A shared molecular mechanism underlies the human rasopathies Legius syndrome and Neurofibromatosis-1

Genes and Development

Volumn 26, Issue 13, 2012, Pages 1421-1426

  Stowe, Irma B ^a   Mercado, Ellen L ^a   Stowe, Timothy R ^b   Bell, Erika L ^a   Oses Prieto, Juan A ^c   Hernández, Hilda ^c   Burlingame, Alma L ^c   McCormick, Frank ^a  

^a UNIVERSITY OF CALIFORNIA   (United States)

^b UNIVERSITY OF CALIFORNIA   (United States)

^c UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

Legius syndrome; NF1; Ras MAPK; Signal transduction; Sprouty

Indexed keywords

EPIDERMAL GROWTH FACTOR; FIBROBLAST GROWTH FACTOR; MITOGEN ACTIVATED PROTEIN KINASE; NEUROFIBROMIN; NUCLEAR FACTOR I; PROTEIN SPRED1; RAS PROTEIN; SPROUTY PROTEIN; UNCLASSIFIED DRUG;

ARTICLE; CELL MEMBRANE; DEVELOPMENTAL DISORDER; DISEASE ASSOCIATION; DOWN REGULATION; ENZYME ACTIVATION; HUMAN; LEGIUS SYNDROME; LOSS OF FUNCTION MUTATION; MOLECULAR DYNAMICS; NEUROFIBROMATOSIS; PRIORITY JOURNAL; PROTEIN BINDING; PROTEIN EXPRESSION; PROTEIN FUNCTION; PROTEIN INTERACTION; PROTEIN LOCALIZATION; SIGNAL TRANSDUCTION;

ANIMALS; CAFE-AU-LAIT SPOTS; CELLS, CULTURED; HUMANS; INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS; MAP KINASE SIGNALING SYSTEM; MEMBRANE PROTEINS; MICE; NEUROFIBROMATOSIS 1; NEUROFIBROMIN 1; PROTEIN BINDING; REPRESSOR PROTEINS;

EID: 84863643200     PISSN: 08909369     EISSN: 15495477     Source Type: Journal    
DOI: 10.1101/gad.190876.112     Document Type: Article

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