Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00151
[1], [2]
m6A modification ADARB1 ADARB1 YTHDF2 : m6A sites Direct Inhibition RNA modification SON SON ADARB1 Methylation : modification sites
m6A Modification:
m6A Regulator YTH domain-containing family protein 2 (YTHDF2) READER
m6A Target Double-stranded RNA-specific editase 1 (ADARB1)
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 Double-stranded RNA-specific editase 1 (ADARB1) WRITER View Details
Regulated Target Protein SON View Details
Crosstalk Relationship m6A  →  A-to-I Inhibition
Crosstalk Mechanism m6A modification directly impacts RNA modification through modulating the expression level of RNA modification regulator
Crosstalk Summary YTHDF2 recognizes the m6A methylation sites and prevents Double-stranded RNA-specific editase 1 (ADARB1) dependent A-to-I RNA editing of Protein SON.
In-vitro Model
A-172 Glioblastoma Homo sapiens CVCL_0131
SH-SY5Y Neuroblastoma Homo sapiens CVCL_0019
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.
Ref 2 ADAR2-dependent A-to-I RNA editing in the extracellular linear and circular RNAs. Neurosci Res. 2019 Oct;147:48-57. doi: 10.1016/j.neures.2018.11.005. Epub 2018 Nov 16.