2.1.1.364: [histone H3]-lysine4 N-methyltransferase

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For detailed information about [histone H3]-lysine4 N-methyltransferase, go to the full flat file.

Reaction

Synonyms

chromatin histone H3-lysine 4 methyltransferase, H3-K4 HMT, histone lysine methyltransferase, histone lysine methyltransferase SET7/9, HKMT, KIAA1717, KMT7, PKMT, protein lysine methyltransferase, SET-domain protein lysine methyltransferase, SET7, SET7/9, SET9, SetD7

ECTree

     2 Transferases

         2.1 Transferring one-carbon groups

             2.1.1 Methyltransferases

                2.1.1.364 [histone H3]-lysine4 N-methyltransferase

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Results	in table
4008	AA Sequence
3	Application
1	Cloned(Commentary)
1	Cofactor
142	Disease/ Diagnostics
1	Expression
7	General Information
1	IC50 Value
2	Inhibitors
1	Natural Substrates/ Products (Substrates)
14	Organism
2	Pathway
1	PDB ID
2	Protein Variants
1	Reaction
14	Reference
8	Source Tissue
18	Substrates and Products (Substrate)
29	Synonyms
1	Systematic Name

General Information

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General Information on EC 2.1.1.364 - [histone H3]-lysine4 N-methyltransferase

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GENERAL INFORMATION

ORGANISM

UNIPROT

COMMENTARY

LITERATURE

malfunction

Homo sapiens

-

SET7/9 deficiency does not affect p65 DNA binding as assessed by electrophoretic mobility shift assays, S100b-induced gene expression is decreased by SET7/9 knockdown

704436

physiological function

6 entries

physiological function

Homo sapiens

-

SET7/9 may act as a transcriptional cofactor of NF-kappaB p65, SET7/9 may regulate NF-kappaB-dependent genes through modifications of chromatin histone lysine at these specific gene promoters, SET7/9 is recruited to the promoters of inflammatory genes and enhances p65 recruitment to these gene promoters, SET7/9 is not involved in monocyte differentiation but affects monocyte adhesion

704436

physiological function

Mus musculus

Q8VHL1

methyltransferase Set9 potentiates TGF-beta signaling by targeting Smad7, an inhibitory downstream effector. Smad7 methylation promotes interaction with the E3 ligase Arkadia and, thus, ubiquitination-dependent degradation. Depletion or pharmacological inhibition of Set9 results in elevated Smad7 protein levels and inhibits TGF-beta-dependent expression of genes encoding extracellular matrix components. Lung fibrosis induced by bleomycin or Ad-TGF-beta treatment is highly compromised in Set9-deficient mice

759026

physiological function

Mus musculus

Q8VHL1

SET9 interacts with SMAD3, the principal mediator of TGFB1 signalling in myofibroblasts. SET9-deficient fibroblasts exhibit globally altered gene expression profiles in response to TGFB1, whilst overexpression of SET9 enhances SMAD3 transcriptional activity. SET9 facilitates nuclear import of SMAD3 and controls SMAD3 protein degradation via ubiquitylation. SET9 is broadly required for the effects of TGFB1 in diseased primary renal fibroblasts. SET9 promotes fibroblast migration into wounds, expression of extracellular matrix proteins, collagen contractility and myofibroblast differentiation. SET9 is recruited to the alpha-smooth muscle actin gene in response to TGFB1

759536

physiological function

Homo sapiens

Q8WTS6

SET9 interacts with the large subunit ribosomal protein, eL42. The N-terminal MORN domain of SET9 is essential for its interaction with eL42. SET9 methylates eL42 at Lys53, Lys80 and Lys100. SET9-mediated methylation of eL42 enhances global translation

758847

physiological function

Homo sapiens

Q8WTS6

Set9 methylates the nuclear and cytoplasmic androgen receptor. Set9 overexpression potentiates androgen receptor-mediated transactivation of the probasin promoter, whereas Set9 depletion inhibits androgen receptor activity and target gene expression. Chromatin occupancy of Set9 at androgen response elements is androgen dependent, and associated with methylated histone H3K4 chromatin activation marks and p300/CBP associated factor acetyltransferase recruitment. Set9 depletion increases the histone H3K9-dimethyl repressive mark at androgen response elements and reduces histone activation marks and occupancy of p300/CBP associated factor. K630A mutation of the androgen receptor reduces amino- and carboxy-terminal interaction in Set9-intact cells, whereas amino- and carboxy-terminal interaction for wild-type androgen receptor is reduced upon Set9 depletion

759776

physiological function

Homo sapiens

Q8WTS6

SET9 promotes HIF-1alpha protein stability in hypoxia and enhances HIF-1 mediated glycolytic gene transcription. SET9 interacts with HIF-1alpha and promotes HIF-1alpha protein stability in hypoxia. Silencing SET9 by siRNA reduces HIF-1alpha protein stability in hypoxia, and attenuates the hypoxic induction of HIF-1 target genes mediating hypoxic glycolysis. SET9 is enriched at the hypoxia response elements within promoters of the HIF-1-responsive glycolytic genes. Silencing SET9 reduces HIF-1alpha levels at these HREs in hypoxia, thereby attenuating HIF-1-mediated gene transcription. Silencing SET9 reduces hypoxia-induced glycolysis and inhibits cell viability of hypoxic cancer cells

758837