Human PEX1 cloned by functional complementation on a CHO cell mutant is responsible for peroxisome-deficient Zellweger syndrome of complementation group I.

@article{Tamura1998HumanPC,
  title={Human PEX1 cloned by functional complementation on a CHO cell mutant is responsible for peroxisome-deficient Zellweger syndrome of complementation group I.},
  author={Shigehiko Tamura and Kanji Okumoto and Reiko Toyama and Nobuyuki Shimozawa and Toshiro Tsukamoto and Yasuyuki Suzuki and Takashi Osumi and Naomi Kondo and Yukio Fujiki},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={1998},
  volume={95 8},
  pages={4350-5}
}
The peroxisome biogenesis disorders (PBDs), including Zellweger syndrome (ZS) and neonatal adrenoleukodystrophy (NALD), are autosomal recessive diseases caused by defects in peroxisome assembly, for which at least 10 complementation groups have been reported. We have isolated a human PEX1 cDNA (HsPEX1) by functional complementation of peroxisome deficiency of a mutant Chinese hamster ovary (CHO) cell line, ZP107, transformed with peroxisome targeting signal type 1-tagged "enhanced" green… CONTINUE READING
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