Target intelligence / Profile preview

Cap-specific mRNA (nucleoside-2'-O-)-methyltransferase 2 (CMTR2)

Target
CMTR2
Molecular classification
Enzyme, Methyltransferase
01

Overview

Cap-specific mRNA (nucleoside-2'-O-)-methyltransferase 2 (CMTR2) is a S-adenosyl-L-methionine-dependent enzyme that catalyzes the methylation of the ribose of the second nucleotide (cap2) in the 5’ cap structure of mRNA and small nuclear RNA (snRNA)[1][10][8]. This modification further enhances the mRNA cap structure beyond the cap0 and cap1 states, contributing to RNA stability, processing, and translation. CMTR2 recognizes the guanosine cap of RNAs independently of its N(7) methylation status and localizes mainly to the cytoplasm and nucleus[1][5]. In mammals, CMTR2 functions largely independently but in concert with other cap methyltransferases to establish the mature mRNA cap structure, and its activity may influence cellular responses such as immune recognition by evading certain innate immune sensors[3][5][1]. No direct disease association or drug targeting is currently established, but perturbations of cap methylation are of growing interest in cancer and virology research.

Other names
Cap methyltransferase 2FTSJD1CMTr2Q8IYT2[1][10]
02

Mechanism of action

Inhibition of methyltransferase activity (hypothetical; targeting cap methyltransferases could affect mRNA stability or translation, but no specific inhibitors are referenced for CMTR2)[3]

03

Biological functions

mRNA 7-methylguanosine (cap) cappingmRNA (nucleoside-2'-O-)-methyltransferase activity2'-O-ribose methylation of messenger RNA cap structure[1][10]
04

Disease associations

Other (relevant to RNA processing, not directly associated with specific disease roles, but such modifications are increasingly implicated in cancer and viral infection through effects on mRNA stability and immune evasion[3])
05

Safety considerations

Disrupting mRNA cap methylation could impact global mRNA stability and translation, possibly affecting essential cellular processes and leading to widespread cellular toxicity[3]

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