Increased BRAF heterodimerization is the common pathogenic mechanism for noonan syndrome-associated RAF1 mutants

Molecular and Cellular Biology

Volumn 32, Issue 19, 2012, Pages 3872-3890

  Wu, Xue ^a,b   Yin, Jiani ^b   Simpson, Jeremy ^d   Kim, Kyoung Han ^c,e   Gu, Shengqing ^a,b   Hong, Jenny H ^a   Bayliss, Peter ^b   Backx, Peter H ^c   Neel, Benjamin G ^a,b   Araki, Toshiyuki ^b  

^a UNIVERSITY OF TORONTO   (Canada)

^b PRINCESS MARGARET HOSPITAL   (Canada)

^c UNIVERSITY OF TORONTO   (Canada)

^d UNIVERSITY OF GUELPH   (Canada)

^e HOSPITAL FOR SICK CHILDREN   (Canada)

Author keywords

[No Author keywords available]

Indexed keywords

B RAF KINASE; MITOGEN ACTIVATED PROTEIN KINASE; PROTEIN SERINE THREONINE KINASE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CONGENITAL HEART DISEASE; CONTROLLED STUDY; DIMERIZATION; FACE DYSMORPHIA; FEMALE; GENE FREQUENCY; GROWTH DISORDER; HEART HYPERTROPHY; MALE; MOUSE; MUTANT; NONHUMAN; NOONAN SYNDROME; PATHOGENESIS; PRIORITY JOURNAL; SHORT STATURE;

ANIMALS; CELLS, CULTURED; ENZYME ACTIVATION; FEMALE; GENE KNOCK-IN TECHNIQUES; HUMANS; MALE; MAP KINASE SIGNALING SYSTEM; MICE; MICE, INBRED C57BL; MODELS, MOLECULAR; MUTAGENESIS, SITE-DIRECTED; NOONAN SYNDROME; PHENOTYPE; POINT MUTATION; PROTEIN MULTIMERIZATION; PROTO-ONCOGENE PROTEINS B-RAF; PROTO-ONCOGENE PROTEINS C-RAF;

MUS;

EID: 84868713216     PISSN: 02707306     EISSN: 10985549     Source Type: Journal    
DOI: 10.1128/MCB.00751-12     Document Type: Article

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