Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00062
[1]
m6A modification ADAR1 ADAR1 YTHDF1 : m6A sites Direct Enhancement RNA modification PSMB2 PSMB2 ADAR1 Methylation : modification sites
m6A Modification:
m6A Regulator YTH domain-containing family protein 1 (YTHDF1) READER
m6A Target Interferon-inducible protein 4 (ADAR1)
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 Proteasome 20S subunit beta 2 (PSMB2) View Details
Crosstalk Relationship m6A  →  A-to-I Enhancement
Crosstalk Mechanism m6A modification directly impacts RNA modification through modulating the expression level of RNA modification regulator
Crosstalk Summary The A-to-I RNA editing activity of Interferon-inducible protein 4 (ADAR1) plays important roles in the YTHDF1-dependent IFN responses. Therefore, m6A and YTHDF1 affect innate immune responses through modulating the ADAR1-mediated A-to-I RNA editing of mRNA (TNKS; EIF2AK2 and Proteasome 20S subunit beta 2 (PSMB2)).
In-vitro Model
A-172 Glioblastoma Homo sapiens CVCL_0131
LN-229 Glioblastoma Homo sapiens CVCL_0393
Vero Normal Chlorocebus sabaeus CVCL_0059
References
Ref 1 N6-methyladenosine promotes induction of ADAR1-mediated A-to-I RNA editing to suppress aberrant antiviral innate immune responses. PLoS Biol. 2021 Jul 29;19(7):e3001292. doi: 10.1371/journal.pbio.3001292. eCollection 2021 Jul.