Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05188
[1]
Non-coding RNA MetBil METTL3  lncRNA       miRNA   circRNA Direct Enhancement m6A modification COL1A2 COL1A2 METTL3 Methylation : m6A sites
m6A Modification:
m6A Regulator Methyltransferase-like 3 (METTL3) WRITER
m6A Target Collagen alpha-2(I) chain (COL1A2)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type Non-coding RNA (ncRNA)
Epigenetic Regulator METTL3 binding lncRNA (MetBil) LncRNA View Details
Regulated Target Methyltransferase-like protein 3 (METTL3) View Details
Crosstalk Relationship ncRNA  →  m6A Enhancement
Crosstalk Mechanism ncRNAs directly impacts m6A modification through recruiting m6A regulator
Crosstalk Summary METBIL as a novel molecular regulator in ischemia-induced cardiac fibrosis via METTL3-mediated m6A modification of Collagen alpha-2(I) chain (COL1A2).
Responsed Disease Vascular disorders of the liver ICD-11: DB98.8
Full List of Potential Compound(s) Related to This m6A-centered Crosstalk
Collagen alpha-2(I) chain (COL1A2) 1 Compound(s) Regulating the Target Click to Show/Hide the Full List
 Compound Name Solubilized type 1 native bovine collagen Phase 2 [2]
Synonyms
Solubilized type 1 native bovine collagen (oral, scleroderma); Solubilized type 1 native bovine collagen (oral, scleroderma), arGentis/University of Tennessee
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MOA Modulator
External Link
References
Ref 1 MetBil as a novel molecular regulator in ischemia-induced cardiac fibrosis via METTL3-mediated m6A modification. FASEB J. 2023 Mar;37(3):e22797. doi: 10.1096/fj.202201734R.
Ref 2 Company report (Argentisrx)