m6A-centered Crosstalk Information
Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
| Crosstalk ID |
M6ACROT05160
|
[1] | |||
Non-coding RNA
Lnc-Gm10532
METTL14
lncRNA miRNA circRNA
Direct
Enhancement
m6A modification
Fis1
Fis1
METTL14
Methylation
 : m6A sites
|
|||||
| m6A Modification: | |||||
|---|---|---|---|---|---|
| m6A Regulator | Methyltransferase-like 14 (METTL14) | WRITER | |||
| m6A Target | Mitochondrial fission 1 protein (FIS1) | ||||
| Epigenetic Regulation that have Cross-talk with This m6A Modification: | |||||
| Epigenetic Regulation Type | Non-coding RNA (ncRNA) | ||||
| Epigenetic Regulator | Lnc-Gm10532 | LncRNA | View Details | ||
| Regulated Target | Methyltransferase-like protein 14 (METTL14) | View Details | |||
| Crosstalk Relationship | ncRNA → m6A | Enhancement | |||
| Crosstalk Mechanism | ncRNAs directly impacts m6A modification through recruiting m6A regulator | ||||
| Crosstalk Summary | Lnc-Gm10532 increased Mitochondrial fission 1 protein (FIS1) expression and mitochondrial fission by recruiting the m6A writer methyltransferase-like 14 (METTL14) and enhancing m6A modification of Fis1 mRNA. Moreover, lnc-Gm10532 was also required for chronic Cd-induced mitochondrial dysfunction and memory deficits in a rodent model. Therefore, data of this study reveal a new epigenetic mechanism of chronic Cd neurotoxicity. | ||||
| Responsed Disease | Cognitive impairment | ICD-11: MB21 | |||
In-vitro Model |
Neuro-2a | Mouse neuroblastoma | Mus musculus | CVCL_0470 | |
| In-vivo Model | To investigate chronic Cd-induced mitochondrial dysfunction and neurotoxicity in vivo, C57BL/6J mice were randomly assigned to 2 groups: (i) control group mice (n = 20) and (ii) Cd exposure group mice (n = 20). | ||||