m6A-centered Crosstalk Information

Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation

m6A Modification:
Crosstalk ID	M6ACROT00090				[1], [2]
m⁶A modification ADARB1 ADARB1 YTHDF2 : m⁶A sites Direct Inhibition RNA modification CDC14B CDC14B ADARB1 Methylation : modification sites
m6A Regulator	YTH domain-containing family protein 2 (YTHDF2)			READER	Regulator Info
m6A Target	Double-stranded RNA-specific editase 1 (ADARB1)				Targert Gene
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	Cell division cycle 14B (CDC14B)				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 Cell division cycle 14B (CDC14B).
In-vitro Model	A-172	Glioblastoma	Homo sapiens		CVCL_0131
In-vitro Model	U-118MG	Astrocytoma	Homo sapiens		CVCL_0633

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-editing activity inhibits glioblastoma growth through the modulation of the CDC14B/Skp2/p21/p27 axis. Oncogene. 2013 Feb 21;32(8):998-1009. doi: 10.1038/onc.2012.125. Epub 2012 Apr 23.