Redundancy of myostatin and growth/differentiation factor 11 function |
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| Authors: | Alexandra C McPherron Thanh V Huynh and Se-Jin Lee |
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| Institution: | (1) Genetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 9000, Rockville Pike, Bethesda, MD 20892, USA;(2) Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA |
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| Abstract: | Background Myostatin (Mstn) and growth/differentiation factor 11 (Gdf11) are highly related transforming growth factor β (TGFβ) family
members that play important roles in regulating embryonic development and adult tissue homeostasis. Despite their high degree
of sequence identity, targeted mutations in these genes result in non-overlapping phenotypes affecting distinct biological
processes. Loss of Mstn in mice causes a doubling of skeletal muscle mass while loss of Gdf11 in mice causes dramatic anterior homeotic transformations of the axial skeleton, kidney agenesis, and an increase in progenitor
cell number in several tissues. In order to investigate the possible functional redundancy of myostatin and Gdf11, we analyzed
the effect of eliminating the functions of both of these signaling molecules. |
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