Diverse biochemical properties of Shp2 mutants. Implications for disease phenotypes. - Wikidata - wikimedia - TriplyDB

Diverse biochemical properties of Shp2 mutants. Implications for disease phenotypes.

Diverse biochemical properties of Shp2 mutants. Implications for disease phenotypes.

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Function, regulation and pathological roles of the Gab/DOS docking proteins Germline missense mutations affecting KRAS Isoform B are associated with a severe Noonan syndrome phenotype Functional effects of PTPN11 (SHP2) mutations causing LEOPARD syndrome on epidermal growth factor-induced phosphoinositide 3-kinase/AKT/glycogen synthase kinase 3beta signaling Reduced phosphatase activity of SHP-2 in LEOPARD syndrome: consequences for PI3K binding on Gab1 Diversity and functional consequences of germline and somatic PTPN11 mutations in human disease.The RASopathies: developmental syndromes of Ras/MAPK pathway dysregulation Leukemia-associated, constitutively active mutants of SHP2 protein tyrosine phosphatase inhibit NF1 transcriptional activation by the interferon consensus sequence binding protein RASopathies: unraveling mechanisms with animal models Structure and function of Gab2 and its role in cancer (Review)Connecting teratogen-induced congenital heart defects to neural crest cells and their effect on cardiac function The RASopathies The neural crest in cardiac congenital anomalies Shp2 knockdown and Noonan/LEOPARD mutant Shp2-induced gastrulation defects Structural and Mechanistic Insights into LEOPARD Syndrome-Associated SHP2 Mutations Molecular Basis of Gain-of-Function LEOPARD Syndrome-Associated SHP2 Mutations Germline gain-of-function mutations in SOS1 cause Noonan syndrome PTPN11 (Shp2) mutations in LEOPARD syndrome have dominant negative, not activating, effects Germline KRAS mutations cause Noonan syndrome Stops along the RAS pathway in human genetic disease Differential biological activity of disease-associated JAK2 mutants SHP-2 is a novel target of Abl kinases during cell proliferation.Evolutionary constraint and disease associations of post-translational modification sites in human genomes Structural, Functional, and Clinical Characterization of a Novel PTPN11 Mutation Cluster Underlying Noonan Syndrome Ras oncogenes: split personalities Aberrant neuronal activity-induced signaling and gene expression in a mouse model of RASopathy.Control of CNS cell-fate decisions by SHP-2 and its dysregulation in Noonan syndrome Tyr66 acts as a conformational switch in the closed-to-open transition of the SHP-2 N-SH2-domain phosphotyrosine-peptide binding cleft.Genome-wide prediction of SH2 domain targets using structural information and the FoldX algorithm.Kinase-activating and kinase-impaired cardio-facio-cutaneous syndrome alleles have activity during zebrafish development and are sensitive to small molecule inhibitors.Structural insights into Noonan/LEOPARD syndrome-related mutants of protein-tyrosine phosphatase SHP2 (PTPN11)Critical Role for GAB2 in Neuroblastoma Pathogenesis through the Promotion of SHP2/MYCN Cooperation.Germline BRAF mutations in Noonan, LEOPARD, and cardiofaciocutaneous syndromes: molecular diversity and associated phenotypic spectrum Inhibition of the Gab2/PI3K/mTOR signaling ameliorates myeloid malignancy caused by Ptpn11 (Shp2) gain-of-function mutations.Noonan syndrome: clinical aspects and molecular pathogenesis.Diverse driving forces underlie the invariant occurrence of the T42A, E139D, I282V and T468M SHP2 amino acid substitutions causing Noonan and LEOPARD syndromes Inhibition of cellular Shp2 activity by a methyl ester analog of SPI-112.SHP2E76K mutant promotes lung tumorigenesis in transgenic mice Identification of cryptotanshinone as an inhibitor of oncogenic protein tyrosine phosphatase SHP2 (PTPN11).Structure-energy-based predictions and network modelling of RASopathy and cancer missense mutations A germline gain-of-function mutation in Ptpn11 (Shp-2) phosphatase induces myeloproliferative disease by aberrant activation of hematopoietic stem cells.

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Diverse biochemical properties of Shp2 mutants. Implications for disease phenotypes.

http://www.wikidata.org/entity/Q42480603

description

2005 nî lūn-bûn

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2005年論文

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2005年论文

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2005年论文

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2005年论文

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name

Diverse biochemical properties of Shp2 mutants. Implications for disease phenotypes.

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Diverse biochemical properties of Shp2 mutants. Implications for disease phenotypes.

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type

label

Diverse biochemical properties of Shp2 mutants. Implications for disease phenotypes.

@en

Diverse biochemical properties of Shp2 mutants. Implications for disease phenotypes.

@nl

prefLabel

Diverse biochemical properties of Shp2 mutants. Implications for disease phenotypes.

@en

Diverse biochemical properties of Shp2 mutants. Implications for disease phenotypes.

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Journal of Biological Chemistry

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Diverse biochemical properties of Shp2 mutants. Implications for disease phenotypes.

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Benjamin G Neel

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Frank S David

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Heike Keilhack

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Lewis C Cantley

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Malcolm McGregor

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P2860

Molecular basis for the dephosphorylation of the activation segment of the insulin receptor by protein tyrosine phosphatase 1B

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

The 64-kDa protein that associates with the platelet-derived growth factor receptor beta subunit via Tyr-1009 is the SH2-containing phosphotyrosine phosphatase Syp

Spatial constraints on the recognition of phosphoproteins by the tandem SH2 domains of the phosphatase SH-PTP2

Crystal structures of peptide complexes of the amino-terminal SH2 domain of the Syp tyrosine phosphatase

Crystal structure of the tyrosine phosphatase SHP-2

Visualization of the cysteinyl-phosphate intermediate of a protein-tyrosine phosphatase by x-ray crystallography

Protein folding and association: insights from the interfacial and thermodynamic properties of hydrocarbons

Tyrosyl phosphorylation of Shp2 is required for normal ERK activation in response to some, but not all, growth factors

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

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10.1074/JBC.M504699200

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35

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280

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