Gene Symbol: Sdhb
Description: succinate dehydrogenase complex iron sulfur subunit B
Alias: succinate dehydrogenase [ubiquinone] iron-sulfur subunit, mitochondrial, iron-sulfur subunit of complex II, succinate dehydrogenase complex, subunit B, iron sulfur (Ip)
Species: rat
Products:     Sdhb

Top Publications

  1. Diaz F, Thomas C, Garcia S, Hernandez D, Moraes C. Mice lacking COX10 in skeletal muscle recapitulate the phenotype of progressive mitochondrial myopathies associated with cytochrome c oxidase deficiency. Hum Mol Genet. 2005;14:2737-48 pubmed
    ..This COX10 KO mouse allowed us to correlate the muscle function with residual COX activity, an estimate that can help predict the progression pattern of human mitochondrial myopathies...
  2. Astuti D, Latif F, Dallol A, Dahia P, Douglas F, George E, et al. Gene mutations in the succinate dehydrogenase subunit SDHB cause susceptibility to familial pheochromocytoma and to familial paraganglioma. Am J Hum Genet. 2001;69:49-54 pubmed
    ..components of succinate dehydrogenase, SDHC and SDHD, anchor the gene products of two other components, SDHA and SDHB, which form the catalytic core, to the inner-mitochondrial membrane...
  3. Bjorkman J, Gould S, Crane D. Pex13, the mouse ortholog of the human peroxisome biogenesis disorder PEX13 gene: gene structure, tissue expression, and localization of the protein to peroxisomes. Genomics. 2002;79:162-8 pubmed
    ..We infer from these findings that targeted disruption of mouse Pex13 would provide an appropriate model for the study of PEX13 dysfunction in humans. ..
  4. Forner F, Kumar C, Luber C, Fromme T, Klingenspor M, Mann M. Proteome differences between brown and white fat mitochondria reveal specialized metabolic functions. Cell Metab. 2009;10:324-35 pubmed publisher
    ..In vivo comparison of organellar proteomes can thus directly address functional questions in metabolism. ..
  5. Yang H, Brosel S, Acin Perez R, Slavkovich V, Nishino I, Khan R, et al. Analysis of mouse models of cytochrome c oxidase deficiency owing to mutations in Sco2. Hum Mol Genet. 2010;19:170-80 pubmed publisher
    ..These mouse models should be of use in further studies of Sco2 function, as well as in testing therapeutic approaches to treat the human disorder. ..
  6. Bardella C, Pollard P, Tomlinson I. SDH mutations in cancer. Biochim Biophys Acta. 2011;1807:1432-43 pubmed publisher
    The SDHA, SDHB, SDHC, SDHD genes encode the four subunits of succinate dehydrogenase (SDH; mitochondrial complex II), a mitochondrial enzyme involved in two essential energy-producing metabolic processes of the cell, the Krebs cycle and ..
  7. Gould S, Subramani S, Scheffler I. Use of the DNA polymerase chain reaction for homology probing: isolation of partial cDNA or genomic clones encoding the iron-sulfur protein of succinate dehydrogenase from several species. Proc Natl Acad Sci U S A. 1989;86:1934-8 pubmed
    ..This application of the polymerase chain reaction should be useful not only for the identification of conserved genes in a variety of species but also for the isolation of previously unknown members of gene families. ..
  8. Brière J, Favier J, El Ghouzzi V, Djouadi F, Benit P, Gimenez A, et al. Succinate dehydrogenase deficiency in human. Cell Mol Life Sci. 2005;62:2317-24 pubmed
    ..Finally we stress the importance of SDH as a target and/or marker in a number of diseases and the need to better delineate the consequences of SDH deficiency in humans. ..
  9. Lashin O, Szweda P, Szweda L, Romani A. Decreased complex II respiration and HNE-modified SDH subunit in diabetic heart. Free Radic Biol Med. 2006;40:886-96 pubmed

More Information


  1. Cervera A, Bayley J, Devilee P, McCreath K. Inhibition of succinate dehydrogenase dysregulates histone modification in mammalian cells. Mol Cancer. 2009;8:89 pubmed publisher
    ..ChIP analysis revealed that the core promoter of IGFBP7, which encodes a secreted protein upregulated after loss of SDHB, showed decreased occupancy by H3K27me3 in the absence of SDH...
  2. Peralta S, Torraco A, Wenz T, Garcia S, Diaz F, Moraes C. Partial complex I deficiency due to the CNS conditional ablation of Ndufa5 results in a mild chronic encephalopathy but no increase in oxidative damage. Hum Mol Genet. 2014;23:1399-412 pubmed publisher
    ..These results showed that a partial defect in CI in neurons can lead to late-onset motor phenotypes without neuronal loss or oxidative damage. ..