Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05450
[1]
m6A modification H19 H19 METTL3 Methylation : m6A sites Direct Enhancement Non-coding RNA H19 Regulated Target  lncRNA       miRNA   circRNA
m6A Modification:
m6A Regulator Methyltransferase-like 3 (METTL3) WRITER
m6A Target H19 imprinted maternally expressed transcript (H19)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type Non-coding RNA (ncRNA)
Epigenetic Regulator H19 imprinted maternally expressed transcript (H19) LncRNA View Details
Crosstalk Relationship m6A  →  ncRNA Enhancement
Crosstalk Mechanism m6A regulators directly modulate the functionality of ncRNAs through specific targeting ncRNA
Crosstalk Summary Either knockdown of METTL3 or METTL14 notably reversed the hypoxic preconditioning-induced enhancement of cell viability, anti-apoptosis ability, and H19 imprinted maternally expressed transcript (H19) expression.
Responsed Disease Abnormalities of breathing ICD-11: MD11
Cell Process Cell viability
Cell apoptosis
In-vitro Model
H9c2(2-1) Normal Rattus norvegicus CVCL_0286
In-vivo Model In vivo myocardial I/R injury was performed by 60 min of ligation of LAD followed by 5 h of reperfusion.
References
Ref 1 N6-methyladenosine methyltransferase plays a role in hypoxic preconditioning partially through the interaction with lncRNA H19. Acta Biochim Biophys Sin (Shanghai). 2020 Dec 29;52(12):1306-1315. doi: 10.1093/abbs/gmaa130.