General Information of the m6A Target Gene (ID: M6ATAR00437)
Target Name Ubiquitin-conjugating enzyme E2 C (UBE2C)
Synonyms
(E3-independent) E2 ubiquitin-conjugating enzyme C; E2 ubiquitin-conjugating enzyme C; UbcH10; Ubiquitin carrier protein C; Ubiquitin-protein ligase C; UBCH10
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Gene Name UBE2C
Chromosomal Location 20q13.12
Family ubiquitin-conjugating enzyme family
Function
Accepts ubiquitin from the E1 complex and catalyzes its covalent attachment to other proteins. In vitro catalyzes 'Lys-11'- and 'Lys-48'-linked polyubiquitination. Acts as an essential factor of the anaphase promoting complex/cyclosome (APC/C), a cell cycle-regulated ubiquitin ligase that controls progression through mitosis. Acts by initiating 'Lys-11'-linked polyubiquitin chains on APC/C substrates, leading to the degradation of APC/C substrates by the proteasome and promoting mitotic exit.
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Gene ID 11065
Uniprot ID
UBE2C_HUMAN
HGNC ID
HGNC:15937
Ensembl Gene ID
ENSG00000175063
KEGG ID
hsa:11065
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
UBE2C 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]
Representative RNA-seq result indicating the expression of this target gene regulated by ALKBH5
Cell Line HaCAT cell line Homo sapiens
Treatment: siALKBH5 HaCAT cells
Control: siControl HaCAT cells
GSE211076
Regulation
logFC: 9.83E-01
p-value: 3.48E-52
More Results Click to View More RNA-seq Results
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary Deregulated Ubiquitin-conjugating enzyme E2 C (UBE2C)-autophagy repression axis drives NSCLC progression which renders varieties of potential molecular targets in cancer therapy of NSCLC. UBE2C is repressed post-transcriptionally via tumor suppressor miR-381 and epitranscriptionally stabilized with maintenance of lower m6A level within its mature RNAs due to the upregulation of m6A demethylase ALKBH5 in NSCLC.
Target Regulation Up regulation
Responsed Disease Non-small-cell lung carcinoma ICD-11: 2C25.Y
Pathway Response Ubiquitin mediated proteolysis hsa04120
Cell Process Cell invasion
Ubiquitination degradation
Cell autophagy
In-vitro Model PLA-801D Lung giant cell carcinoma Homo sapiens CVCL_7110
A-549 Lung adenocarcinoma Homo sapiens CVCL_0023
Calu-6 Lung adenocarcinoma Homo sapiens CVCL_0236
NCI-H1299 Lung large cell carcinoma Homo sapiens CVCL_0060
NCI-H520 Lung squamous cell carcinoma Homo sapiens CVCL_1566
HBEC (Human lung cancer cell)
PC-9 Lung adenocarcinoma Homo sapiens CVCL_B260
Lung cancer [ICD-11: 2C25]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary Deregulated Ubiquitin-conjugating enzyme E2 C (UBE2C)-autophagy repression axis drives NSCLC progression which renders varieties of potential molecular targets in cancer therapy of NSCLC. UBE2C is repressed post-transcriptionally via tumor suppressor miR-381 and epitranscriptionally stabilized with maintenance of lower m6A level within its mature RNAs due to the upregulation of m6A demethylase ALKBH5 in NSCLC.
Responsed Disease Non-small-cell lung carcinoma [ICD-11: 2C25.Y]
Target Regulator RNA demethylase ALKBH5 (ALKBH5) ERASER
Target Regulation Up regulation
Pathway Response Ubiquitin mediated proteolysis hsa04120
Cell Process Cell invasion
Ubiquitination degradation
Cell autophagy
In-vitro Model PLA-801D Lung giant cell carcinoma Homo sapiens CVCL_7110
A-549 Lung adenocarcinoma Homo sapiens CVCL_0023
Calu-6 Lung adenocarcinoma Homo sapiens CVCL_0236
NCI-H1299 Lung large cell carcinoma Homo sapiens CVCL_0060
NCI-H520 Lung squamous cell carcinoma Homo sapiens CVCL_1566
HBEC (Human lung cancer cell)
PC-9 Lung adenocarcinoma Homo sapiens CVCL_B260
References
Ref 1 Deregulation of UBE2C-mediated autophagy repression aggravates NSCLC progression. Oncogenesis. 2018 Jun 13;7(6):49. doi: 10.1038/s41389-018-0054-6.