m6A-centered Crosstalk Information

Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation

m6A Modification:
Crosstalk ID	M6ACROT00122				[1], [2]
m⁶A modification ADARB1 ADARB1 YTHDF2 : m⁶A sites Direct Inhibition RNA modification IGFBP7 IGFBP7 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	Insulin-like growth factor-binding protein 7 (IGFBP7)				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 Insulin-like growth factor-binding protein 7 (IGFBP7).
In-vitro Model	A-172	Glioblastoma	Homo sapiens		CVCL_0131
In-vitro Model	KYSE-30	Esophageal squamous cell carcinoma	Homo sapiens		CVCL_1351

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 functions as a tumor suppressor via editing IGFBP7 in esophageal squamous cell carcinoma. Int J Oncol. 2017 Feb;50(2):622-630. doi: 10.3892/ijo.2016.3823. Epub 2016 Dec 29.