SPRED proteins provide a NF-ty link to Ras suppression

被引:9
作者
McClatchey, Andrea I. [1 ]
Cichowski, Karen [2 ,3 ,4 ]
机构
[1] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Canc Res,Dept Pathol, Charlestown, MA 02129 USA
[2] Brigham & Womens Hosp, Dept Med, Div Genet, Boston, MA 02115 USA
[3] Harvard Univ, Sch Med, Boston, MA 02115 USA
[4] Harvard Canc Ctr, Ludwig Ctr Dana Farber, Boston, MA 02115 USA
关键词
Legius syndrome; NF1; signal transduction; Ras/MAPK; Sprouty; NEUROFIBROMATOSIS TYPE-1 PROTEIN; TUMOR-SUPPRESSOR; LEGIUS SYNDROME; SPROUTY; PHENOTYPE; GAP; ACTIVATION; MUTATIONS; MECHANISM; GENOTYPE;
D O I
10.1101/gad.197434.112
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Mutations in the SPRED1 (Sprouty-related protein with an EVH [Ena/Vasp homology] domain 1) and NF1 (neurofibromatosis 1) genes underlie clinically related human disorders. The NF1-encoded protein neurofibromin is a Ras GTPase-activating protein (GAP) and can directly limit Ras activity. Spred proteins also negatively regulate Ras signaling, but the mechanism by which they do so is not clear. In the July 1, 2012, issue of Genes & Development, Stowe and colleagues (pp. 1421-1426) present evidence that Spred1 recruits neurofibromin to the membrane, where it dampens growth factor-induced Ras activity, providing a satisfying explanation for the overlapping features of two human diseases.
引用
收藏
页码:1515 / 1519
页数:5
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