Literature summary for 1.14.11.65 extracted from

Zhang, Q.J.; Tran, T.A.T.; Wang, M.; Ranek, M.J.; Kokkonen-Simon, K.M.; Gao, J.; Luo, X.; Tan, W.; Kyrychenko, V.; Liao, L.; Xu, J.; Hill, J.A.; Olson, E.N.; Kass, D.A.; Martinez, E.D.; Liu, Z.P.
Histone lysine dimethyl-demethylase KDM3A controls pathological cardiac hypertrophy and fibrosis (2018), Nat. Commun., 9, 5230 .

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Organism

Organism	UniProt	Comment	Textmining
Mus musculus	Q6PCM1	isoform KDM3A	-

Synonyms

Synonyms	Comment	Organism
Kdm3a	-	Mus musculus

General Information

General Information	Comment	Organism
physiological function	Kdm3a promotes left ventricular hypertrophy and fibrosis in response to pressure-overload. KDM3A gene deletion protects mice against trans-aortic constriction-induced left ventricular hypertrophy. Cardiomyocyte KDM3A activates Timp1 transcription with profibrotic activity. A pan-KDM inhibitor, JIB-04, suppresses pressure overload-induced left ventricular hypertrophy and fibrosis. JIB-04 inhibits KDM3A and suppresses the transcription of fibrotic genes that overlap with genes downregulated in KDM3A-knockout mice versus wild-type controls	Mus musculus

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Release 2023.1 (January 2023)