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机译:A nonsense mutation 1669Glu--Ter within the regulatory domain of human erythroid ankyrin leads to a selective deficiency of the major ankyrin isoform (band 2.1) and a phenotype of autosomal dominant hereditary spherocytosis.
Department of Biomedical Research, St. Elizabeth's Medical Center, Tufts University School of Medicine, Boston, Massachusetts 02135.;
Ankyrins; Erythrocytes; Abnormal; RNA; Messenger; band-2.1-protein; Spectrin; 锚蛋白类; 红细胞; 异常;