2.1.1.203: tRNA (cytosine34-C5)-methyltransferase
This is an abbreviated version!
For detailed information about tRNA (cytosine34-C5)-methyltransferase, go to the full flat file.
Word Map on EC 2.1.1.203
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2.1.1.203
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5-methylcytosine
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anticodon
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homocysteine
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wobble
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ualcan
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5-formylcytosine
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biallelic
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omnibus
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shrinkage
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hyperhomocysteinemia
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encephalomyopathy
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nsun2-mediated
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epitranscriptome
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early-onset
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medicine
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pharmacology
- 2.1.1.203
- 5-methylcytosine
-
anticodon
- homocysteine
-
wobble
-
ualcan
- 5-formylcytosine
-
biallelic
-
omnibus
-
shrinkage
-
hyperhomocysteinemia
- encephalomyopathy
-
nsun2-mediated
-
epitranscriptome
-
early-onset
- medicine
- pharmacology
Reaction
Synonyms
5-methylcytosine RNA methyltransferase, cytosine-5 RNA methyltransferase, cytosine-5 tRNA methyltransferase, DnmA, EC 2.1.1.29, hTrm4, M5C RNA methyltransferase, NOP2/Sun domain family member 2, NSUN2, NSUN3, NSUN3 methylase, PMT1, RCMT, RNA:m5C methyltransferase, SAKI, substrate of AIM-1/Aurora kinase B
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Engineering
Engineering on EC 2.1.1.203 - tRNA (cytosine34-C5)-methyltransferase
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A37G
naturally occurring mutation, mitochondrial disease-associated point mutations with the gene encoding mt-tRNAMet that lead to A37G substitution, impede methylation of C34 by NSUN3, lack of NSUN3-mediated modification impairs mitochondrial translation, leading to reduced mitochondrial function
C39U
naturally occurring mutation, mitochondrial disease-associated point mutations with the gene encoding mt-tRNAMet that lead to C39U substitution, impede methylation of C34 by NSUN3, lack of NSUN3-mediated modification impairs mitochondrial translation, leading to reduced mitochondrial function
G679R
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site-directed mutaegensis, the mutation to arginine at this residue causes NSUN2 to fail to localize within the nucleolus
K190M
additional information
generation of an insertion mutation in Drosophila NSun2 (NSun2DELTA21.5), which is viable and fertile and loses RNA methylation at known tRNA substrates. RNAi-mediated knockdown of NSun2 in follicle cells. Functional Gypsy retroviral particles can be formed in NSun2 mutants. Specific eccDNAs accumulate in RCMT mutants. RCMT mutants display reduced tRNA stability and tRNA abundance
additional information
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combined knockdown of NSUN2 and METTL1, EC 2.1.1.33, in HeLa cells
additional information
generation of enzyme depeleted NSUN2-/- cells. Rescue for loss of NSUN2 by reexpressing the wild-type or enzymatic dead protein. The number of m5C per tRNA in all tRNAs or tRNA leucine is quantified by mass spectrometry in NSUN2-/- cells reexpressing wild-type NSUN2, the catalytically inactive NSUN2 K190M mutant, or the empty vector control. Reexpression of NSUN2 significantly restores 525 methylation sites when compared to the empty vector control and 431 sites when compared to K190M-overexpressing cells
additional information
generation of NSUN3 knockout cells. When the knockout strain is rescued by plasmid-encoded NSUN3, f5C34 in mt-tRNAMet is partially restored
additional information
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generation of NSUN3 knockout cells. When the knockout strain is rescued by plasmid-encoded NSUN3, f5C34 in mt-tRNAMet is partially restored
additional information
mutation of the cysteine in motif IV in human NSUN3 to alanine or serine results in a stable covalent intermediate. Mutations in NSUN3 that lead to either aberrant splicing and frameshifting (p.Glu42Valfs*11) or the introduction of a premature stop codon (c.295C>T/p.Arg99*) have been detected in patients with a mitochondrial deficiency disorder
additional information
mutation of the cysteine in motif IV in human NSUN3 to alanine or serine results in a stable covalent intermediate