A defect in glycosylphosphatidylinositol (GPI) transamidase activity in mutant K cells is responsible for their inability to display GPI surface proteins.

@article{Chen1996ADI,
  title={A defect in glycosylphosphatidylinositol (GPI) transamidase activity in mutant K cells is responsible for their inability to display GPI surface proteins.},
  author={Rui Chen and Sidney Udenfriend and George M. Prince and Stephen E. Maxwell and Sandhya Ramalingam and Louise Diekmann Gerber and Jozo Knez and M. Edward Medof},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={1996},
  volume={93 6},
  pages={
          2280-4
        }
}
The final step in the pathway that provides for glycosylphosphatidylinositol (GPI) anchoring of cell-surface proteins occurs in the lumen of the endoplasmic reticulum and consists of a transamidation reaction in which fully assembled GPI anchor donors are substituted for specific COOH-terminal signal peptide sequences contained in nascent polypeptides. In previous studies we described a human K562 cell mutant line, designated class K, which assembles all the known intermediates of the GPI… CONTINUE READING

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Cloning of murine glycosyl phosphatidylinositol anchor attachment protein, GPAA1.

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