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Peroxisome biogenesis disorders: identification of a new complementation group distinct from peroxisome-deficient CHO mutants and not complemented by human PEX 13.

Abstract
Ten complementation groups of generalized peroxisome biogenesis disorders (PBD), (excluding rhizomelic chondrodysplasia punctata) have been identified using complementation analysis. Four of the genes involved have been identified using two different methods of (1) genetic functional complementation of peroxisome deficient CHO cell mutants and (2) homology searches for human dbEST, based on yeast genes involved in peroxisome biogenesis (PEX genes). We report here the first identification of a new complementation group which is genetically different from peroxisome deficient CHO mutants. There were no complementations by the human PEX 13 gene. The nature of the related gene is being investigated.
AuthorsN Shimozawa, Y Suzuki, Z Zhang, A Imamura, T Tsukamoto, T Osumi, K Tateishi, K Okumoto, Y Fujiki, T Orii, P G Barth, R J Wanders, N Kondo
JournalBiochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 243 Issue 2 Pg. 368-71 (Feb 13 1998) ISSN: 0006-291X [Print] United States
PMID9480815 (Publication Type: Case Reports, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • DNA, Complementary
  • Membrane Proteins
  • PEX13 protein, human
  • Catalase
Topics
  • Animals
  • CHO Cells
  • Catalase (immunology)
  • Chromosome Mapping
  • Cloning, Molecular
  • Cricetinae
  • DNA, Complementary (genetics)
  • Fibroblasts
  • Fluorescent Antibody Technique
  • Genetic Complementation Test
  • Humans
  • Infant
  • Male
  • Membrane Proteins (genetics)
  • Peroxisomal Disorders (genetics)
  • Phenotype
  • Transfection (genetics)

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