Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT02108
[1]
m6A modification MeCP2 MeCP2 YTHDF1 : m6A sites Direct Enhancement DNA methylation MeCP2 SLC31A1
m6A Modification:
m6A Regulator YTH domain-containing family protein 1 (YTHDF1) READER
m6A Target Methyl-CpG-binding protein 2 (MECP2)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type DNA methylation (DNAMeth)
Epigenetic Regulator Methyl-CpG-binding protein 2 (MECP2) READER View Details
Regulated Target Solute carrier family 31 member 1 (SLC31A1) View Details
Crosstalk Relationship m6A  →  DNA methylation Enhancement
Crosstalk Mechanism m6A modification directly impacts DNA methylation through modulating the expression level of DNA methyltransferases or demethylases.
Crosstalk Summary YTHDF1 recognizes target Methyl-CpG-binding protein 2 (MECP2) mRNA and induces its translation. Solute carrier family 31 member 1 (SLC31A1) inhibition due to increased MeCP2-recognized methylating CpG islands of SLC31A1 in the promoter region restrains its transcription. Conversely, MeCP2 knockdown rescued SLC31A1 expression, resulting in contradictory effects.
Responsed Disease Vascular disorders of the liver ICD-11: DB98.8
Full List of Potential Compound(s) Related to This m6A-centered Crosstalk
Methyl-CpG-binding protein 2 (MECP2) 1 Compound(s) Regulating the Target Click to Show/Hide the Full List
 Compound Name AVXS-201 Phase 1 [2]
External Link
References
Ref 1 SLC31A1 loss depletes mitochondrial copper and promotes cardiac fibrosis. Eur Heart J. 2025 Mar 6:ehaf130. doi: 10.1093/eurheartj/ehaf130. Online ahead of print.
Ref 2 Clinical pipeline report, company report or official report of Novartis