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• W2121315227 abstract "The Ras/mitogen-activated protein kinase (MAPK) pathway plays a critical role in transducing mitogenic signals from receptor tyrosine kinases. Loss-of-function mutations in one feedback regulator of Ras/MAPK signaling, SPRED1 (Sprouty-related protein with an EVH1 domain), cause Legius syndrome, an autosomal dominant human disorder that resembles Neurofibromatosis-1 (NF1). Spred1 functions as a negative regulator of the Ras/MAPK pathway; however, the underlying molecular mechanism is poorly understood. Here we show that neurofibromin, the NF1 gene product, is a Spred1-interacting protein that is necessary for Spred1's inhibitory function. We show that Spred1 binding induces the plasma membrane localization of NF1, which subsequently down-regulates Ras-GTP levels. This novel mechanism for the regulation of neurofibromin provides a molecular bridge for understanding the overlapping pathophysiology of NF1 and Legius syndrome." @default.
• W2121315227 created "2016-06-24" @default.
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• W2121315227 date "2012-07-01" @default.
• W2121315227 modified "2023-10-16" @default.
• W2121315227 title "A shared molecular mechanism underlies the human rasopathies Legius syndrome and Neurofibromatosis-1" @default.
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• W2121315227 doi "https://doi.org/10.1101/gad.190876.112" @default.
• W2121315227 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3403010" @default.
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• W2121315227 hasPublicationYear "2012" @default.
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