Search results for "Teas"

showing 10 items of 619 documents

The Role of Osteoprotegerin and Its Ligands in Vascular Function

2019

International audience; The superfamily of tumor necrosis factor (TNF) receptors includes osteoprotegerin (OPG) and its ligands, which are receptor activators of nuclear factor kappa-B ligand (RANKL) and TNF-related apoptosis-inducing ligand (TRAIL). The OPG/RANKL/RANK system plays an active role in pathological angiogenesis and inflammation as well as cell survival. It has been demonstrated that there is crosstalk between endothelial cells and osteoblasts during osteogenesis, thus establishing a connection between angiogenesis and osteogenesis. This OPG/RANKL/RANK/TRAIL system acts on specific cell surface receptors, which are then able to transmit their signals to other intracellular comp…

0301 basic medicineAngiogenesismedicine.medical_treatmentReview030204 cardiovascular system & hematologyLigandslcsh:ChemistryTNF-Related Apoptosis-Inducing Ligand0302 clinical medicineReceptorlcsh:QH301-705.5Cellular SenescenceSpectroscopyReceptor Activator of Nuclear Factor-kappa BbiologyChemistryvascular diseaseGeneral MedicineComputer Science ApplicationsProtein Transportmedicine.anatomical_structureCytokineRANKLTumor necrosis factor alphaDisease Susceptibilitymedicine.symptomProtein BindingSignal Transductionmusculoskeletal diseasesProteasome Endopeptidase ComplexEndotheliumendotheliumNeovascularization PhysiologicInflammationCatalysisInorganic ChemistryStructure-Activity Relationship03 medical and health sciencesOsteoprotegerin[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemmedicineAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyMyocardiumRANK LigandOrganic ChemistryEndothelial Cells030104 developmental biologylcsh:Biology (General)lcsh:QD1-999osteoprotegerinOPG/RANKL/RANKCancer researchbiology.proteinBlood VesselsBiomarkers
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Proteases, Protease-Activated Receptors, and Atherosclerosis

2018

Coagulation activation by the TF (tissue factor) pathway plays pivotal roles in triggering platelets and precipitating acute coronary syndromes. Although dual antiplatelet therapy is effective in secondary cardiovascular prevention, combining platelet antagonism with low-dose aspirin and the oral coagulation FXa antagonist rivaroxaban has a synergistic clinical benefit over monotherapy in preventing the composite outcome of cardiovascular death, stroke, or myocardial infarction.1 It is, therefore, of considerable interest to understand the roles of coagulation proteases and their cell signaling effects in the development of atherosclerosis and vascular inflammation. Acute thrombosis in anim…

0301 basic medicineApolipoprotein EProteasesReceptors Proteinase-Activated030204 cardiovascular system & hematologyArticleMice03 medical and health sciencesTissue factor0302 clinical medicineThrombinEndopeptidasesAnimalsReceptor PAR-2MedicinePlateletbusiness.industryArteriosclerosisAtherosclerosismedicine.diseaseThrombosis030104 developmental biologyCoagulationCancer researchCardiology and Cardiovascular MedicinebusinessPeptide Hydrolasesmedicine.drugArteriosclerosis, Thrombosis, and Vascular Biology
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Ubiquitin-Dependent And Independent Signals In Selective Autophagy.

2015

Selective autophagy regulates the abundance of specific cellular components via a specialized arsenal of factors, termed autophagy receptors, that target protein complexes, aggregates, and whole organelles into lysosomes. Autophagy receptors bind to LC3/GABARAP proteins on phagophore and autophagosome membranes, and recognize signals on cargoes to deliver them to autophagy. Ubiquitin (Ub), a well-known signal for the degradation of polypeptides in the proteasome, also plays an important role in the recognition of cargoes destined for selective autophagy. In addition, a variety of cargoes are committed to selective autophagy pathways by Ub-independent mechanisms employing protein-protein int…

0301 basic medicineAutophagosomebiologyUbiquitinGABARAPAutophagyUbiquitinationCell BiologyBAG3BioinformaticsCell biology03 medical and health sciences030104 developmental biologyProteasomeUbiquitinProteolysisbiology.proteinAutophagyAnimalsHumansTarget proteinATG16L1Signal TransductionTrends in cell biology
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The receptor protein tyrosine phosphatase PTPRJ negatively modulates the CD98hc oncoprotein in lung cancer cells.

2018

PTPRJ, a receptor protein tyrosine phosphatase strongly downregulated in human cancer, displays tumor suppressor activity by negatively modulating several proteins involved in proliferating signals. Here, through a proteomic-based approach, we identified a list of potential PTPRJ-interacting proteins and among them we focused on CD98hc, a type II glycosylated integral membrane protein encoded by SLC3A2, corresponding to the heavy chain of a heterodimeric transmembrane amino-acid transporter, including LAT1. CD98hc is widely overexpressed in several types of cancers and contributes to the process of tumorigenesis by interfering with cell proliferation, adhesion, and migration. We first valid…

0301 basic medicineCD98hcChemistryCell growthCellPTPRJProtein tyrosine phosphatasemedicine.disease_causeProtein tyrosine phosphatase03 medical and health scienceschemistry.chemical_compound030104 developmental biologymedicine.anatomical_structureProteasomal degradationOncologyMG132Cancer cellCancer researchmedicineProteasome inhibitorGene silencingLung cancerCarcinogenesismedicine.drugResearch Paper
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Comment on “Endothelial Protein C Receptor (EPCR), Protease Activated Receptor-1 (PAR-1) and Their Interplay in Cancer Growth and Metastatic Dissemin…

2019

Although the interplay between tumor progression and blood coagulation has been recognized [...]

0301 basic medicineCancer ResearchEndothelial protein C receptorChemistryCancermedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenslcsh:RC254-28203 medical and health sciences030104 developmental biology0302 clinical medicineProtease-Activated Receptor 1n/aOncologyCoagulationTumor progression030220 oncology & carcinogenesisCancer researchmedicineCancers
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HDAC1 and HDAC2 integrate the expression of p53 mutants in pancreatic cancer.

2015

Mutation of p53 is a frequent genetic lesion in pancreatic cancer being an unmet clinical challenge. Mutants of p53 have lost the tumour-suppressive functions of wild type p53. In addition, p53 mutants exert tumour-promoting functions, qualifying them as important therapeutic targets. Here, we show that the class I histone deacetylases HDAC1 and HDAC2 contribute to maintain the expression of p53 mutants in human and genetically defined murine pancreatic cancer cells. Our data reveal that the inhibition of these HDACs with small molecule HDAC inhibitors (HDACi), as well as the specific genetic elimination of HDAC1 and HDAC2, reduce the expression of mutant p53 mRNA and protein levels. We fur…

0301 basic medicineCancer ResearchProteasome Endopeptidase ComplexMutantHistone Deacetylase 2Histone Deacetylase 1Biologymedicine.disease_causeMolecular oncologyProto-Oncogene Proteins c-myc03 medical and health sciencesMicePancreatic cancerGeneticsmedicineAnimalsHumansRNA MessengerPromoter Regions GeneticMolecular BiologyRegulation of gene expressionMice KnockoutMutationWild typeCancerProto-Oncogene Proteins c-mdm2medicine.diseaseGenes p53HDAC13. Good healthGene Expression Regulation NeoplasticHistone Deacetylase InhibitorsPancreatic NeoplasmsDisease Models Animal030104 developmental biologyMutationCancer researchOncogene
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Interleukin-6 increases expression of serine protease inhibitor Kazal type 1 through STAT3 in colorectal adenocarcinoma

2015

Inflammation promotes colorectal cancer (CRC) tumorigenesis, but the underlying molecular mechanisms are still being uncovered. Proinflammatory cytokine interleukin-6 (IL-6) stimulates survival signaling in CRC; inflammatory signals also regulate production and activity of proteases and their inhibitors. Over-expression of serine protease inhibitor Kazal type 1 (SPINK1) predicts an unfavorable outcome in colon cancer. The SPINK1 gene contains an IL-6 responsive element, suggesting it could act as an acute phase reactant. We assessed the connection between IL-6 and SPINK1, and the function and mechanism of this signaling. Our results show that Colo205 and HT-29 cells express and secrete SPIN…

0301 basic medicineCancer ResearchTumor microenvironmentProteasesStromal cellBiologymedicine.disease_cause3. Good healthProinflammatory cytokine03 medical and health sciencesParacrine signalling030104 developmental biology0302 clinical medicine030220 oncology & carcinogenesisCancer cellCancer researchbiology.proteinmedicineInterleukin 6CarcinogenesisMolecular BiologyMolecular Carcinogenesis
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Tissue Factor-Expressing Tumor-Derived Extracellular Vesicles Activate Quiescent Endothelial Cells via Protease-Activated Receptor-1

2017

Tissue factor (TF)-expressing tumor-derived extracellular vesicles (EVs) can promote metastasis and pre-metastatic niche formation, but the mechanisms by which this occurs remain largely unknown. We hypothesized that generation of activated factor X (FXa) by TF expressed on tumor-derived EV could activate protease-activated receptors (PARs) on non-activated endothelial cells to induce a pro-adhesive and pro-inflammatory phenotype. We obtained EV from TF-expressing breast (MDA-MB-231) and pancreatic (BxPC3 and Capan-1) tumor cell lines. We measured expression of E-selectin and secretion of interleukin-8 (IL-8) in human umbilical vein endothelial cells after exposure to EV and various immunol…

0301 basic medicineCancer Researchcell-derived microparticlesprotease-activated receptorsexosomesBiologylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenslcsh:RC254-282In vitroMicrovesiclesUmbilical vein3. Good healthCell biology03 medical and health sciencesTissue factor030104 developmental biologyOncologyDownregulation and upregulationthromboplastincancerThromboplastinSecretionReceptorOriginal ResearchFrontiers in Oncology
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Replacement of miR-155 Elicits Tumor Suppressive Activity and Antagonizes Bortezomib Resistance in Multiple Myeloma

2019

Aberrant expression of microRNAs (miRNAs) has been associated to the pathogenesis of multiple myeloma (MM). While miR-155 is considered a therapeutic target in several malignancies, its role in MM is still unclear. The analysis of miR-155 expression indicates its down-regulation in MM patient-derived as compared to healthy plasma cells, thus pointing to a tumor suppressor role in this malignancy. On this finding, we investigated miR-155 replacement as a potential anti-tumor strategy in MM. The miR-155 enforced expression triggered anti-proliferative and pro-apoptotic effects in vitro. Given the lower miR-155 levels in bortezomib-resistant as compared to sensitive MM cells, we analyzed the p…

0301 basic medicineCancer Researchlcsh:RC254-282ArticlemiR-155PathogenesismiR-15503 medical and health sciences0302 clinical medicineIn vivomicroRNAmedicineMultiple myelomamiRNAmicroRNABortezomibbusiness.industrybortezomiblcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseIn vitromultiple myeloma030104 developmental biologyOncologyProteasome030220 oncology & carcinogenesisCancer researchbusinessmedicine.drugCancers
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Development of Novel Peptide-Based Michael Acceptors Targeting Rhodesain and Falcipain-2 for the Treatment of Neglected Tropical Diseases (NTDs)

2017

This paper describes the development of a class of peptide-based inhibitors as novel antitrypanosomal and antimalarial agents. The inhibitors are based on a characteristic peptide sequence for the inhibition of the cysteine proteases rhodesain of Trypanosoma brucei rhodesiense and falcipain-2 of Plasmodium falciparum. We exploited the reactivity of novel unsaturated electrophilic functions such as vinyl-sulfones, -ketones, -esters, and -nitriles. The Michael acceptors inhibited both rhodesain and falcipain-2, at nanomolar and micromolar levels, respectively. In particular, the vinyl ketone 3b has emerged as a potent rhodesain inhibitor (k2nd = 67 × 106 M-1 min-1), endowed with a picomolar b…

0301 basic medicineCathepsin LAntimalarialPeptideHeLa Cell01 natural sciencesCysteine Proteinase InhibitorDipeptideDrug DiscoveryPeptide sequencechemistry.chemical_classificationTrypanocidal AgentbiologyNeglected DiseasesStereoisomerismDipeptidesTrypanocidal AgentsMAJOR CYSTEINE PROTEASE PLASMODIUM-FALCIPARUM TRYPANOSOMA-BRUCEI CONFORMATIONAL-ANALYSIS BIOLOGICAL EVALUATION HIGHLY POTENT VINYL-ESTER INHIBITORS PEPTIDOMIMETICS SUBSTRATEMolecular Docking SimulationCysteine EndopeptidasesBiochemistryMolecular MedicineHumanProteasesNeglected DiseaseStereochemistryPhenylalaninePlasmodium falciparumTrypanosoma brucei bruceiCysteine Proteinase InhibitorsMolecular Dynamics SimulationTrypanosoma bruceiAntimalarialsStructure-Activity Relationship03 medical and health sciencesparasitic diseasesHumansStructure–activity relationship010405 organic chemistryDrug Discovery3003 Pharmaceutical ScienceHydrogen BondingTrypanosoma brucei rhodesiensePlasmodium falciparumbiology.organism_classificationMalaria0104 chemical sciencesTrypanosomiasis African030104 developmental biologychemistryCarbamateCarbamatesCysteine EndopeptidaseHeLa CellsCysteineJournal of Medicinal Chemistry
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