m6A-centered Crosstalk Information
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 | ||||
: m6A sites