m6A Target Gene Information
General Information of the m6A Target Gene (ID: M6ATAR00799)
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
UBE2I
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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RNA demethylase ALKBH5 (ALKBH5) [ERASER]
In total 1 item(s) under this regulator | ||||
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene | [1] | |||
Response Summary | ROS promotes ALKBH5 SUMOylation through activating ERK/EPHB2/JNK signaling, leading to inhibition of ALKBH5 m6A demethylase activity by blocking substrate accessibility. Post-translational modification of ALKBH5 regulates ROS-induced DNA damage response. ROS specifically promotes ALKBH5 but not FTO, METTL3 and METTL14 SUMOylation by enhancing the interaction of ALKBH5 and Ubiquitin conjugating enzyme E2 I (UBE2I/UBC9) and inhibiting the association between ALKBH5 and SENP1. | |||
Target Regulation | Up regulation | |||
Responsed Disease | Diseases of the circulatory system | ICD-11: BE2Z | ||
Pathway Response | Apoptosis | hsa04210 | ||
Chemical carcinogenesis - reactive oxygen species | hsa05208 | |||
Cell Process | Oxygen species(ROS)-induced stress | |||
In-vitro Model | HEK293T | Normal | Homo sapiens | CVCL_0063 |
In-vivo Model | For the ROS-induced DNA damage analysis, the indicated cell lines were treated with or without 100 uM hydrogen peroxide (H2O2), or 80 uM Carbonyl cyanide m-chlorophenylhydrazone (CCCP) for 6 hours. For the in vivo ROS study, DMSO and 5 mg/kg CCCP was intraperitoneally injected in to three pairs of mice. | |||
Diseases of the circulatory system [ICD-11: BE2Z]
In total 1 item(s) under this disease | ||||
Experiment 1 Reporting the m6A-centered Disease Response | [1] | |||
Response Summary | ROS promotes ALKBH5 SUMOylation through activating ERK/EPHB2/JNK signaling, leading to inhibition of ALKBH5 m6A demethylase activity by blocking substrate accessibility. Post-translational modification of ALKBH5 regulates ROS-induced DNA damage response. ROS specifically promotes ALKBH5 but not FTO, METTL3 and METTL14 SUMOylation by enhancing the interaction of ALKBH5 and Ubiquitin conjugating enzyme E2 I (UBE2I/UBC9) and inhibiting the association between ALKBH5 and SENP1. | |||
Responsed Disease | Diseases of the circulatory system [ICD-11: BE2Z] | |||
Target Regulator | RNA demethylase ALKBH5 (ALKBH5) | ERASER | ||
Target Regulation | Up regulation | |||
Pathway Response | Apoptosis | hsa04210 | ||
Chemical carcinogenesis - reactive oxygen species | hsa05208 | |||
Cell Process | Oxygen species(ROS)-induced stress | |||
In-vitro Model | HEK293T | Normal | Homo sapiens | CVCL_0063 |
In-vivo Model | For the ROS-induced DNA damage analysis, the indicated cell lines were treated with or without 100 uM hydrogen peroxide (H2O2), or 80 uM Carbonyl cyanide m-chlorophenylhydrazone (CCCP) for 6 hours. For the in vivo ROS study, DMSO and 5 mg/kg CCCP was intraperitoneally injected in to three pairs of mice. | |||