Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05342
[1]
Non-coding RNA SNHG4 METTL3  lncRNA       miRNA   circRNA Direct Inhibition m6A modification STAT2 STAT2 METTL3 Methylation : m6A sites
m6A Modification:
m6A Regulator Methyltransferase-like 3 (METTL3) WRITER
m6A Target Signal transducer and activator of transcription 2 (STAT2)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type Non-coding RNA (ncRNA)
Epigenetic Regulator Small nucleolar RNA host gene 4 (SNHG4) LncRNA View Details
Regulated Target Methyltransferase-like protein 3 (METTL3) View Details
Crosstalk Relationship ncRNA  →  m6A Inhibition
Crosstalk Mechanism ncRNAs directly impacts m6A modification through modulating the expression level of m6A regulator
Crosstalk Summary SNHG4 promotes LPS induced inflammation in human lung fibroblasts and mouse lung tissues in vitro and in vivo by inhibiting METTL3-mediated m6A level of Signal transducer and activator of transcription 2 (STAT2) mRNA, which may provide a potential therapeutic mechanism for NP.
Responsed Disease Congenital pneumonia ICD-11: KB24
Pathway Response Apoptosis hsa04210
Cell Process Cell apoptosis
References
Ref 1 Long noncoding RNA SNHG4 remits lipopolysaccharide-engendered inflammatory lung damage by inhibiting METTL3 - Mediated m(6)A level of STAT2 mRNA. Mol Immunol. 2021 Nov;139:10-22. doi: 10.1016/j.molimm.2021.08.008. Epub 2021 Aug 25.