BRENDA - Enzyme Database

Attenuated mitochondrial NADP+-dependent isocitrate dehydrogenase activity induces apoptosis and hypertrophy of H9c2 cardiomyocytes

Lee, J.H.; Park, J.W.; Biochimie 99, 110-118 (2014)

Data extracted from this reference:

Engineering
EC Number
Amino acid exchange
Commentary
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
Commentary
Organism
GeneOntology No.
Textmining
1.1.1.42
mitochondrion
-
Rattus norvegicus
5739
-
Natural Substrates/ Products (Substrates)
EC Number
Natural Substrates
Organism
Commentary (Nat. Sub.)
Natural Products
Commentary (Nat. Pro.)
Organism (Nat. Pro.)
Reversibility
1.1.1.42
isocitrate + NADP+
Rattus norvegicus
-
2-oxoglutarate + CO2 + NADPH + H+
-
-
r
Organism
EC Number
Organism
Primary Accession No. (UniProt)
Commentary
Textmining
1.1.1.42
Rattus norvegicus
P56574
-
-
Source Tissue
EC Number
Source Tissue
Commentary
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
Commentary Substrates
Literature (Substrates)
Organism
Products
Commentary (Products)
Literature (Products)
Organism (Products)
Reversibility
1.1.1.42
isocitrate + NADP+
-
740117
Rattus norvegicus
2-oxoglutarate + CO2 + NADPH + H+
-
-
-
r
Cofactor
EC Number
Cofactor
Commentary
Organism
Structure
1.1.1.42
NADP+
-
Rattus norvegicus
1.1.1.42
NADPH
-
Rattus norvegicus
Cofactor (protein specific)
EC Number
Cofactor
Commentary
Organism
Structure
1.1.1.42
NADP+
-
Rattus norvegicus
1.1.1.42
NADPH
-
Rattus norvegicus
Engineering (protein specific)
EC Number
Amino acid exchange
Commentary
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 (protein specific)
EC Number
Localization
Commentary
Organism
GeneOntology No.
Textmining
1.1.1.42
mitochondrion
-
Rattus norvegicus
5739
-
Natural Substrates/ Products (Substrates) (protein specific)
EC Number
Natural Substrates
Organism
Commentary (Nat. Sub.)
Natural Products
Commentary (Nat. Pro.)
Organism (Nat. Pro.)
Reversibility
1.1.1.42
isocitrate + NADP+
Rattus norvegicus
-
2-oxoglutarate + CO2 + NADPH + H+
-
-
r
Source Tissue (protein specific)
EC Number
Source Tissue
Commentary
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) (protein specific)
EC Number
Substrates
Commentary Substrates
Literature (Substrates)
Organism
Products
Commentary (Products)
Literature (Products)
Organism (Products)
Reversibility
1.1.1.42
isocitrate + NADP+
-
740117
Rattus norvegicus
2-oxoglutarate + CO2 + NADPH + H+
-
-
-
r
General Information
EC Number
General Information
Commentary
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
General Information (protein specific)
EC Number
General Information
Commentary
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