ArticleMammalian genome : official journal of the International Mammalian Genome Society1996
Molecular markers near the mouse brachymorphic (bm) gene, which affects connective tissues and bleeding time.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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3 citing papers in PubMed, 19 citations in OpenAlex.
- A member of a family of sulfate-activating enzymes causes murine brachymorphism.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- The mouse pale ear (ep) mutation is the homologue of human Hermansky-Pudlak syndrome.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Mapping and retinal phenotype of the hugger mutation in the mouse.Mammalian genome : official journal of the International Mammalian Genome Society · 1997Article
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7 authors at 1 institution in 1 country.
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Abstract
Several inherited skeletal/connective tissue defects are associated with hemorrhagic disorders in humans. Accordingly, three mouse mutants (brachymorphic [bm], hemimelic extra toes [Hx], and ulnaless [Ul]), with inherited skeletal abnormalities, were analyzed for hemorrhagic tendencies. All three had prolonged bleeding times. Platelet numbers, size, and function, as well as common soluble plasma clotting factors, were not measurably affected. To further define the bm mutation, its chromosomal location relative to 19 other molecular markers was determined to a high resolution in a large interspecific backcross. Several microsatellite markers were found to be very closely linked to bm and should provide useful entry points for the eventual identification of this gene by positional/candidate cloning techniques. These results suggest that inherited skeletal abnormalities and bleeding tendencies are associated more frequently in both humans and animal models than is commonly recognized. Identification of these genes may reveal novel relationships between osteogenesis and hemostasis.
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