Mutation of juxtamembrane tyrosine residue 1001 suppresses loss-of-function mutations of the met receptor in epithelial cells.
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Use of signal specific receptor tyrosine kinase oncoproteins reveals that pathways downstream from Grb2 or Shc are sufficient for cell transformation and metastasisHepatocyte growth factor receptor tyrosine kinase met is a substrate of the receptor protein-tyrosine phosphatase DEP-1The Gab1 PH domain is required for localization of Gab1 at sites of cell-cell contact and epithelial morphogenesis downstream from the met receptor tyrosine kinaseThe MET axis as a therapeutic target.Essential role of Gab1 for signaling by the c-Met receptor in vivoMet receptor tyrosine kinase: enhanced signaling through adapter proteinsCoupling of Gab1 to c-Met, Grb2, and Shp2 mediates biological responsesGab3, a new DOS/Gab family member, facilitates macrophage differentiation.Expression of c-Met in developing rat hippocampus: evidence for HGF as a neurotrophic factor for calbindin D-expressing neurons.Disassociation of met-mediated biological responses in vivo: the natural hepatocyte growth factor/scatter factor splice variant NK2 antagonizes growth but facilitates metastasis.Suppression of Ras-mediated tumorigenicity and metastasis through inhibition of the Met receptor tyrosine kinaseEnhanced transformation by a plasma membrane-associated met oncoprotein: activation of a phosphoinositide 3'-kinase-dependent autocrine loop involving hyaluronic acid and CD44.Exocyst is involved in cystogenesis and tubulogenesis and acts by modulating synthesis and delivery of basolateral plasma membrane and secretory proteinsThe role of the c-Met pathway in lung cancer and the potential for targeted therapy.Sequential requirement of hepatocyte growth factor and neuregulin in the morphogenesis and differentiation of the mammary gland.Motogenic and morphogenic activity of epithelial receptor tyrosine kinases.Degradation of the Met tyrosine kinase receptor by the ubiquitin-proteasome pathwayFrom Tpr-Met to Met, tumorigenesis and tubes.The multisubstrate docking site of the MET receptor is dispensable for MET-mediated RAS signaling and cell scattering.Down-regulation of the met receptor tyrosine kinase by presenilin-dependent regulated intramembrane proteolysis.MET as a target for treatment of chest tumorsInhibition of neoplastic development in the liver by hepatocyte growth factor in a transgenic mouse model.Positive and negative tissue-specific signaling by a nematode epidermal growth factor receptor.MET exon 14 juxtamembrane splicing mutations: clinical and therapeutical perspectives for cancer therapy.Hepatocyte growth factor in lung repair and pulmonary fibrosis.MET: a new promising biomarker in non-small-cell lung carcinoma.Exon 14 Deleted MET Receptor as a New Biomarker and Target in Cancers.Amplification of apoptosis through sequential caspase cleavage of the MET tyrosine kinase receptor.Proapoptotic function of the MET tyrosine kinase receptor through caspase cleavage.A conserved DpYR motif in the juxtamembrane domain of the Met receptor family forms an atypical c-Cbl/Cbl-b tyrosine kinase binding domain binding site required for suppression of oncogenic activation.Potent blockade of hepatocyte growth factor-stimulated cell motility, matrix invasion and branching morphogenesis by antagonists of Grb2 Src homology 2 domain interactions.Loss of the exon encoding the juxtamembrane domain is essential for the oncogenic activation of TPR-MET.Branching tubulogenesis but not scatter of madin-darby canine kidney cells requires a functional Grb2 binding site in the Met receptor tyrosine kinase.Effect of Mini-Tyrosyl-tRNA Synthetase/Mini-Tryptophanyl-tRNA Synthetase on Angiogenesis in Rhesus Monkeys after Acute Myocardial Infarction.The proto-oncogene c-Cbl is a positive regulator of Met-induced MAP kinase activation: a role for the adaptor protein Crk.Protein tyrosine phosphatase PTP-S binds to the juxtamembrane region of the hepatocyte growth factor receptor Met.Reconstitution of mammary gland development in vitro: requirement of c-met and c-erbB2 signaling for branching and alveolar morphogenesis.Activating mutations in the Met receptor overcome the requirement for autophosphorylation of tyrosines crucial for wild type signaling.Structural basis of oncogenic activation caused by point mutations in the kinase domain of the MET proto-oncogene: modeling studies.Hepatocyte growth factor/scatter factor activates proliferation in melanoma cells through p38 MAPK, ATF-2 and cyclin D1.
P2860
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P2860
Mutation of juxtamembrane tyrosine residue 1001 suppresses loss-of-function mutations of the met receptor in epithelial cells.
description
1995 nî lūn-bûn
@nan
1995 թուականի Մարտին հրատարակուած գիտական յօդուած
@hyw
1995 թվականի մարտին հրատարակված գիտական հոդված
@hy
1995年の論文
@ja
1995年論文
@yue
1995年論文
@zh-hant
1995年論文
@zh-hk
1995年論文
@zh-mo
1995年論文
@zh-tw
1995年论文
@wuu
name
Mutation of juxtamembrane tyro ...... receptor in epithelial cells.
@ast
Mutation of juxtamembrane tyro ...... receptor in epithelial cells.
@en
Mutation of juxtamembrane tyro ...... receptor in epithelial cells.
@nl
type
label
Mutation of juxtamembrane tyro ...... receptor in epithelial cells.
@ast
Mutation of juxtamembrane tyro ...... receptor in epithelial cells.
@en
Mutation of juxtamembrane tyro ...... receptor in epithelial cells.
@nl
prefLabel
Mutation of juxtamembrane tyro ...... receptor in epithelial cells.
@ast
Mutation of juxtamembrane tyro ...... receptor in epithelial cells.
@en
Mutation of juxtamembrane tyro ...... receptor in epithelial cells.
@nl
P2093
P2860
P356
P1476
Mutation of juxtamembrane tyro ...... t receptor in epithelial cells
@en
P2093
K M Weidner
W Birchmeier
P2860
P304
P356
10.1073/PNAS.92.7.2597
P407
P577
1995-03-01T00:00:00Z