Methylation of adenosine at position 1 produces a drastic functional change in the nucleobase. 1-Methyladenosine (pKa 8.25) is a much stronger base than adenosine (pKa 3.5). N-1 methylation excludes participation of the adenine base in canonical Watson–Crick base pairing and provides a positive charge to the nucleobase. This modification also alters the hydrophobicity of the base, the stacking properties, the ordering of water molecules and the chelation properties. The base may become involved in non-canonical hydrogen bonding, in electrostatic interactions and, in general, it may contribute to the conformational dynamics of the tRNA.
In the central dogma of molecular biology, genetic information flows from DNA to RNA and then to protein. Reversible epigenetic modifications on genomic DNA and histone have been known to substantially regulate gene expression. On the other hand, there exists more than 100 naturally occurring chemical modifications in RNA; however, the functions of these RNA modifications are largely unknown. Whether some of these modifications in RNA can be reversed and could impact gene expression in the central dogma was unknown until the recent discovery of N6-methyladenosine (N6-Me-A) as the first example of reversible RNA methylation.1 We offer the N6-Me-A RNA monomer with a phenoxyacetyl protecting group to minimize potential branching. We have shown N6-Me-A-CE Phosphoramidite to be completely compatible with all popular RNA synthesis and deprotection methods, from UltraMild to the most popular procedure using AMA for deprotection.
|Storage||Refrigerated storage, maximum of 2-8°C, dry|
|Stability||Similar to dA,C,G,T-CE Phosphoramidites|
The table below show pack size data and, for solutions, dilution and approximate coupling based on normal priming procedures.
|Catalog #||Pack Size||Grams/Pack||0.1M Dil. (mL)||Approximate Number of Additions|
|Catalog #||Pack Size||Grams/Pack||Dilution (mL)||Approximate Number of Additions|
REFERENCE(S)| 1 Y. Fu, D. Dominissini, G. Rechavi, and C. He, Nat Rev Genet, 2014, 15, 293-306.