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Title: (Inborn anemias of mice): Terminal progress report

Technical Report ·
OSTI ID:6590085

Mutations located at 11 different chromosomal locations in the mouse all affecting hemopoiesis have been studied. These include: Hertwig's anemia (an), W-anemias (W, W/sup v/, W/sup 17J/ to W/sup 41J/), Steel anemias (Sl, Sl/sup d/, etc.), Normoblastic anemia (nb), Jaundiced (ja), Spherocytic anemias (sph, sph/sup ha/), sph/sup 2J/, sph/sup 2BC/, Flexed-tail anemia (f), Microcytic anemia (mk), Sex-linked anemia (Sla), Alpha thallasemia (Hba/sup th/), and a hypochromic anemia associated with low transferrin levels (hpx). Our findings indicate that the erythroid defect in W-anemias stem from an intrinsic defect in the erythroid progenitor cells, and that all other erythroid hemostatic mechanisms are fully functional. Hertwig's anemia (an) is affected in a similar fashion. However, in the case of Steel anemias, the erythroid progenitors are repressed, but when transplanted to appropriate recipients were found to be fully functional. 70 refs., 4 tabs.

Research Organization:
Jackson Lab., Bar Harbor, ME (USA)
DOE Contract Number:
AC02-76EV03264
OSTI ID:
6590085
Report Number(s):
DOE/EV/03264-1; ON: DE87009259
Country of Publication:
United States
Language:
English