m6A-centered Crosstalk Information
Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
| Crosstalk ID |
M6ACROT00009
|
[1] | |||
.png)
.png)
 : m6A sites
Direct
Inhibition
RNA modification
IL17RD
IL17RD
ADAR1
Methylation
 : modification sites
|
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| m6A Modification: | |||||
|---|---|---|---|---|---|
| m6A Regulator | Methyltransferase-like 3 (METTL3) | WRITER | |||
| m6A Target | Interleukin-17 receptor D (IL17RD) | ||||
| Epigenetic Regulation that have Cross-talk with This m6A Modification: | |||||
| Epigenetic Regulation Type | RNA modification (RNAMod) >> Adenosine-to-Inosine editing (A-to-I) | ||||
| Epigenetic Regulator | Interferon-inducible protein 4 (ADAR1) | WRITER | View Details | ||
| Regulated Target | Interleukin-17 receptor D (IL17RD) | View Details | |||
| Crosstalk Relationship | m6A → A-to-I | Inhibition | |||
| Crosstalk Mechanism | m6A modification directly impacts RNA modification through targeting the shared RNA | ||||
| Crosstalk Summary | Both the presence and extent of A-to-I sites in m6A-negative RNA transcripts suggest a negative correlation between m6A and A-to-I. Suppression of m6A-catalyzing enzymes results in global A-to-I RNA editing changes. Further depletion of m6A modification increases the association of m6A-depleted transcripts with adenosine deaminase acting on RNA (ADAR) enzymes, resulting in upregulated A-to-I editing on the same m6A-depleted transcripts. Inhibition of METTL3 enhances ADAR1-mediated A-to-I editing of Interleukin-17 receptor D (IL17RD) by reducing its m6A modification. | ||||
In-vitro Model |
HeLa | Endocervical adenocarcinoma | Homo sapiens | CVCL_0030 | |
| HEK293-FT | Normal | Homo sapiens | CVCL_6911 | ||
| H9 | Sezary syndrome | Homo sapiens | CVCL_1240 | ||