Search results for "GAS6"

showing 3 items of 3 documents

GAS6

2017

Venous thrombosis is determined by the recruitment of monocytes and neutrophils to the inflamed endothelium and is primarily influenced by the plasmatic coagulation system.1 Monocyte tissue factor (TF) was identified as the causative trigger for intraluminal fibrin formation and thrombus load in the inferior vena cava (IVC) stenosis model, resembling human deep vein thrombosis.1 Although monocyte TF is prothrombotic, the TF expressed by activated endothelial cells triggers proinflammatory protease-activated receptor signaling pathways.2,3 See accompanying article on page 1315 In the past years, GAS6 (growth arrest–specific gene-6) was described as a major regulatory protein of prothrombotic…

0301 basic medicineEndotheliumVena Cava Inferior030204 cardiovascular system & hematologyFibrinogenInferior vena cavaMonocytes03 medical and health sciencesTissue factor0302 clinical medicinemedicineHumansPlateletThrombusVenous ThrombosisGAS6business.industryImpaired platelet aggregationmedicine.disease030104 developmental biologymedicine.anatomical_structuremedicine.veinAnesthesiaCancer researchCardiology and Cardiovascular MedicinebusinessGasolinemedicine.drugArteriosclerosis, Thrombosis, and Vascular Biology
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Reply to ‘Genetic and clinical data reinforce the role of GAS6 and TAM receptors in liver fibrosis’

2016

Proto-Oncogene ProteinHepatologyCirrosis hepaticaTam receptorsGAS6business.industryLiver CirrhosiLiver fibrosisReceptor Protein-Tyrosine KinasesReceptor Protein-Tyrosine Kinases03 medical and health sciences0302 clinical medicine030220 oncology & carcinogenesisIntercellular Signaling Peptides and ProteinCancer researchMedicine030211 gastroenterology & hepatologyProto-Oncogene ProteinsbusinessHumanJournal of Hepatology
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MERTK rs4374383 polymorphism affects the severity of fibrosis in non-alcoholic fatty liver disease

2015

Background & Aim Homozygosity for a common non-coding rs4374383 G>A polymorphism in MERTK (myeloid-epithelial-reproductive tyrosine kinase) has been associated with the protection against fibrosis progression in chronic hepatitis C. The main study objective was to assess whether MERTK AA genotype influences liver fibrosis, and secondarily MERTK expression in patients with non-alcoholic fatty liver disease (NAFLD). We also investigated whether MERTK is expressed in human hepatic stellate cells (HSC) and in murine models of fibrogenesis. Methods We considered 533 consecutive patients who underwent liver biopsy for suspected non-alcoholic steatohepatitis (NASH) without severe obesity from two …

Liver CirrhosisMale0301 basic medicineMessengerMice0302 clinical medicineNon-alcoholic Fatty Liver DiseaseFibrosisInbred BALB CCells CulturedMice Inbred BALB CCulturedmedicine.diagnostic_testMedicine (all)Fatty liverNASHMiddle AgedLiver biopsyFemale030211 gastroenterology & hepatologyAdultmedicine.medical_specialtyMERTKCellsBiology03 medical and health sciencesGeneticProto-Oncogene ProteinsInternal medicinemedicineAnimalsHumansFibrosis; MERTK; NASH; Adult; Animals; Cells Cultured; Female; Humans; Liver Cirrhosis; Male; Mice Inbred BALB C; Middle Aged; Non-alcoholic Fatty Liver Disease; Proto-Oncogene Proteins; RNA Messenger; Receptor Protein-Tyrosine Kinases; Polymorphism Genetic; Medicine (all); HepatologyRNA MessengerPolymorphismPolymorphism Geneticc-Mer Tyrosine KinaseHepatologyGAS6Receptor Protein-Tyrosine Kinasesnafld fibrosis mertkMERTKHepatologymedicine.diseaseFibrosis030104 developmental biologyImmunologyHepatic stellate cellRNASteatohepatitisJournal of Hepatology
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