m6A-centered Crosstalk Information
Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
| Crosstalk ID |
M6ACROT05552
|
[1] | |||
m6A modification
MALAT1
MALAT1
ALKBH5
Demethylation
 : m6A sites
Direct
Enhancement
Non-coding RNA
MALAT1
Regulated Target
lncRNA miRNA circRNA
|
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| m6A Modification: | |||||
|---|---|---|---|---|---|
| m6A Regulator | RNA demethylase ALKBH5 (ALKBH5) | ERASER | |||
| m6A Target | Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) | ||||
| Epigenetic Regulation that have Cross-talk with This m6A Modification: | |||||
| Epigenetic Regulation Type | Non-coding RNA (ncRNA) | ||||
| Epigenetic Regulator | Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) | LncRNA | View Details | ||
| Crosstalk Relationship | m6A → ncRNA | Enhancement | |||
| Crosstalk Mechanism | m6A regulators directly modulate the functionality of ncRNAs through specific targeting ncRNA | ||||
| Crosstalk Summary | ALKBH5 could up-regulate Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) expression by demethylation. Furthermore, dexmedetomidine inhibited the expression of ALKBH5 in LPS-treated HK-2 cells. Dexmedetomidine suppressed the biological behavior of HK-2 cells treated with LPS by inhibiting the expression of ALKBH5 in vitro, which provides potential targets for the prevention and treatment of sepsis-induced kidney injury. Dexmedetomidine suppressed the biological behavior of HK-2 cells treated with LPS by inhibiting the expression of ALKBH5 in vitro, which provides potential targets for the prevention and treatment of sepsis-induced kidney injury. | ||||
| Responsed Disease | Injury of kidney | ICD-11: NB92.0 | |||
| Responsed Drug | Dexmedetomidine* | ||||
| Cell Process | Cell viability | ||||
| Cell apoptosis | |||||
| Inflammation | |||||
In-vitro Model |
HK-2 [Human kidney] | Normal | Homo sapiens | CVCL_0302 | |