General Information of the m6A Target Gene (ID: M6ATAR00799)
Target Name Ubiquitin conjugating enzyme E2 I (UBE2I/UBC9)
Synonyms
SUMO-conjugating enzyme UBC9; RING-type E3 SUMO transferase UBC9; SUMO-protein ligase; Ubiquitin carrier protein 9; Ubiquitin carrier protein I; Ubiquitin-conjugating enzyme E2 I
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Gene Name UBE2I
Chromosomal Location 16p13.3
Family Ubiquitin-conjugating enzyme family
Function
Accepts the ubiquitin-like proteins SUMO1, SUMO2, SUMO3, SUMO4 and SUMO1P1/SUMO5 from the UBLE1A-UBLE1B E1 complex and catalyzes their covalent attachment to other proteins with the help of an E3 ligase such as RANBP2, CBX4 and ZNF451. Can catalyze the formation of poly-SUMO chains. Necessary for sumoylation of FOXL2 and KAT5. Essential for nuclear architecture and chromosome segregation. Sumoylates p53/TP53 at 'Lys-386'. Mediates sumoylation of ERCC6 which is essential for its transcription-coupled nucleotide excision repair activity.
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Gene ID 7329
Uniprot ID
UBC9_HUMAN
HGNC ID
HGNC:12485
Ensembl Gene ID
ENSG00000103275
KEGG ID
hsa:7329
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).
Browse Regulator
Browse Disease
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.
References
Ref 1 Post-translational modification of RNA m6A demethylase ALKBH5 regulates ROS-induced DNA damage response. Nucleic Acids Res. 2021 Jun 4;49(10):5779-5797. doi: 10.1093/nar/gkab415.