Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00493
[1], [2], [3]
RNA modification MIR222 MIR222 ADARB1 Methylation : modification sites Indirect Inhibition m6A modification CDKN1B CDKN1B HNRNPA2B1 : m6A sites
m6A Modification:
m6A Regulator Heterogeneous nuclear ribonucleoproteins A2/B1 (HNRNPA2B1) READER
m6A Target Cyclin-dependent kinase inhibitor 1B (CDKN1B/p27)
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 MicroRNA 222 (MIR222) View Details
Crosstalk Relationship A-to-I  →  m6A Inhibition
Crosstalk Mechanism RNA modification indirectly impacts m6A modification through downstream signaling pathways
Crosstalk Summary ADARB1 interacts with MicroRNA 222 (MIR222), increasing it's A-to-I level and inhibiting its physical interaction with Cyclin-dependent kinase inhibitor 1B (CDKN1B/p27), which was regulated by HNRNPA2B1-mediated m6A modification.
In-vitro Model
U-118MG Astrocytoma Homo sapiens CVCL_0633
References
Ref 1 Heterogeneous nuclear ribonucleoprotein A2/B1 regulates the self-renewal and pluripotency of human embryonic stem cells via the control of the G1/S transition. Stem Cells. 2013 Dec;31(12):2647-58. doi: 10.1002/stem.1366.
Ref 2 Modulation of microRNA editing, expression and processing by ADAR2 deaminase in glioblastoma. Genome Biol. 2015 Jan 13;16(1):5. doi: 10.1186/s13059-014-0575-z.
Ref 3 MiR-222 promotes the progression of polycystic ovary syndrome by targeting p27 Kip1. Pathol Res Pract. 2019 May;215(5):918-923. doi: 10.1016/j.prp.2019.01.038. Epub 2019 Jan 28.