Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00001
[1]
RNA modification CDKN1A CDKN1A NSUN2 Methylation : modification sites Direct Enhancement m6A modification CDKN1A CDKN1A METTL3 Methylation : m6A sites
m6A Modification:
m6A Regulator Methyltransferase-like 3 (METTL3) WRITER
m6A Target Cyclin-dependent kinase inhibitor 1 (CDKN1A)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type RNA modification (RNAMod)  >> 5-methylcytidine (m5C)
Epigenetic Regulator RNA cytosine C(5)-methyltransferase NSUN2 (NSUN2) WRITER View Details
Regulated Target Cyclin-dependent kinase inhibitor 1 (CDKN1A) View Details
Crosstalk Relationship m5C  →  m6A Enhancement
Crosstalk Mechanism RNA modification directly impacts m6A modification through targeting the shared RNA
Crosstalk Summary NSUN2-mediated m5C and METTL3/METTL14-mediated m6A methylation synergistically enhance Cyclin-dependent kinase inhibitor 1 (CDKN1A) expression at the translational level, leading to elevated expression of p21 in oxidative stress-induced cellular senescence.
Cell Process Cellular senescence
In-vitro Model
HCT 116 TP53(-/-) Colon carcinoma Homo sapiens CVCL_HD97
HeLa Endocervical adenocarcinoma Homo sapiens CVCL_0030
References
Ref 1 NSUN2-Mediated m5C Methylation and METTL3/METTL14-Mediated m6A Methylation Cooperatively Enhance p21 Translation. J Cell Biochem. 2017 Sep;118(9):2587-2598. doi: 10.1002/jcb.25957. Epub 2017 May 3.