficiency results in differential expression of 3505 genes during arteriogenesis and, more specifically, in impaired induction of multiple proinflammatory genes. Recruitment from the bone marrow of inflammatory cells, in particular proinflammatory Ly6Chi monocytes, is severely impaired in PCAF-/- mice
malfunction
abrogation of HBO1 activity caused by either RNA interference or dominant negative mutation (e.g. S57A) does not affect the recruitment of ORC, CDC6 and CDT1 to replication origins, but remarkably impairs the loading of MCMs to the origins and subsequently delays DNA replication licensing. In immune-related disease, HBO1 is upregulated in synovial fibroblasts, which are the key pathogenic factors contributing to the development and progression of rheumatoid arthritis. Protein HBZ (HTLV-1 basic zipper factor, from a human T cell leukemia virus) interacts with HBO1 during pathogenesis and inhibits its acetylation activity to reduce p53-mediated transcription activation of p21/CDKN1A and Gadd45a, and subsequently delays G2-cell cycle arrest
malfunction
deletion of Gcn5 or PCAF do not affect Treg development or suppressive function in vitro, but do affect inducible Treg (iTreg) development, and in vivo, abrogate Treg-dependent allograft survival. Deletion of either CBP or p300 results in only a modest decrease in Treg suppressive function. Activated CD4+T cell population in mesenteric lymph nodes of PCAF-/- mice, contribution of PCAF to iTreg development. PCAF deletion in Foxp3+ Treg cells causes lethal autoimmunity
malfunction
enzyme deficiency is associated with congenital malformations and embryolethality. Enzyme inhibition induces oxidative stress
malfunction
homozygous enzyme loss leads to lethal hematopoietic failure in mice at an early postnatal stage. Enzyme loss in adult mice results in dramatic hematopoietic failure
malfunction
-
knockdown of the enzyme inhibits differentiation of mesenchymal stem cells into osteoblast cells. The impaired osteogenic differentiation by enzyme knockdown is blocked by inhibition of nuclear factor kappaB
malfunction
oocyte enzyme deletion results in female infertility, with follicle development failure in the secondary and preantral follicle stages. Enzyme deletion results in abnormal heterochromatin configurations in oocytes. Granulosa cell-specific deletion of the enzyme does not affect follicle development or female fertility
metabolism
HBO1 can be either ubiquitinated or act as an ubiquitin ligase. HBO1 acetyltransferase complexes and activity regulation, overview. The tumor suppressor p53, adipogenesis regulator FAD24 (factor for adipocyte differentiation 24, also called NOC3L) and cell cycle kinases CDK1, CDK2, CDK11 and PLK1 are linked to HBO1. Moreover, cell growth inhibitor Niam and homeobox protein SIX1 that potentiates the Warburg effect by interaction with HBO1 are also presented. HBO1 complexes mainly consist of accessory proteins MEAF6, ING4 or ING5, and two types of cofactors for chromatin binding: Jade-1/2/3 and BRPF1/2/3. HBO1 is associated with the key events of the cell cycle, especially in mitosis through physical interaction with PLK1 and CDK1. Acetylation and autoacetylation regulates HBO1 activity
metabolism
-
the enzyme regulates osteogenic differentiation of mesenchymal stem cells by inhibiting nuclear factor kappaB. The enzyme represses nuclear factor kappa B-dependent transcription and inhibits the nuclear factor kappaB signaling pathway
metabolism
two prototypical GNAT family members, GCN5 (general control nonrepressed-protein 5, lysine acetyltransferase (KAT)2a) and p300/CBP-associated factor (p300/CBP-associated factor (PCAF), Kat2b) contribute to Treg functions through partially distinct and partially overlapping mechanisms. Transplants in mice lacking PCAF undergo acute allograft rejection. PCAF deletion also enhances anti-tumor immunity in immunocompetent mice. Dual deletion of GCN5 and PCAF leads to decreased Treg stability and numbers in peripheral lymphoid tissues, and mice succumbed to severe autoimmunity by 3-4 weeks of life
physiological function
-
ATAC2 not only carries out an enzymatic function but also plays an architectural role in the stability of mammalian ATAC
physiological function
-
CBP regulates neurobehavioural development, the enzyme activity and histone acetylation is required for control of neural cortical precursor competency to differentiate, regulation via environmental factors
physiological function
-
histone acetylation is one of the major epigenetic mechanisms to regulate gene expression. MOZ is essential for the generation and maintenance of hematopoietic stem cells and for the appropriate development of myeloid, erythroid and B-lineage cell progenitors. MOZ is also required for self-renewal of hematopoietic stem cells
physiological function
-
Qkf/Morf requirement in neural stem cell/neural progenitor self-renewal with an additional role in some other cell types such as osteoblasts and germ cells. Qkf in adult neurogenesis in vivo, overview
physiological function
-
the enzyme activity of MOZ is critical for the proliferation of hematopoietic precursors, overview
physiological function
-
histone acetyltransferase Mof plays an essential role in the maintenance of embryonic stem cell self-renewal and pluripotency. Embryonic stem cells with Mof deletion lose characteristic morphology, alkaline phosphatase staining, and differentiation potential. They also have aberrant expression of the core transcription factors Nanog, Oct4, and Sox2. The phenotypes of Mof null embryonic stem cells can be partially suppressed by Nanog overexpression, supporting the idea that Mof functions as an upstream regulator of Nanog in embryonic stem cells. Mof is an integral component of the embryonic stem cell core transcriptional network and Mof primes genes for diverse developmental programs. Mof is also required for Wdr5 recruitment and histone H3K4 methylation at key regulatory loci
physiological function
an important role for PCAF in arteriogenesis. Enzyme PCAF modulates post-ischemic gene regulation
physiological function
-
the enzyme GCN5 plays essential roles in various developmental processes, it has a critical function in osteogenic commitment of mesenchymal stem cells. In this role, the histone acetyltransferase activity of GCN5 is not required. Enzyme GCN5 represses nuclear factor kappa B-dependent transcription and inhibits the NF-kappaB signaling pathway. GCN5 is responsible for degradation of RelA. Acetylase activity of GCN5 is dispensable for the regulation of osteogenic differentiation of mesenchymal stem cells
physiological function
enzyme HBO1 is responsible for the bulk acetylation of histone H4 and H3K14. HBO1 functions as the core catalytic subunit in multimeric complexes established by cofactors and accessory proteins. HBO1 affords multiple functions in various processes such as DNA replication, gene transcription, protein ubiquitination, immune regulation, stem cell pluripotent and self-renewal maintenance as well as embryonic development. HBO1 functions as the core catalytic subunit in multimeric complexes established by cofactors and accessory proteins. HBO1 is reported to participate in transcriptional regulation in alternative complexes such as HBO1-SIX1 and HBO1-Niam. HBO1 encourages tissue-specific gene expression, for it participates in intragenic histone acetylation and mediated Pol II binding in regulating the expression of endothelial VEGFR-2. HBO1-mediated histone acetylation enables the accession of transcriptional factors to the chromatin and regulates the initiation of transcription. Alternatively, HBO1 complexes occupies the coding region to afford a direct role in transcriptional elongation. HBO1 might acetylate the transcriptional factors and change their protein-protein interactions. HBO1 facilitates chromatin loading of minichromosome maintenance (MCM) complexes and promotes DNA replication licensing. Loading of MCM complexes to chromatin is the final step of the prereplicative complexes assembly. Indispensable roles of HBO1 in chromosome remodeling and DNA replication, the mechanism regarding how HBO1 facilitates MCM loading and the involved protein-protein interactions is analyzed. HBO1 is required for T cell development and immune regulation. HBO1 acetyltransferase complexes and activity regulation, overview. Multiple functions of HBO1 are realized by the formation of protein complexes with different cofactors or partner proteins. HBO1 functions in spermatogenesis
physiological function
histone acetyltransferases (HATs) play critical roles in controlling T-regulation (Treg) development. PCAF helps protect Tregs from undergoing apoptosis upon TCR stimulation
physiological function
the enzyme has an essential function in oogenesis and is essential for female fertility by regulating antioxidant gene expression. The enzyme directly regulates antioxidant gene expression in oocytes
physiological function
the enzyme is a developmental-stage-specific chromatin regulator whose activity is essential for adult but not early and midgestational murine hematopoietic maintenance. Enzyme activity is required for adult hematopoietic cell survival
UNIPROT
ENTRY NAME
ORGANISM
NO. OF AA
NO. OF TRANSM. HELICES
MOLECULAR WEIGHT[Da]
SOURCE
SEQUENCE
LOCALIZATION PREDICTION
The reliability class of the localization prediction ranges from 1 (very reliable) to 5 (not reliable).
The reliability class of the localization prediction ranges from 1 (very reliable) to 5 (not reliable). KAT2A_MOUSE
830
0
93394
Swiss-Prot
other Location (Reliability: 4)
MOLECULAR WEIGHT
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
SUBUNIT
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
additional information
additional information
-
NCOAT contains a motif similar to the histone binding domain in the MYST family of HATs, a zinc finger-like motif responsible for substrate recognition
additional information
-
MOZ encodes a large multidomain protein that contains, among others, 2 domains shown to interact with the transcription factor Runx1, a C4H3 domain also referred to as plant homeodomain, an atypical Cys(2)-His-Cys (C2HC) zinc finger domain with a putative nucleosome-binding activity, and a region with homology to the active acetyl-CoA binding site of several HAT proteins
additional information
HBO1 consists of the N-terminal domain (NTD) and the conserved C-terminal MYST domain. The NTD of HBO1 consists of a number of loops and a small part of the helix. The structure is highly flexible, which may provide abundant conformation changes for HBO1 activity regulation or protein binding. The MYST domain of HBO1 contains two typical sites for molecule binding, the acetyl-CoA-binding site and histone tail binding site
POSTTRANSLATIONAL MODIFICATION
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
acetylation
acetylation and autoacetylation regulates HBO1 activity. This regulation mainly occurs on Lys201. In contrast, acetylation occurs at another conserve site Lys279 in RNSGLSK(ac)EQ is downregulated in response to heat or X-ray treatments in mouse testis, indicating its functions in spermatogenesis
phosphoprotein
additional information
HBO1 can be either ubiquitinated or act as an ubiquitin ligase
phosphoprotein
-
CBP phosphorylation at Ser436 by atypical protein kinase zeta is necessary for histone acetylation at neural gene promoters and appropriate differentiation
phosphoprotein
phosphorylations regulate HBO1 activity and connect it to the cell cycle
PROTEIN VARIANTS
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
G657E
-
site-directed mutagenesis, loss-of-function mutation in the HAT catalytic domain of MOZ, mutation of the HAT catalytic domain affects B-lineage differentiation and hematopoietic stem/progenitor cell frequencies, analysis of hematopoietic cell populations in HAT-/-, HAT-/+, and HAT+/+ mice, overview. The HAT activity of MOZ is essential for maintaining the functionality of hematopoietic stem cells
Y891F
-
site-directed mutagenesis, catalytically inactive mutant, stable binding of unacetylated histone H4, useful for purification of the histone protein
additional information
additional information
generation of a strain of T cell-specific Gcn5 knockout (GCN5 KO) mice by breeding Lck-Cre transgenic mice with Gcn5 floxed mice. In these mice, Cre recombinase expression driven by the Lck promoter mediates Gcn5 deletion from the CD4/CD8 double-negative stage. Immunoblot analysis demonstrates that GCN5 is efficiently deleted from thymic T cells. The percentages of cells at CD4/CD8 double-positive and single-positive stages are not altered in the thymus of GCN5 KO mice. But GCN5 gene deletion results in an about 20% reduction in the total thymocyte numbers in mice. As a consequence, a similar level reduction in the absolute numbers of CD4/CD8 double-positive and single-positive cells. While a slight but statistically significant increase in the percentage of double-negative cells is observed upon Gcn5 gene deletion, their absolute number is not altered due to the reduction in total thymocytes in GCN5 KO mice. Ectopic GCN5 expression significantly enhances EGR2 acetylation without affecting total protein expression levels. Gene expression profiles in the GCN5 knockdown DN32, overview
additional information
generation of mKO mice, mice harboring LoxP sites flanking exons 3-19 of the GCN5 gene, referred to as GCN5flox/flox, usage of Cre-LoxP methodology to generate mice with muscle-specific knockout of GCN5 (mKO) and floxed, wildtype littermates. Despite successful knockdown of GCN5 activity in skeletal muscle of mKO mice, whole-body energy expenditure as well as skeletal muscle mitochondrial abundance and maximal respiratory capacity are comparable between mKO and wild-type mice. No differences in skeletal muscle expression of several genes between wild-type and GCN5 mKO mice, overview. Skeletal muscle gene expression of metabolic, angiogenic, and mitochondrial genes is not affected by loss of GCN5. Loss of GCN5 does not alter body composition, in vivo metabolism or energy expenditure
additional information
-
TIP (tension-induced/inhibited) proteins are identified as interacting partners of p300. TIPs do not have intrinsic catalytic activity but they recruit p300 HAT activity. TIP-6 binds directly and indirectly to p300 and histone H4 (H4). Deletion of the SANT domain does not abolish TIP-6 interaction with p300 and H4 but eliminates direct TIP-6 binding to p300. Chromatin immunoprecipitation assays show the recruitment of TIP-6, TIP-6DELTASANT, and p300 to the PPARgamma2 promoter, but H3/H4 acetylation occurres only when p300 is directly associated with TIP-6
additional information
-
generation of ATAC2-knockout mice, loss of Atac2 leads to reduced histone acetylation, cell death, and G2/M arrest
additional information
-
hematopoietic deficiency in MOZ-DELTAC mice occurs in terms of decreased numbers of blood cells, significantly reduced hematopoietic progenitors and HSC and an increase in nucleated erythrocytes, phenotype, overview. When MOZ-deficient fetal liver cells are transplanted into irradiated mice, recipient mice do not develop a reconstituted hematopoietic system, even when excess numbers of fetal liver cells are transplanted
additional information
-
knockdown of PRMT1 by RNAi in erythroid progenitor cells prevents histone acetylation, enhancer and promoter interaction, and recruitment of transcription complexes to the active beta-globin promoter. Restoration of PRMT1 expression in PRMT1 knockout cells rescues erythroid differentiation and beta-globin transcription
additional information
-
loss of function of Moz causes defects in the hematopoietic stem cell compartment. Generation of different Moz mutant alleles with similar consequences for the hematopoietic system, phenotypes, overview. Qkf gt/gt mutants that survive to weaning age, which are less than 50% on an inbred 129Sv/Pas background, are smaller than littermate controls, have craniofacial abnormalities, skeletal abnormalities, and a disproportional reduction in the size of the cerebral cortex. Developing Qkf gt/gt mutant forebrain at embryonic day 11.5 contains fewer cerebrocortical progenitor cells, the cerebral cortex primordium, the cortical plate, contains fewer neurons and is reduced in size at embryonic days 13.5, 15.5, and 17.5. Mof mutant mouse embryos arrest in development at the blastocyst stage. RNAi screening in mouse embryonic stem cells reveals that Tip60 is required for pluripotency, and genome-wide expression analysis of Tip60-depleted embryonic stem cells suggests that Tip60 represses a large number of genes that are expressed during differentiation. Tip60 mutant mouse embryos die before implantation
additional information
-
neonatal cbp+/- mice are behaviourally impaired and display perturbed vocalization behaviour. Knockdown of CBP by siRNA causes a reduction in betaII-tubulin-positive neurons, and inhibits neurogenesis and gliogenesis, cell phenotype, overview
additional information
contribution of PCAF to post-ischemic neovascularization in a hind limb ischemia model23, using enzyme-deficient PCAF-/- mice, phenotype, overview
additional information
deletion of PCAF, PCAF targeting in wild-type mice impairs inhibits Treg function in vitro and in vivo, phenotype, overview
additional information
deletion of PCAF, PCAF targeting in wild-type mice impairs inhibits Treg function in vitro and in vivo, phenotype, overview
additional information
in vitro-expressed full-length HBO1 exerts less acetylation activity compared to that of the separate MYST domain
PURIFICATION (Commentary)
ORGANISM
UNIPROT
LITERATURE
recombinant GST-tagged enzyme from BSC40 cells by glutathione affinity chromatography
-
recombinant His-tagged wild-type and mutant enzymes by nickel affinity chromatography
-
CLONED (Commentary)
ORGANISM
UNIPROT
LITERATURE
gene Kat2a, recombinant expression of FLAG-tagged enzyme in DN32.D3 cells, interaction of FLAG-tagged GCN5 with HA-tagged EGR2 in transiently transfected DN32.D3 cells by coimmunoprecipitation and immunoblotting
expression of GST-tagged enzyme in BSC40 cells via VTF-7 vaccinia virus transfection vector
-
expression of His-tagged wild-type and mutant enzymes using the baculovrius transfection system
-
expression of Tip60 in H-1299 human lung carcinoma cells, leads to increased c-Myc protein stability in the transfected cells
-
EXPRESSION
ORGANISM
UNIPROT
LITERATURE
during oocyte development, there is about 5fold increase between 14 days and full-grown germinal vesicle stage oocytes
in immune-related disease, HBO1 is upregulated in synovial fibroblasts, which are the key pathogenic factors contributing to the development and progression of rheumatoid arthritis
the enzyme expression is decreased significantly in the bone tissue sections of ovariectomized mice or aged mice
-
the expression of nuclear and total cellular enzyme proteins is decreased following 5 mM valproic acid exposure for 6 h
APPLICATION
ORGANISM
UNIPROT
COMMENTARY
LITERATURE
molecular biology
pharmacology
-
the GCN5-NF-kB pathway is a potentialmolecular target for stem cell mediated regenerative medicine and the treatment of metabolic bone diseases such as osteoporosis
molecular biology
-
the catalytically inactive mutant Y891F is useful for stable binding and purification of unacetylated histone H4 protein
molecular biology
-
the results demonstrate the importance of TIPs in the recruitment of p300 to specific promoters and in the regulation of p300 HAT activity through the involvement of the SANT domain
REF.
AUTHORS
TITLE
JOURNAL
VOL.
PAGES
YEAR
ORGANISM (UNIPROT)
PUBMED ID
SOURCE
Hasan, S.; Hottiger, M.O.
Histone acetyl transferases: a role in DNA repair and DNA replication
J. Mol. Med.
80
463-474
2002
Arabidopsis thaliana, Saccharomyces cerevisiae, Drosophila melanogaster, Homo sapiens, Mus musculus, Tetrahymena thermophila, Homo sapiens GCN5
Toleman, C.; Paterson, A.J.; Whisenhunt, T.R.; Kudlow, J.E.
Characterization of the histone acetyltransferase (HAT) domain of a bifunctional protein with activable O-GlcNAcase and HAT activities
J. Biol. Chem.
279
53665-53673
2004
Mus musculus (Q9EQQ9)
Toleman, C.A.; Paterson, A.J.; Kudlow, J.E.
The histone acetyltransferase NCOAT contains a zinc finger-like motif involved in substrate recognition
J. Biol. Chem.
281
3918-3925
2006
Mus musculus
Yang, Y.; Wolf, L.V.; Cvekl, A.
Distinct embryonic expression and localization of CBP and p300 histone acetyltransferases at the mouse alphaA-crystallin locus in lens
J. Mol. Biol.
369
917-926
2007
Mus musculus
Badri, K.R.; Zhou, Y.; Dhru, U.; Aramgam, S.; Schuger, L.
Tension Induced/inhibited Proteins (TIPs) are novel partners of the histone acetyltransferase p300: TIPs SANT domain in p300 activity and TIP-6-induced adipogenesis
Mol. Cell. Biol.
28
6358-6372
2008
Mus musculus
Voss, A.K.; Thomas, T.
MYST family histone acetyltransferases take center stage in stem cells and development
Bioessays
31
1050-1061
2009
Arabidopsis thaliana, Danio rerio, Saccharomyces cerevisiae, Caenorhabditis elegans, Drosophila melanogaster, Homo sapiens, Mus musculus, Danio rerio zMoz
Perez-Campo, F.M.; Borrow, J.; Kouskoff, V.; Lacaud, G.
The histone acetyl transferase activity of monocytic leukemia zinc finger is critical for the proliferation of hematopoietic precursors
Blood
113
4866-4874
2009
Mus musculus, Mus musculus C57BL/6
Li, X.; Hu, X.; Patel, B.; Zhou, Z.; Liang, S.; Ybarra, R.; Qiu, Y.; Felsenfeld, G.; Bungert, J.; Huang, S.
H4R3 methylation facilitates beta-globin transcription by regulating histone acetyltransferase binding and H3 acetylation
Blood
115
2028-2037
2010
Mus musculus
Katsumoto, T.; Yoshida, N.; Kitabayashi, I.
Roles of the histone acetyltransferase monocytic leukemia zinc finger protein in normal and malignant hematopoiesis
Cancer Sci.
99
1523-1527
2008
Mus musculus
Wang, J.; Weaver, I.; Gauthier-Fisher, A.; Wang, H.; He, L.; Yeomans, J.; Wondisford, F.; Kaplan, D.; Miller, F.
CBP histone acetyltransferase activity regulates embryonic neural differentiation in the normal and Rubinstein-Taybi syndrome brain
Dev. Cell
18
114-125
2010
Mus musculus
Ravindra, K.C.; Selvi, B.R.; Arif, M.; Reddy, B.A.; Thanuja, G.R.; Agrawal, S.; Pradhan, S.K.; Nagashayana, N.; Dasgupta, D.; Kundu, T.K.
Inhibition of lysine acetyltransferase KAT3B/p300 activity by a naturally occurring hydroxynaphthoquinone, plumbagin
J. Biol. Chem.
284
24453-24464
2009
Homo sapiens, Mus musculus
Guelman, S.; Kozuka, K.; Mao, Y.; Pham, V.; Solloway, M.J.; Wang, J.; Wu, J.; Lill, J.R.; Zha, J.
The double-histone-acetyltransferase complex ATAC is essential for mammalian development
Mol. Cell. Biol.
29
1176-1188
2009
Mus musculus, Homo sapiens (Q9H8E8)
Li, X.; Li, L.; Pandey, R.; Byun, J.S.; Gardner, K.; Qin, Z.; Dou, Y.
The histone acetyltransferase MOF is a key regulator of the embryonic stem cell core transcriptional network
Cell stem cell
11
163-178
2012
Mus musculus
Bastiaansen, A.J.; Ewing, M.M.; de Boer, H.C.; van der Pouw Kraan, T.C.; de Vries, M.R.; Peters, E.A.; Welten, S.M.; Arens, R.; Moore, S.M.; Faber, J.E.; Jukema, J.W.; Hamming, J.F.; Nossent, A.Y.; Quax, P.H.
Lysine acetyltransferase PCAF is a key regulator of arteriogenesis
Arterioscler. Thromb. Vasc. Biol.
33
1902-1910
2013
Mus musculus (Q9JHD1)
Zhang, P.; Liu, Y.; Jin, C.; Zhang, M.; Tang, F.; Zhou, Y.
Histone acetyltransferase GCN5 regulates osteogenic differentiation of mesenchymal stem cells by inhibiting NF-kappaB
J. Bone Miner. Res.
31
391-402
2015
Mus musculus, Mus musculus C57BL/6
Valerio, D.; Xu, H.; Eisold, M.; Woolthuis, C.; Pandita, T.; Armstrong, S.
Histone acetyltransferase activity of MOF is required for adult but not early fetal hematopoiesis in mice
Blood
129
48-59
2017
Mus musculus (Q9D1P2), Mus musculus
Liu, Y.; Bao, C.; Wang, L.; Han, R.; Beier, U.H.; Akimova, T.; Cole, P.A.; Dent, S.Y.R.; Hancock, W.W.
Complementary roles of GCN5 and PCAF in Foxp3+ T-regulatory cells
Cancers (Basel)
11
554
2019
Mus musculus (Q9JHD1), Mus musculus (Q9JHD2)
Wang, Y.; Yun, C.; Gao, B.; Xu, Y.; Zhang, Y.; Wang, Y.; Kong, Q.; Zhao, F.; Wang, C.R.; Dent, S.Y.R.; Wang, J.; Xu, X.; Li, H.B.; Fang, D.
The lysine acetyltransferase GCN5 is required for iNKT cell development through EGR2 acetylation
Cell Rep.
20
600-612
2017
Mus musculus (Q9JHD2), Mus musculus C57BL/6 (Q9JHD2)
Lan, R.; Wang, Q.
Deciphering structure, function and mechanism of lysine acetyltransferase HBO1 in protein acetylation, transcription regulation, DNA replication and its oncogenic properties in cancer
Cell. Mol. Life Sci.
77
637-649
2020
Homo sapiens (O95251), Mus musculus (Q5SVQ0)
Yin, S.; Jiang, X.; Jiang, H.; Gao, Q.; Wang, F.; Fan, S.; Khan, T.; Jabeen, N.; Khan, M.; Ali, A.; Xu, P.; Pandita, T.; Fan, H.; Zhang, Y.; Shi, Q.
Histone acetyltransferase KAT8 is essential for mouse oocyte development by regulating reactive oxygen species levels
Development
144
2165-2174
2017
Mus musculus (Q9D1P2)
-
Zhang, P.; Liu, Y.; Jin, C.; Zhang, M.; Tang, F.; Zhou, Y.
Histone acetyltransferase GCN5 regulates osteogenic differentiation of mesenchymal stem cells by inhibiting NF-kappaB
J. Bone Miner. Res.
31
391-402
2016
Mus musculus
Leaver, D.; Cleary, B.; Nguyen, N.; Priebbenow, D.; Lagiakos, H.; Sanchez, J.; Xue, L.; Huang, F.; Sun, Y.; Mujumdar, P.; Mudududdla, R.; Varghese, S.; Teguh, S.; Charman, S.; White, K.; Katneni, K.; Cuellar, M.; Strasser, J.; Dahlin, J.; Walters, M.
Discovery of benzoylsulfonohydrazides as potent inhibitors of the histone acetyltransferase KAT6A
J. Med. Chem.
62
7146-7159
2019
Mus musculus (Q8BZ21)
-
Dent, J.R.; Martins, V.F.; Svensson, K.; LaBarge, S.A.; Schlenk, N.C.; Esparza, M.C.; Buckner, E.H.; Meyer, G.A.; Hamilton, D.L.; Schenk, S.; Philp, A.
Muscle-specific knockout of general control of amino acid synthesis 5 (GCN5) does not enhance basal or endurance exercise-induced mitochondrial adaptation
Mol. Metab.
6
1574-1584
2017
Mus musculus (Q9JHD2)
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