Data extracted from this reference:
Cloned(Commentary)
2.1.1.1
stable recombinant expression of enzyme NNMT in the SH-SY5Y human neuroblastoma cell line, which has no endogenous enzyme expression, at levels of activity comparable with that in Parkinson's disease brain, recombinant expression of enzyme NNMT in SH-SY5Y human neuroblastoma and N27 rat mesencephalic dopaminergic neurones increases neurite branching, synaptophysin expression and dopamine accumulation and release. Recombinant NNMT-V5 expression in SH-SY5Y cells changes cellular morphology and increases dopamine uptake and release. Transient expression of enzyme NNMT in N27 cells
Homo sapiens
Engineering
2.1.1.1
additional information
enzyme expression in SH-SY5Y neuroblastoma and N27 mesencephalic neurones induces changes in cell morphology via ephrin-B2 and Akt signalling
Homo sapiens
Natural Substrates/ Products (Substrates)
2.1.1.1
S-adenosyl-L-methionine + nicotinamide
Homo sapiens
S-adenosyl-L-homocysteine + 1-methylnicotinamide
?
Organism
Source Tissue
2.1.1.1
additional information
no activity in the SH-SY5Y human neuroblastoma cell line and in N27 cells
Homo sapiens
2.1.1.1
neuron
Homo sapiens
Substrates and Products (Substrate)
2.1.1.1
S-adenosyl-L-methionine + nicotinamide
733625
Homo sapiens
S-adenosyl-L-homocysteine + 1-methylnicotinamide
?
Synonyms
2.1.1.1
NNMT
Homo sapiens
Cofactor
2.1.1.1
S-adenosyl-L-methionine
Homo sapiens
Cloned(Commentary) (protein specific)
2.1.1.1
stable recombinant expression of enzyme NNMT in the SH-SY5Y human neuroblastoma cell line, which has no endogenous enzyme expression, at levels of activity comparable with that in Parkinson's disease brain, recombinant expression of enzyme NNMT in SH-SY5Y human neuroblastoma and N27 rat mesencephalic dopaminergic neurones increases neurite branching, synaptophysin expression and dopamine accumulation and release. Recombinant NNMT-V5 expression in SH-SY5Y cells changes cellular morphology and increases dopamine uptake and release. Transient expression of enzyme NNMT in N27 cells
Homo sapiens
Cofactor (protein specific)
2.1.1.1
S-adenosyl-L-methionine
Homo sapiens
Engineering (protein specific)
2.1.1.1
additional information
enzyme expression in SH-SY5Y neuroblastoma and N27 mesencephalic neurones induces changes in cell morphology via ephrin-B2 and Akt signalling
Homo sapiens
Natural Substrates/ Products (Substrates) (protein specific)
2.1.1.1
S-adenosyl-L-methionine + nicotinamide
Homo sapiens
S-adenosyl-L-homocysteine + 1-methylnicotinamide
?
Source Tissue (protein specific)
2.1.1.1
additional information
no activity in the SH-SY5Y human neuroblastoma cell line and in N27 cells
Homo sapiens
2.1.1.1
neuron
Homo sapiens
Substrates and Products (Substrate) (protein specific)
2.1.1.1
S-adenosyl-L-methionine + nicotinamide
733625
Homo sapiens
S-adenosyl-L-homocysteine + 1-methylnicotinamide
?
General Information
2.1.1.1
malfunction
the enzyme effects on neurons are reduced in cells lacking epinephrin EFNB2 or Akt
Homo sapiens
2.1.1.1
metabolism
the effects of enzyme NNMT expression in SH-SY5Y cells, e.g. protection against the toxicity of the Complex I (CxI) inhibitors 1-methyl-4-phenylpyridinium ion and rotenone, are mediated via increased CxI activity and ATP production and the sequential activation of the epinephrin EFNB2 and Akt signalling pathways
Homo sapiens
2.1.1.1
physiological function
the enzyme NNMT expression protects against neurotoxin-mediated cell death by increasing Complex I (CxI) activity, resulting in increased ATP synthesis, mediated via protection of the NDUFS3 subunit of CxI from degradation by increased 1-methylnicotinamide production. The enzyme expression increases neurite branching and the presynaptic marker synaptophysin, synaptophysin expression is induced by the enzyme. 1-Methylnicotinamide replicates the effects of enzyme NNMT expression upon SH-SY5Y neurite branching, effects of NNMT expression on neuron morphology and differentiation, overview. Recombinant NNMT-V5 expression in SH-SY5Y cells changes cellular morphology and increases dopamine uptake and release. The effects of enzyme NNMT expression in SH-SY5Y cells, e.g. protection against the toxicity of the Complex I (CxI) inhibitors 1-methyl-4-phenylpyridinium ion and rotenone, are mediated via increased CxI activity and ATP production and the sequential activation of the epinephrin EFNB2 and Akt signalling pathways. The enzyme NNMT reduces cholinergic phenotype but does not induce terminal differentiation
Homo sapiens
General Information (protein specific)
2.1.1.1
malfunction
the enzyme effects on neurons are reduced in cells lacking epinephrin EFNB2 or Akt
Homo sapiens
2.1.1.1
metabolism
the effects of enzyme NNMT expression in SH-SY5Y cells, e.g. protection against the toxicity of the Complex I (CxI) inhibitors 1-methyl-4-phenylpyridinium ion and rotenone, are mediated via increased CxI activity and ATP production and the sequential activation of the epinephrin EFNB2 and Akt signalling pathways
Homo sapiens
2.1.1.1
physiological function
the enzyme NNMT expression protects against neurotoxin-mediated cell death by increasing Complex I (CxI) activity, resulting in increased ATP synthesis, mediated via protection of the NDUFS3 subunit of CxI from degradation by increased 1-methylnicotinamide production. The enzyme expression increases neurite branching and the presynaptic marker synaptophysin, synaptophysin expression is induced by the enzyme. 1-Methylnicotinamide replicates the effects of enzyme NNMT expression upon SH-SY5Y neurite branching, effects of NNMT expression on neuron morphology and differentiation, overview. Recombinant NNMT-V5 expression in SH-SY5Y cells changes cellular morphology and increases dopamine uptake and release. The effects of enzyme NNMT expression in SH-SY5Y cells, e.g. protection against the toxicity of the Complex I (CxI) inhibitors 1-methyl-4-phenylpyridinium ion and rotenone, are mediated via increased CxI activity and ATP production and the sequential activation of the epinephrin EFNB2 and Akt signalling pathways. The enzyme NNMT reduces cholinergic phenotype but does not induce terminal differentiation
Homo sapiens