Mechanism of Crosstalk between m6A Modification and Epigenetic Regulation
Crosstalk ID
M6ACROT05782
[1]
m6A modification RNU6-1 RNU6-1 METTL16 Methylation : m6A sites Direct Enhancement Non-coding RNA RNU6-1 Regulated Target  lncRNA       miRNA   circRNA
m6A Modification:
m6A Regulator Methyltransferase-like 16 (METTL16) WRITER
m6A Target RNA, U6 small nuclear 1 (RNU6-1)
Epigenetic Regulation that have Cross-talk with This m6A Modification:
Epigenetic Regulation Type Non-coding RNA (ncRNA)
Epigenetic Regulator RNA, U6 small nuclear 1 (RNU6-1) snRNA View Details
Crosstalk Relationship m6A  →  ncRNA Enhancement
Crosstalk Mechanism m6A regulators directly modulate the functionality of ncRNAs through specific targeting ncRNA
Crosstalk Summary Inhibition of METTL16 activity significantly reduces the m6A modification levels of RNA, U6 small nuclear 1 (RNU6-1)
In-vitro Model
HEK293 Normal Homo sapiens CVCL_0045
HEK293T Normal Homo sapiens CVCL_0063
HEK293-A Normal Homo sapiens CVCL_6910
References
Ref 1 The U6 snRNA m(6)A Methyltransferase METTL16 Regulates SAM Synthetase Intron Retention. Cell. 2017 May 18;169(5):824-835.e14. doi: 10.1016/j.cell.2017.05.003.