Reduced phosphatase activity of SHP-2 in LEOPARD syndrome: consequences for PI3K binding on Gab1 (Q24321087)

Michel Vidal

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Wen Hwa Lee

Wen Hwa Lee

3

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Alexandra Montagner

Alexandra Montagner

2

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Maria A Miteva

Maria Miteva

4

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author name string

Michel Vidaud

6

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Béatrice Parfait

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Patrick Raynal

Grouping of multiple-lentigines/LEOPARD and Noonan syndromes on the PTPN11 gene

8

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language of work or name

English

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publication date

1 May 2006

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published in

FEBS Letters

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volume

580

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issue

10

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page(s)

2477-82

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cites work

1 reference

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Mutations in PTPN11, encoding the protein tyrosine phosphatase SHP-2, cause Noonan syndrome

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Somatic mutations in PTPN11 in juvenile myelomonocytic leukemia, myelodysplastic syndromes and acute myeloid leukemia

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The 'Shp'ing news: SH2 domain-containing tyrosine phosphatases in cell signaling

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A novel role for Gab1 and SHP2 in epidermal growth factor-induced Ras activation

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Receptor-specific regulation of phosphatidylinositol 3'-kinase activation by the protein tyrosine phosphatase Shp2.

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Diversity and functional consequences of germline and somatic PTPN11 mutations in human disease

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Diverse biochemical properties of Shp2 mutants. Implications for disease phenotypes

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Noonan syndrome-associated SHP2/PTPN11 mutants cause EGF-dependent prolonged GAB1 binding and sustained ERK2/MAPK1 activation

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Crystal structure of the tyrosine phosphatase SHP-2

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Noonan syndrome type I with PTPN11 3 bp deletion: structure-function implications.

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Phosphotyrosines 627 and 659 of Gab1 constitute a bisphosphoryl tyrosine-based activation motif (BTAM) conferring binding and activation of SHP2

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A critical role for phosphoinositide 3-kinase upstream of Gab1 and SHP2 in the activation of ras and mitogen-activated protein kinases by epidermal growth factor.

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PTPN11 (Shp2) mutations in LEOPARD syndrome have dominant negative, not activating, effects

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