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2 tified, we find that individuals with severe achondrogenesis 1B phenotype have null mutations on both
3 skeletal dysplasia in humans, suggested that achondrogenesis type 1A may be caused by GMAP-210 defici
5 pes in these mice and those in patients with achondrogenesis type 1A, a neonatal lethal form of skele
6 t a third even more severe chondrodysplasia, achondrogenesis type IB, is also caused by mutations in
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