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Gene Review

Idh2  -  isocitrate dehydrogenase 2 (NADP+),...

Mus musculus

Synonyms: E430004F23, ICD-M, IDH, IDP, IDPm, ...
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Disease relevance of Idh2


High impact information on Idh2

  • HEK293 cells and intact respiring mitochondria treated with oxidants inducing GSH oxidation such as H(2)O(2) or diamide showed a decrease in IDPm activity and the accumulation of glutathionylated enzyme [1].
  • Recently, we demonstrated that the control of mitochondrial redox balance and oxidative damage is one of the primary functions of mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDPm) [1].
  • Oxidized glutathione led to enzyme inactivation with simultaneous formation of a mixed disulfide between glutathione and the cysteine residue(s) in IDPm, which was detected by immunoblotting with anti-GSH IgG [1].
  • Because cysteine residue(s) in IDPm are susceptible to inactivation by a number of thiol-modifying reagents, we hypothesized that IDPm is likely a target for regulation by an oxidative mechanism, specifically glutathionylation [1].
  • The results of the current study indicate that IDPm activity appears to be modulated through enzymatic glutathionylation and deglutathionylation during oxidative stress [1].

Biological context of Idh2

  • We demonstrate in this report that IDPm is induced by ROS and that decreased expression of IDPm markedly elevates the ROS generation, DNA fragmentation, lipid peroxidation, and concurrent mitochondrial damage with a significant reduction in ATP level [2].
  • The results suggest that IDPm plays an important protective role in apoptosis of HEK293 cells induced by a high concentration of glucose and may contribute to various pathologies associated with the long-term complications of diabetes [3].
  • Cells with decreased expression of IDPc or IDPm had elevated reactive oxygen species generation, lipid peroxidation and protein oxidation [4].

Anatomical context of Idh2

  • Our results strongly indicate that IDPm is a major NADPH producer in the mitochondria and thus plays a key role in cellular defense against oxidative stress-induced damage [2].
  • In this report, we demonstrate that modulation of IDPm activity in HEK293 cells, an embryonic kidney cell line, regulates high glucose-induced apoptosis [3].

Associations of Idh2 with chemical compounds

  • We investigated the role of mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDPm) in controlling the mitochondrial redox balance and subsequent cellular defense against oxidative damage [2].
  • The protective role of IDPm against oxidative damage may be attributed to increased levels of a reducing equivalent, NADPH, needed for regeneration of glutathione in the mitochondria [2].
  • When exposed to cadmium, IDPm was susceptible to loss of enzyme activity and structural alterations [5].

Regulatory relationships of Idh2


Other interactions of Idh2


Analytical, diagnostic and therapeutic context of Idh2


  1. Regulation of mitochondrial NADP+-dependent isocitrate dehydrogenase activity by glutathionylation. Kil, I.S., Park, J.W. J. Biol. Chem. (2005) [Pubmed]
  2. Control of mitochondrial redox balance and cellular defense against oxidative damage by mitochondrial NADP+-dependent isocitrate dehydrogenase. Jo, S.H., Son, M.K., Koh, H.J., Lee, S.M., Song, I.H., Kim, Y.O., Lee, Y.S., Jeong, K.S., Kim, W.B., Park, J.W., Song, B.J., Huh, T.L., Huhe, T.L. J. Biol. Chem. (2001) [Pubmed]
  3. Regulation of high glucose-induced apoptosis by mitochondrial NADP+-dependent isocitrate dehydrogenase. Shin, A.H., Kil, I.S., Yang, E.S., Huh, T.L., Yang, C.H., Park, J.W. Biochem. Biophys. Res. Commun. (2004) [Pubmed]
  4. Role of NADP+-dependent isocitrate dehydrogenase (NADP+-ICDH) on cellular defence against oxidative injury by gamma-rays. Lee, S.H., Jo, S.H., Lee, S.M., Koh, H.J., Song, H., Park, J.W., Lee, W.H., Huh, T.L. Int. J. Radiat. Biol. (2004) [Pubmed]
  5. Mitochondrial NADP+-dependent isocitrate dehydrogenase protects cadmium-induced apoptosis. Kil, I.S., Shin, S.W., Yeo, H.S., Lee, Y.S., Park, J.W. Mol. Pharmacol. (2006) [Pubmed]
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