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

Nobuyuki Shimozawa, Yasuyuki Suzuki, Zhongyi Zhang, Atsushi Imamura, Toshiro Tsukamoto, Takashi Osumi, Keita Tateishi, Kanji Okumoto, Yukio Fujiki, Tadao Orii, Peter G. Barth, Ronald J.A. Wanders, Naomi Kondo

Research output: Contribution to journalArticle

19 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)368-371
Number of pages4
JournalBiochemical and Biophysical Research Communications
Volume243
Issue number2
DOIs
Publication statusPublished - Feb 13 1998

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Fingerprint Dive into the research topics of 'Peroxisome biogenesis disorders: Identification of a new complementation group distinct from peroxisome-deficient CHO mutants and not complemented by human PEX 13'. Together they form a unique fingerprint.

  • Cite this

    Shimozawa, N., Suzuki, Y., Zhang, Z., Imamura, A., Tsukamoto, T., Osumi, T., Tateishi, K., Okumoto, K., Fujiki, Y., Orii, T., Barth, P. G., Wanders, R. J. A., & Kondo, N. (1998). Peroxisome biogenesis disorders: Identification of a new complementation group distinct from peroxisome-deficient CHO mutants and not complemented by human PEX 13. Biochemical and Biophysical Research Communications, 243(2), 368-371. https://doi.org/10.1006/bbrc.1997.8067