m6A Target Gene Information

General Information of the m6A Target Gene (ID: M6ATAR00717)
Target Name miR-503
Synonyms
hsa-mir-503; MIRN503
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Gene Name MIR503
Chromosomal Location Xq26.3
Gene ID 574506
HGNC ID
HGNC:32138
miRBase ID
MI0003188
Ensembl Gene ID
ENSG00000208005
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
MIR503 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
Methyltransferase-like 3 (METTL3) [WRITER]
 Regulator Info 
Representative RNA-seq result indicating the expression of this target gene regulated by METTL3
Cell Line MDA-MB-231 Homo sapiens
Treatment: METTL3 knockdown MDA-MB-231 cells
Control: MDA-MB-231 cells
 GSE70061
Regulation
logFC: 1.48E+00
p-value: 8.87E-04
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 Hypoxia induced rapid H3K4 methylation of the promoter of the methyltransferase-like 3 gene (METTL3) and resulted in its overexpression. METTL3 overexpression evokes N6-methyladenosine (m6A)-dependent miR-503 biogenesis in endothelial cells. In summary, this study highlights a novel endogenous mechanism wherein EVs aggravate myocardial injury during the onset of AMI via endothelial cell-secreted miR-503 shuttling.
Target Regulation Up regulation
Responsed Disease Myocardial injury ICD-11: NB31.Z
 Disease Info 
Cell Process Mitochondrial metabolic dysfunction
In-vivo Model To generate an AMI mouse model, mice were anesthetised by intraperitoneal injection of sterile pentobarbital sodium at 50 mg/kg body weight.
Injury of heart [ICD-11: NB31]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary Hypoxia induced rapid H3K4 methylation of the promoter of the methyltransferase-like 3 gene (METTL3) and resulted in its overexpression. METTL3 overexpression evokes N6-methyladenosine (m6A)-dependent miR-503 biogenesis in endothelial cells. In summary, this study highlights a novel endogenous mechanism wherein EVs aggravate myocardial injury during the onset of AMI via endothelial cell-secreted miR-503 shuttling.
Responsed Disease Myocardial injury [ICD-11: NB31.Z]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
 Regulator Info 
Target Regulation Up regulation
Cell Process Mitochondrial metabolic dysfunction
In-vivo Model To generate an AMI mouse model, mice were anesthetised by intraperitoneal injection of sterile pentobarbital sodium at 50 mg/kg body weight.
References
Ref 1 Extracellular vesicle-packaged mitochondrial disturbing miRNA exacerbates cardiac injury during acute myocardial infarction. Clin Transl Med. 2022 Apr;12(4):e779. doi: 10.1002/ctm2.779.