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Literature summary for 1.15.1.1 extracted from

  • Park, K.H.; Vincent, I.
    Presymptomatic biochemical changes in hindlimb muscle of G93A human Cu/Zn superoxide dismutase 1 transgenic mouse model of amyotrophic lateral sclerosis (2008), Biochim. Biophys. Acta, 1782, 462-468.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 1.15.1.1

Cloned(Commentary)

Cloned (Comment) Organism
overexpression of wild-type and mutant enzymes in hind limb muscle of transgenic mice Homo sapiens

Protein Variants

Protein Variants Comment Organism
E93A construction of transgenic mice overexpressing wild-type and mutant SOD1, biochemical changes occur in the hindlimb muscle of young, presymptomatic G93A hSOD1 transgenic mice, cdk5 activity is reduced in hindlimb muscle of 27-day-old G93A hSOD1 transgenic mice by suppression through the mutant E93A enzyme, phenotype, overview, mutant G93A SOD1 also suppresses muscle cdk5 activity in vitro Homo sapiens

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
O2.- + H+ Homo sapiens the enzyme mutation E93A leads to a decrease in muscle cdk5 activity accompanied by a significant reduction in MyoD and cyclin D1 levels causing amyotrophic lateral sclerosis, a primarily a motor neuron disorder with early muscle denervation preceding motor neuron loss, the progressive deterioration of muscle function is potentiated by altered muscle biochemistry in these mice at a very young, presymptomatic age, overview O2 + H2O2
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 ?

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Purification (Commentary)

Purification (Comment) Organism
large scale immunoisolation of native mutant and wildtype SOD1 Homo sapiens

Source Tissue

Source Tissue Comment Organism Textmining

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
O2.- + H+
-
 Homo sapiens O2 + H2O2
-
 ?
O2.- + H+ the enzyme mutation E93A leads to a decrease in muscle cdk5 activity accompanied by a significant reduction in MyoD and cyclin D1 levels causing amyotrophic lateral sclerosis, a primarily a motor neuron disorder with early muscle denervation preceding motor neuron loss, the progressive deterioration of muscle function is potentiated by altered muscle biochemistry in these mice at a very young, presymptomatic age, overview Homo sapiens O2 + H2O2
-
 ?

Synonyms

Synonyms Comment Organism
Cu/Zn superoxide dismutase 1
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 Homo sapiens
SOD1
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 Homo sapiens