Abstract
Noonan syndrome, a developmental disorder characterized by congenital heart defects, reduced growth, facial dysmorphism and variable cognitive deficits, is caused by constitutional dysregulation of the RAS-MAPK signaling pathway. Here we report that germline NRAS mutations conferring enhanced stimulus-dependent MAPK activation account for some cases of this disorder. These findings provide evidence for an obligate dependency on proper NRAS function in human development and growth.
Publication types
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Case Reports
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Research Support, Non-U.S. Gov't
MeSH terms
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Adolescent
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Amino Acid Sequence
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Animals
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Base Sequence
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COS Cells
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Child
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Child, Preschool
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Chlorocebus aethiops
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DNA Mutational Analysis
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Female
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Genes, ras*
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Humans
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Male
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Middle Aged
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Mitogen-Activated Protein Kinases / metabolism
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Models, Molecular
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Molecular Sequence Data
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Mutation*
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Noonan Syndrome / genetics*
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Noonan Syndrome / metabolism
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Noonan Syndrome / pathology
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Phosphorylation
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Protein Structure, Tertiary
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Sequence Homology, Amino Acid
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Transfection
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Young Adult
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ras Proteins / chemistry
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ras Proteins / genetics*
Substances
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Mitogen-Activated Protein Kinases
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ras Proteins