Figure 6.
Figure 6. Complementation of deficient surface expression of DAF and MIRL (CD59) on paroxysmal nocturnal hemoglobinuria (PNH) cells. Three glycosyl phosphatidylinositol (GPI)–anchor-deficient cell lines derived from B lymphocytes of patients with PNH (panels A, B & C) were stained with anti-DAF and anti-MIRL (CD59) and analyzed by flow cytometry. The same cell lines transfected with PIGA cDNA (panels D, E & F) were analyzed under the same conditions as the controls. These experiments implied that PIGA is the gene that is mutant in PNH. That mutations in PIGA account for the deficiency of GPI-anchored proteins in PNH was demonstrated by Dr. Junji Takeda, Dr. Taroh Kinoshita and colleagues in this same landmark paper.
 Reproduced from Takeda J, Miyata T, Kawagoe K, et al. Deficiency of the GPI anchor caused by a somatic mutation of the PIGA gene in paroxysmal nocturnal hemoglobinuria. Cell. 1993;73:703–711 by copyright permission from Elsevier Science.

Complementation of deficient surface expression of DAF and MIRL (CD59) on paroxysmal nocturnal hemoglobinuria (PNH) cells. Three glycosyl phosphatidylinositol (GPI)–anchor-deficient cell lines derived from B lymphocytes of patients with PNH (panels A, B & C) were stained with anti-DAF and anti-MIRL (CD59) and analyzed by flow cytometry. The same cell lines transfected with PIGA cDNA (panels D, E & F) were analyzed under the same conditions as the controls. These experiments implied that PIGA is the gene that is mutant in PNH. That mutations in PIGA account for the deficiency of GPI-anchored proteins in PNH was demonstrated by Dr. Junji Takeda, Dr. Taroh Kinoshita and colleagues in this same landmark paper.
 Reproduced from

Takeda J, Miyata T, Kawagoe K, et al. Deficiency of the GPI anchor caused by a somatic mutation of the PIGA gene in paroxysmal nocturnal hemoglobinuria. Cell. 1993;73:703–711
by copyright permission from Elsevier Science.

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