Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT00018
[1]
RNA modification TINCR TINCR TRMT61A Methylation : modification sites Direct Enhancement m6A modification TINCR TINCR YTHDF2 : m6A sites
m6A Modification:
m6A Regulator YTH domain-containing family protein 2 (YTHDF2) READER
m6A Target Ubiquitin domain-containing protein TINC (TINCR)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type RNA modification (RNAMod)  >> N1-methyladenosine (m1A)
Epigenetic Regulator tRNA (adenine(58)-N(1))-methyltransferase catalytic subunit TRMT61A (TRMT61A) WRITER View Details
Regulated Target TINCR ubiquitin domain containing (TINCR) View Details
Crosstalk Relationship m1A  →  m6A Enhancement
Crosstalk Mechanism RNA modification directly impacts m6A modification through recruiting m6A regulator and targeting the shared RNA
Crosstalk Summary A subset of endogenous RNAs (Ubiquitin domain-containing protein TINC (TINCR); cMATR3; cFAM20B and cSLC45A4) that harbor m6A and associate with YTHDF2 in an HRSP12-dependent manner is also subjected to m1A-facilitated rapid degradation. The m1A modification is mediated by the TRMT6/TRMT61A complex.
Pathway Response RNA degradation hsa03018
Cell Process mRNA decay
In-vitro Model
HeLa Endocervical adenocarcinoma Homo sapiens CVCL_0030
References
Ref 1 m(1)A and m(6)A modifications function cooperatively to facilitate rapid mRNA degradation. Cell Rep. 2022 Sep 6;40(10):111317. doi: 10.1016/j.celrep.2022.111317.