m6A Target Gene Information
General Information of the m6A Target Gene (ID: M6ATAR00479)
Target Name | Androgen receptor (AR) | ||||
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Synonyms |
Dihydrotestosterone receptor; Nuclear receptor subfamily 3 group C member 4; DHTR; NR3C4
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Gene Name | AR | ||||
Family | nuclear hormone receptor family. NR3 subfamily. {ECO:0000305}. | ||||
Function |
Steroid hormone receptors are ligand-activated transcription factors that regulate eukaryotic gene expression and affect cellular proliferation and differentiation in target tissues. Transcription factor activity is modulated by bound coactivator and corepressor proteins like ZBTB7A that recruits NCOR1 and NCOR2 to the androgen response elements/ARE on target genes, negatively regulating androgen receptor signaling and androgen-induced cell proliferation. Transcription activation is also down-regulated by NR0B2. Activated, but not phosphorylated, by HIPK3 and ZIPK/DAPK3; [Isoform 3]: Lacks the C-terminal ligand-binding domain and may therefore constitutively activate the transcription of a specific set of genes independently of steroid hormones; [Isoform 4]: Lacks the C-terminal ligand-binding domain and may therefore constitutively activate the transcription of a specific set of genes independently of steroid hormones.
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Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
AR
can be regulated by the following regulator(s), and cause disease/drug response(s). You can browse detail information of regulator(s) or disease/drug response(s).
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ETS-related transcription factor Elf-3 (ELF3) [WRITER]
In total 1 item(s) under this regulator | ||||
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene | [1] | |||
Response Summary | ELF3 is a member of the ETS family of transcription factors, is a repressor of Androgen receptor (AR) transcriptional activity. Modulation of ELF3 expression and/or AR/ELF3 interaction has utility in the treatment of PC. | |||
Responsed Disease | Prostate cancer | ICD-11: 2C82 | ||
In-vitro Model | LNCaP | Prostate carcinoma | Homo sapiens | CVCL_0395 |
HeLa | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 | |
Hep-G2 | Hepatoblastoma | Homo sapiens | CVCL_0027 | |
In-vivo Model | NOD.CB17-Prkdcscid/J none castrated SCID male mice 4 weeks old were purchased from Jackson Laboratories. After a one week period of acclimation, the mice were injected with 6×106 TetOn-Flag-ELF3 LNCaP suspended in 200 uL of a 50% mixture containing RPMI 1640 medium and Matrigel matrix basement membrane (BD Corporation, Bedford, MA) subcutaneously into the right flank region. The mice were either fed with doxycycline 200 mg/kg containing diet (BioServ, NJ) to induce the ELF3 expression or with a control regular diet. The sizes of the resultant tumors were measured weekly. | |||
Prostate cancer [ICD-11: 2C82]
In total 1 item(s) under this disease | ||||
Experiment 1 Reporting the m6A-centered Disease Response | [1] | |||
Response Summary | ELF3 is a member of the ETS family of transcription factors, is a repressor of Androgen receptor (AR) transcriptional activity. Modulation of ELF3 expression and/or AR/ELF3 interaction has utility in the treatment of PC. | |||
Responsed Disease | Prostate cancer [ICD-11: 2C82] | |||
Target Regulator | ETS-related transcription factor Elf-3 (ELF3) | WRITER | ||
In-vitro Model | LNCaP | Prostate carcinoma | Homo sapiens | CVCL_0395 |
HeLa | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 | |
Hep-G2 | Hepatoblastoma | Homo sapiens | CVCL_0027 | |
In-vivo Model | NOD.CB17-Prkdcscid/J none castrated SCID male mice 4 weeks old were purchased from Jackson Laboratories. After a one week period of acclimation, the mice were injected with 6×106 TetOn-Flag-ELF3 LNCaP suspended in 200 uL of a 50% mixture containing RPMI 1640 medium and Matrigel matrix basement membrane (BD Corporation, Bedford, MA) subcutaneously into the right flank region. The mice were either fed with doxycycline 200 mg/kg containing diet (BioServ, NJ) to induce the ELF3 expression or with a control regular diet. The sizes of the resultant tumors were measured weekly. | |||