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
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]
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
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]
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
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.
Full List of Crosstalk(s) between m6A Modification and Epigenetic Regulation Related to This Regulator
Histone modification
m6A Regulator: Methyltransferase-like 3 (METTL3)
In total 1 item(s) under this m6A regulator
Crosstalk ID: M6ACROT03071
Epigenetic Regulator Histone-lysine N-methyltransferase 2A (KMT2A)
Regulated Target Histone H3 lysine 4 trimethylation (H3K4me3)
Crosstalk relationship Histone modification → m6A
Disease Myocardial injury
Drug C646
Non-coding RNA
m6A Regulator: Methyltransferase-like 3 (METTL3)
In total 1 item(s) under this m6A regulator
Crosstalk ID: M6ACROT05626
Epigenetic Regulator MiR-503
Regulated Target PPARG coactivator 1 beta (PPARGC1B)
Crosstalk relationship m6A → ncRNA
Disease Injury of heart
RNA Modification Sequencing Data Associated with the Target (ID: M6ATAR00717)
miR-503
Adenosine-to-Inosine editing (A-to-I)
In total 1 m6A sequence/site(s) in this target gene
mod ID: A2ISITE003920 Click to Show/Hide the Full List
mod site chrX:134546391-134546392:- [2]
Sequence CCCGCGCTCAGCCGTGCCCTAGCAGCGGGAACAGTTCTGCA
Transcript ID List ENST00000385270.1; MIMAT0002874; ENST00000441492.1; ENST00000440570.5; ENST00000414769.1
External Link RMBase: RNA-editing_site_143326