Literature summary for 1.14.11.66 extracted from

Cui, S.Z.; Lei, Z.Y.; Guan, T.P.; Fan, L.L.; Li, Y.Q.; Geng, X.Y.; Fu, D.X.; Jiang, H.W.; Xu, S.H.
Targeting USP1-dependent KDM4A protein stability as a potential prostate cancer therapy (2020), Cancer Sci., 111, 1567-1581 .

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Application

Application	Comment	Organism
medicine	KDM4A expression is upregulated in phosphatase and tensin homolog knockout mouse prostate tissue. Depletion of KDM4A in prostate cancer cells inhibits their proliferation and survival in vivo and vitro. Upregulation of KDM4A expression with high USP1 expression is observed in most prostate tumors and inhibition of USP1 promotes prostate cancer cells response to therapeutic agent enzalutamide	Mus musculus

Organism

Organism	UniProt	Comment	Textmining
Mus musculus	Q8BW72	isoform KDM4A, cf. EC 1.14.11.69	-

Synonyms

Synonyms	Comment	Organism
KDM4A	-	Mus musculus

Expression

Organism	Comment	Expression
Mus musculus	KDM4A expression is upregulated in phosphatase and tensin homolog knockout mouse prostate tissue	up

General Information

General Information	Comment	Organism
physiological function	depletion of KDM4A in prostate cancer cells inhibits their proliferation and survival in vivo and vitro. Deubiquitinase USP1 regulates KDM4A K48-linked deubiquitination and stability. c-Myc is a key downstream effector of the USP1-KDM4A/androgen receptor axis in driving prostate cancer cell proliferation. Upregulation of KDM4A expression with high USP1 expression is observed in most prostate tumors and inhibition of USP1 promotes prostate cancer cells response to therapeutic agent enzalutamide	Mus musculus

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Release 2023.1 (January 2023)