m6A Regulator Information

General Information of the m6A Regulator (ID: REG00016)
Regulator Name Methyltransferase-like 13 (METTL13)
Synonyms
eEF1A-KNMT; eEF1A lysine and N-terminal methyltransferase; EEF1AKNMT; FEAT; KIAA0859; CGI-01
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Gene Name METTL13
Sequence
MNLLPKSSREFGSVDYWEKFFQQRGKKAFEWYGTYLELCGVLHKYIKPREKVLVIGCGNS
ELSEQLYDVGYRDIVNIDISEVVIKQMKECNATRRPQMSFLKMDMTQMEFPDASFQVVLD
KGTLDAVLTDEEEKTLQQVDRMLAEVGRVLQVGGRYLCISLAQAHILKKAVGHFSREGWM
VRVHQVANSQDQVLEAEPQFSLPVFAFIMTKFRPVPGSALQIFELCAQEQRKPVRLESAE
RLAEAVQERQQYAWLCSQLRRKARLGSVSLDLCDGDTGEPRYTLHVVDSPTVKPSRDNHF
AIFIIPQGRETEWLFGMDEGRKQLAASAGFRRLITVALHRGQQYESMDHIQAELSARVME
LAPAGMPTQQQVPFLSVGGDIGVRTVQHQDCSPLSGDYVIEDVQGDDKRYFRRLIFLSNR
NVVQSEARLLKDVSHKAQKKRKKDRKKQRPADAEDLPAAPGQSIDKSYLCCEHHKAMIAG
LALLRNPELLLEIPLALLVVGLGGGSLPLFVHDHFPKSCIDAVEIDPSMLEVATQWFGFS
QSDRMKVHIADGLDYIASLAGGGEARPCYDVIMFDVDSKDPTLGMSCPPPAFVEQSFLQK
VKSILTPEGVFILNLVCRDLGLKDSVLAGLKAVFPLLYVRRIEGEVNEILFCQLHPEQKL
ATPELLETAQALERTLRKPGRGWDDTYVLSDMLKTVKIV
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Family methyltransferase superfamily
Function
Dual methyltransferase that catalyzes methylation of elongation factor 1-alpha (EEF1A1 and EEF1A2) at two different positions, and is therefore involved in the regulation of mRNA translation. Via its C-terminus, methylates EEF1A1 and EEF1A2 at the N-terminal residue 'Gly-2'. Via its N-terminus dimethylates EEF1A1 and EEF1A2 at residue 'Lys-55'. Has no activity towards core histones H2A, H2B, H3 and H4 . Negatively regulates cell proliferation at G1/S transition via transcriptional suppression of cell cycle regulatory genes such as CDK4 and CDK6.
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Gene ID 51603
Uniprot ID
EFNMT_HUMAN
Regulator Type WRITER ERASER READER
Mechanism Diagram Click to View the Original Diagram
Full List of Target Gene(s) of This m6A Regulator and Corresponding Disease/Drug Response(s)
METTL13 can regulate the m6A methylation of following target genes, and result in corresponding disease/drug response(s). You can browse corresponding disease or drug response(s) resulted from the regulation of certain target gene.
Browse Target Gene related Disease
Browse Target Gene related Drug
PI3-kinase subunit beta (PIK3CB)
 Target Gene 
Pancreatic cancer [ICD-11: 2C10]
In total 1 item(s) under this disease
 Disease Info 
Experiment 1 Reporting the m6A-centered Disease Response of This Target Gene [1]
Responsed Disease Pancreatic cancer [ICD-11: 2C10]
Responsed Drug AZD6482 Terminated
 Drug Info 
Target Regulation Up regulation
Pathway Response PI3K-Akt signaling pathway hsa04151
Glycolysis / Gluconeogenesis hsa00010
Cell Process Glucose metabolism
In-vitro Model
 BxPC-3 Pancreatic ductal adenocarcinoma Homo sapiens CVCL_0186
PANC-1 Pancreatic ductal adenocarcinoma Homo sapiens CVCL_0480
In-vivo Model Established cohorts of mice bearing tumour xenografts driven by PTEN-deficient BxPC-3 and PANC-1 cells with PIK3CB overexpression. When tumours grew to ~300 mm3, mice were grouped and administered with vehicle (DMSO) or KIN-193 via intraperitoneal injection (20 mg/kg) once daily.
Response Summary N6-methyladenosine mRNA methylation of PIK3CB regulates AKT signalling to promote PTEN-deficient pancreatic cancer progression. Rs142933486 is significantly associated with the overall survival of PDAC by reducing the PIK3CB m6A level, which facilitated its mRNA and protein expression levels mediated by the m6A 'writer' complex (METTL13/METTL14/WTAP) and the m6A 'reader' YTHDF2. KIN-193, a PI3-kinase subunit beta (PIK3CB)-selective inhibitor, is shown to serve as an effective anticancer agent for blocking PTEN-deficient PDAC.
PI3-kinase subunit beta (PIK3CB)
 Target Gene 
AZD6482 [Terminated]
In total 1 item(s) under this drug
 Drug Info 
Experiment 1 Reporting the m6A-centered Drug Response of This Target Gene [1]
Responsed Disease Pancreatic cancer ICD-11: 2C10
 Disease Info 
Target Regulation Up regulation
Pathway Response PI3K-Akt signaling pathway hsa04151
Glycolysis / Gluconeogenesis hsa00010
Cell Process Glucose metabolism
In-vitro Model BxPC-3 Pancreatic ductal adenocarcinoma Homo sapiens CVCL_0186
PANC-1 Pancreatic ductal adenocarcinoma Homo sapiens CVCL_0480
In-vivo Model Established cohorts of mice bearing tumour xenografts driven by PTEN-deficient BxPC-3 and PANC-1 cells with PIK3CB overexpression. When tumours grew to ~300 mm3, mice were grouped and administered with vehicle (DMSO) or KIN-193 via intraperitoneal injection (20 mg/kg) once daily.
Response Summary N6-methyladenosine mRNA methylation of PIK3CB regulates AKT signalling to promote PTEN-deficient pancreatic cancer progression. Rs142933486 is significantly associated with the overall survival of PDAC by reducing the PIK3CB m6A level, which facilitated its mRNA and protein expression levels mediated by the m6A 'writer' complex (METTL13/METTL14/WTAP) and the m6A 'reader' YTHDF2. KIN-193, a PI3-kinase subunit beta (PIK3CB)-selective inhibitor, is shown to serve as an effective anticancer agent for blocking PTEN-deficient PDAC.
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References
Ref 1 N(6)-methyladenosine mRNA methylation of PIK3CB regulates AKT signalling to promote PTEN-deficient pancreatic cancer progression. Gut. 2020 Dec;69(12):2180-2192. doi: 10.1136/gutjnl-2019-320179. Epub 2020 Apr 20.