부산대학교 도서관

Research concerning the chronic faults that emerge in hematopoiesis for mice, homozygous for the recessive allelic mutation motheaten (me) or viable motheaten (mev) on chromosome 6, focussed on testing whether the faults at the me locus could be due to mutations inside the hematopoietic cell protein-tyrosine phosphatase (Hcph) gene. The similar map positions of the Hcph and me loci and the believable function of hematopoietic cell phosphatase (HCP) as a decisive signaling molecule in hematopoietic cell control and development prompted this focus. The me and mev mutations were inside the Hcph gene.