Search results for "Hepatocyte Growth Factor Receptor"

showing 5 items of 5 documents

Dual Constant Domain-Fab: A novel strategy to improve half-life and potency of a Met therapeutic antibody

2016

The kinase receptor encoded by the Met oncogene is a sensible target for cancer therapy. The chimeric monovalent Fab fragment of the DN30 monoclonal antibody (MvDN30) has an odd mechanism of action, based on cell surface removal of Met via activation of specific plasma membrane proteases. However, the short half-life of the Fab, due to its low molecular weight, is a severe limitation for the deployment in therapy. This issue was addressed by increasing the Fab molecular weight above the glomerular filtration threshold through the duplication of the constant domains, in tandem (DCD-1) or reciprocally swapped (DCD-2). The two newly engineered molecules showed biochemical properties comparable…

0301 basic medicineCancer ResearchMice SCIDCancer targeted therapy0302 clinical medicineMice Inbred NODEpidermal growth factor receptorPhosphorylationbiologyChemistryImmunoglobulin Fab FragmentsAntibodies MonoclonalGeneral MedicineArticlesProto-Oncogene Proteins c-metHalf-lifeCell biologyOncology030220 oncology & carcinogenesisColonic NeoplasmsMetMolecular MedicineFemalemedicine.symptomSignal transductionAntibodySignal Transductionmedicine.drug_classColonAntibody; Cancer targeted therapy; Fab; Half-life; Met; Protein engineering; Cancer Research; Genetics; Molecular MedicineAntineoplastic AgentsMonoclonal antibody03 medical and health sciencesImmunoglobulin Fab FragmentsProtein DomainsCell Line TumormedicineGeneticsAnimalsHumansFabAntibodyCell growthMolecular biology030104 developmental biologyHEK293 CellsMechanism of actionHepatocyte Growth Factor ReceptorA549 Cellsbiology.proteinProtein engineering
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MET/HGF Co-Targeting in Pancreatic Cancer: A Tool to Provide Insight into the Tumor/Stroma Crosstalk

2018

The ‘onco-receptor’ MET (Hepatocyte Growth Factor Receptor) is involved in the activation of the invasive growth program that is essential during embryonic development and critical for wound healing and organ regeneration during adult life. When aberrantly activated, MET and its stroma-secreted ligand HGF (Hepatocyte Growth Factor) concur to tumor onset, progression, and metastasis in solid tumors, thus representing a relevant target for cancer precision medicine. In the vast majority of tumors, wild-type MET behaves as a ‘stress-response’ gene, and relies on ligand stimulation to sustain cancer cell ‘scattering’, invasion, and protection form apoptosis. …

0301 basic medicineStromal cellpancreatic cancerReviewHGF; MET; Metastasis; Pancreatic cancer; Target therapy; Tumor microenvironment; Animals; Hepatocyte Growth Factor; Humans; Neoplasm Metastasis; Pancreatic Neoplasms; Proto-Oncogene Proteins c-metCatalysisMetastasisInorganic Chemistrylcsh:Chemistry03 medical and health sciences0302 clinical medicinePancreatic cancermedicineAnimalsHumansmetastasistumor microenvironmentHGFPhysical and Theoretical ChemistryNeoplasm MetastasisMolecular Biologylcsh:QH301-705.5SpectroscopyTumor microenvironmentbusiness.industryHepatocyte Growth Factortarget therapyOrganic ChemistryGeneral MedicineProto-Oncogene Proteins c-metmedicine.diseaseComputer Science ApplicationsPancreatic Neoplasms030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Tumor progressionHepatocyte Growth Factor Receptor030220 oncology & carcinogenesisCancer cellCancer researchMETHepatocyte growth factorbusinessmedicine.drugInternational Journal of Molecular Sciences
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Thiocarbamate-Linked Polysulfonate–Peptide Conjugates As Selective Hepatocyte Growth Factor Receptor Binders

2014

The capacity of many proteins to interact with natural or synthetic polyanions has been exploited for modulating their biological action. However, the polydispersity of these macromolecular polyanions as well as their poor specificity is a severe limitation to their use as drugs. An emerging trend in this field is the synthesis of homogeneous and well-defined polyanion–peptide conjugates, which act as bivalent ligands, with the peptide part bringing the selectivity of the scaffold. Alternately, this strategy can be used for improving the binding of short peptides to polyanion-binding protein targets. This work describes the design and first synthesis of homogeneous polysulfonate–peptide con…

DendrimersBiomedical EngineeringPharmaceutical ScienceBioengineeringPeptidemacromolecular substancesPlasma protein bindingArticleReceptor tyrosine kinaseSubstrate SpecificityStructure-Activity RelationshipThiocarbamatesmedicineHumansStructure–activity relationshipPharmacologychemistry.chemical_classificationDose-Response Relationship DrugMolecular StructurebiologyHepatocyte Growth FactorChemistryOrganic Chemistrytechnology industry and agricultureProto-Oncogene Proteins c-metProtein Structure TertiaryThiocarbamateBiochemistryHepatocyte Growth Factor ReceptorProto-Oncogene Proteins c-metbiology.proteinHepatocyte growth factorSulfonic AcidsPeptidesProtein BindingBiotechnologymedicine.drugBioconjugate Chemistry
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Chronic lymphocytic leukemia nurse-like cells express hepatocyte growth factor receptor (c-MET) and indoleamine 2,3-dioxygenase and display features …

2014

Hepatocyte growth factor, produced by stromal and follicular dendritic cells, and present at high concentrations in the sera of patients with chronic lymphocytic leukemia, prolongs the survival of leukemic B cells by interacting with their receptor, c-MET. It is, however, unknown whether hepatocyte growth factor influences microenvironmental cells, such as nurse-like cells, which deliver survival signals to the leukemic clone. We evaluated the expression of c-MET on nurse-like cells and monocytes from patients with chronic lymphocytic leukemia and searched for phenotypic/functional features supposed to be influenced by the hepatocyte growth factor/c-MET interaction. c-MET is expressed at hi…

STAT3 Transcription FactorC-MetStromal cellmedicine.medical_treatmentGene ExpressionBiologyMonocyteschemistry.chemical_compoundT-Lymphocyte SubsetsmedicineHumansIndoleamine-Pyrrole 23-DioxygenaseGrowth factor receptor inhibitorPhosphorylationIndoleamine 23-dioxygenaseCells CulturedFollicular dendritic cellsMacrophagesGrowth factorArticlesHematologyProto-Oncogene Proteins c-metLeukemia Lymphocytic Chronic B-CellCoculture TechniquesInterleukin-10C-MET; INDOLEAMINE 23-DIOXYGENASEchronic lymphocytic leukemia hepatocyte growth factor c-MET nurse-like cellshepatocyte growth factornurse-like cellschemistryHepatocyte Growth Factor ReceptorCancer researchchronic lymphocytic leukemiaHepatocyte growth factorC-METINDOLEAMINE 23-DIOXYGENASEmedicine.drugHaematologica
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Getting the Fat out of Met and Fas

2008

Lack of Fas antagonism by Met in human fatty liver disease. Zou C, Ma J, Wang X, Guo L, Zhu Z, Stoops J, Eaker AE, Johnson CJ, Strom S, Michalopoulos GK, DeFrances MC, Zarnegar R. Hepatocytes in fatty livers are hypersensitive to apoptosis and undergo escalated apoptotic activity via death receptor-mediated pathways, particularly that of Fas–FasL, causing hepatic injury that can eventually proceed to cirrhosis and end-stage liver disease. Here we report that the hepatocyte growth factor receptor, Met, plays an important part in preventing Fas-mediated apoptosis of hepatocytes by sequestering Fas. We also show that Fas antagonism by Met is abrogated in human fatty liver disease (FLD). Throug…

medicine.medical_specialtyCirrhosisHepatologyFatty liverBiologymedicine.diseaseMolecular biologyFas ligandLiver diseaseEndocrinologyHepatocyte Growth Factor ReceptorApoptosisInternal medicinemedicineExtracellularAntagonismJournal of Hepatology
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