Cloned (Comment) | Organism |
---|---|
recombinant ectopic expression of NNMT in enzyme-deficient SH-SY5Y human neuroblastoma cells increasing adenosine triphosphate synthesis and complex I activity | Homo sapiens |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
S-adenosyl-L-methionine + nicotinamide | Homo sapiens | - |
S-adenosyl-L-homocysteine + 1-methylnicotinamide | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
brain | the enzyme is robustly expressed in neurones in all regions of the brain | Homo sapiens | - |
additional information | no enzyme activity in SH-SY5Y human neuroblastoma cells | Homo sapiens | - |
neuron | - |
Homo sapiens | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
S-adenosyl-L-methionine + nicotinamide | - |
Homo sapiens | S-adenosyl-L-homocysteine + 1-methylnicotinamide | - |
? |
Synonyms | Comment | Organism |
---|---|---|
NNMT | - |
Homo sapiens |
Cofactor | Comment | Organism | Structure |
---|---|---|---|
S-adenosyl-L-methionine | - |
Homo sapiens |
General Information | Comment | Organism |
---|---|---|
additional information | recombinant ectopic expression of NNMT in enzyme-deficient SH-SY5Y human neuroblastoma cells increased adenosine triphosphate synthesis and complex I activity, effects of which are replicated by the addition of 1-methylnicotinamide. The enzyme expression protects against the toxicity of mitochondrial toxins and abolishes the toxic effects of KCN, 2,4-dinitrophenol, and 6-hydroxydopamine, and reduced that of rotenone, while 1-methylnicotinamide significantly reduces the toxicity of rotenone, but has no effect on the toxicity of KCN, 2,4-dinitrophenol, and 6-hydroxydopamine. The enzyme is cytoprotective against toxins that inhibit various aspects of mitochondrial function, which are not mediated solely via increased 1-methylnicotinamide production, but in combination with other unidentified mechanisms | Homo sapiens |