m6A-centered Crosstalk Information
Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
| Crosstalk ID |
M6ACROT05685
|
[1] | |||
m6A modification
pri-miR-3591
pri-miR-3591
FTO
Demethylation
 : m6A sites
Direct
Inhibition
Non-coding RNA
pri-miR-3591
PRKAA2
lncRNA miRNA circRNA
|
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| m6A Modification: | |||||
|---|---|---|---|---|---|
| m6A Regulator | Fat mass and obesity-associated protein (FTO) | ERASER | |||
| m6A Target | pri-miR-3591 | ||||
| Epigenetic Regulation that have Cross-talk with This m6A Modification: | |||||
| Epigenetic Regulation Type | Non-coding RNA (ncRNA) | ||||
| Epigenetic Regulator | MicroRNA 3591 | microRNA | View Details | ||
| Regulated Target | Protein kinase AMP-activated catalytic subunit alpha 2 (PRKAA2) | View Details | |||
| Crosstalk Relationship | m6A → ncRNA | Inhibition | |||
| Crosstalk Mechanism | m6A regulators directly modulate the functionality of ncRNAs through specific targeting ncRNA | ||||
| Crosstalk Summary | FTO-mediated m6A demethylation of pri-miR-3591 leaded to a maturation block of miR-3591-5p, which relieved the inhibitory effect of miR-3591-5p on Protein kinase AMP-activated catalytic subunit alpha 2 (PRKAA2) and then promoted the increase of PRKAA2, thereby alleviating OA cartilage damage. | ||||
| Responsed Disease | Osteoarthritis | ICD-11: FA05 | |||
| Cell Process | Cell proliferation | ||||
| Cell apoptosis | |||||