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Literature summary extracted from

  • Lee, J.H.; Park, J.W.
    Attenuated mitochondrial NADP+-dependent isocitrate dehydrogenase activity induces apoptosis and hypertrophy of H9c2 cardiomyocytes (2014), Biochimie, 99, 110-118.
    View publication on PubMed

Protein Variants

EC Number Protein Variants Comment Organism
1.1.1.42 additional information knockdown of IDPm by siRNA in H9c2 cells, the suppression of IDPm expression by siRNA induces apoptosis and hypertrophy of cultured cardiomyocytes through the disruption of cellular redox balance, phenotype, overview Rattus norvegicus

Localization

EC Number Localization Comment Organism GeneOntology No. Textmining
1.1.1.42 mitochondrion
-
 Rattus norvegicus 5739
-

Natural Substrates/ Products (Substrates)

EC Number Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
1.1.1.42 isocitrate + NADP+ Rattus norvegicus
-
 2-oxoglutarate + CO2 + NADPH + H+
-
 r

Organism

EC Number Organism UniProt Comment Textmining
1.1.1.42 Rattus norvegicus P56574
-
-

Source Tissue

EC Number Source Tissue Comment Organism Textmining
1.1.1.42 H9c2 cell
-
 Rattus norvegicus
-
1.1.1.42 heart
-
 Rattus norvegicus
-
1.1.1.42 myoblast
-
 Rattus norvegicus
-

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
1.1.1.42 isocitrate + NADP+
-
 Rattus norvegicus 2-oxoglutarate + CO2 + NADPH + H+
-
 r

Synonyms

EC Number Synonyms Comment Organism
1.1.1.42 IDPm
-
 Rattus norvegicus
1.1.1.42 NADP+-dependent isocitrate dehydrogenase
-
 Rattus norvegicus

Cofactor

EC Number Cofactor Comment Organism Structure
1.1.1.42 NADP+
-
 Rattus norvegicus
1.1.1.42 NADPH
-
 Rattus norvegicus

General Information

EC Number General Information Comment Organism
1.1.1.42 malfunction transfection of H9c2 clonal myoblastic cells with small interfering RNA (siRNA) specific for IDPm markedly attenuates IDPm expression and substantially induces apoptosis, senescence, and hypertrophy as indicated by increased atrial natriuretic peptide gene expression, a marker of cardiomyocyte hypertrophy, and a larger cell size. Knockdown of IDPm expression results in the modulation of cellular and mitochondrial redox status, mitochondrial function, and cellular oxidative damage. The suppression of IDP expression by siRNA induces apoptosis and hypertrophy of cultured cardiomyocytes through the disruption of cellular redox balance. IDPm knockdown alters cellular redox status and induces oxidative damage. Apoptosis induced by IDPm knockdown is ROS-mediated. Substantially increased desmin and vimentin abundance is observed in IDPm siRNA-transfected H9c2 cells compared to the control cells. Mitochondrial fission and fusion involve enzymatic reactions mediated by large dynamin-associated GTPases. IDPm knockdown induces mitochondrial damage by altering the redox status Rattus norvegicus
1.1.1.42 physiological function mitochondrial NADP+s-dependent isocitrate dehydrogenase (IDPm) functions as an antioxidant and antiapoptotic protein by supplying NADPH to antioxidant systems Rattus norvegicus