Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary for 1.1.1.42 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

Protein Variants Comment Organism
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

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

Natural Substrates/ Products (Substrates)

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

Organism

Organism UniProt Comment Textmining
Rattus norvegicus P56574
-
-

Source Tissue

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

Substrates and Products (Substrate)

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

Synonyms

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

Cofactor

Cofactor Comment Organism Structure
NADP+
-
Rattus norvegicus
NADPH
-
Rattus norvegicus

General Information

General Information Comment Organism
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
physiological function mitochondrial NADP+s-dependent isocitrate dehydrogenase (IDPm) functions as an antioxidant and antiapoptotic protein by supplying NADPH to antioxidant systems Rattus norvegicus