Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00145
[1], [2]
m6A modification ADARB1 ADARB1 YTHDF2 : m6A sites Direct Inhibition RNA modification HNRNPLL HNRNPLL 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 Heterogeneous nuclear ribonucleoprotein L like (HNRNPLL) 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 Heterogeneous nuclear ribonucleoprotein L like (HNRNPLL).
In-vitro Model
A-172 Glioblastoma Homo sapiens CVCL_0131
HeLa Endocervical adenocarcinoma Homo sapiens CVCL_0030
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 Tumor-associated intronic editing of HNRPLL generates a novel splicing variant linked to cell proliferation. J Biol Chem. 2018 Jun 29;293(26):10158-10171. doi: 10.1074/jbc.RA117.001197. Epub 2018 May 16.