Search results for "Decoy"

showing 10 items of 14 documents

Does beak coloration of male blackbirds play a role in intra and/or intersexual selection?

2002

In many bird species, males may show brightly coloured traits and variance in male mating success may be explained by female preference and/or competition between males favouring the most coloured males. Male beak coloration has been suggested to play an important role in the pairing pattern of European blackbirds. Here, we investigate female preference and male-male interactions in relation to male beak coloration in this species. We used a field experiment to measure female and male responses toward stuffed decoys showing either of two beak coloration representing the extremes of the natural variation from yellow to orange. Decoys were situated on the centre of plots and behaviours of mal…

0106 biological sciencesEcology[SDV]Life Sciences [q-bio]05 social sciencesZoologyGeneral MedicineBiological evolutionBiologyNatural variation010603 evolutionary biology01 natural sciencesBehavioral NeuroscienceBeakInvestigation methodsMate choicePair formationSexual selection0501 psychology and cognitive sciencesAnimal Science and Zoology050102 behavioral science & comparative psychologyDecoyComputingMilieux_MISCELLANEOUSBehavioural Processes
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Targeting the MET oncogene by concomitant inhibition of receptor and ligand via an antibody-"decoy" strategy

2018

MET, a master gene sustaining "invasive growth," is a relevant target for cancer precision therapy. In the vast majority of tumors, wild-type MET behaves as a "stress-response" gene and relies on the ligand (HGF) to sustain cell "scattering," invasive growth and apoptosis protection (oncogene "expedience"). In this context, concomitant targeting of MET and HGF could be crucial to reach effective inhibition. To test this hypothesis, we combined an anti-MET antibody (MvDN30) inducing "shedding" (i.e., removal of MET from the cell surface), with a "decoy" (i.e., the soluble extracellular domain of the MET receptor) endowed with HGF-sequestering ability. To avoid antibody/decoy interaction-and …

0301 basic medicineCancer ResearchLung NeoplasmsCellContext (language use)ApoptosisMice SCIDLigands03 medical and health sciencesMice0302 clinical medicineMice Inbred NODanti-HGF therapy; antibodies; decoy; MET oncogene; MET target therapyMET oncogeneExtracellularmedicineTumor Cells CulturedantibodiesAnimalsHumansdecoyCell ProliferationOncogenebiologyMET target therapyChemistryAntibodies MonoclonalProto-Oncogene Proteins c-metXenograft Model Antitumor AssaysIn vitro030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer cellColonic NeoplasmsCancer researchbiology.proteinanti-HGF therapyFemaleAntibodyDecoyGlioblastoma
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Death Receptor 5 Displayed on Extracellular Vesicles Decreases TRAIL Sensitivity of Colon Cancer Cells

2020

Tumor necrosis factor-related apoptosis inducing ligand (TRAIL) is considered to be a promising antitumor drug because of its selective proapoptotic properties on tumor cells. However, the clinical application of TRAIL is until now limited because of the resistance of several cancer cells, which can occur at various levels in the TRAIL signaling pathway. The role of decoy receptors that can side-track TRAIL, thereby preventing the formation of an activated death receptor, has been extensively studied. In this study, we have focused on extracellular vesicles (EVs) that are known to play a role in cell-to-cell communication and that can be released by donor cells into the medium transferring …

0301 basic medicineENDOCYTOSISTRAILSURFACE EXPRESSIONCell and Developmental Biology03 medical and health sciences0302 clinical medicineSecretionDR5Decoy receptorsReceptorlcsh:QH301-705.5Original Researchreceptor-ligand traffickingEXOSOMESChemistryapoptosisCell BiologyMicrovesiclesconditioned medium030104 developmental biologylcsh:Biology (General)Apoptosis030220 oncology & carcinogenesisCancer cellCancer researchTumor necrosis factor alphareceptor–ligand traffickingextracellular vesiclesDecoyDevelopmental BiologyFrontiers in Cell and Developmental Biology
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PCSK9-D374Y mediated LDL-R degradation can be functionally inhibited by EGF-A and truncated EGF-A peptides: An in vitro study.

2019

Abstract Background and aims Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to low density lipoprotein receptor (LDLR) through the LDLR epidermal growth factor-like repeat A (EGF-A) domain and induces receptor internalization and degradation. PCSK9 has emerged as a novel therapeutic target for hypercholesterolemia. Clinical studies with PCSK9 inhibiting antibodies have demonstrated strong LDL-c lowering effects, but other therapeutic approaches using small molecule inhibitors for targeting PCSK9 functions may offer supplementary therapeutic options. The aim of our study was to evaluate the effect of synthetic EGF-A analogs on mutated (D374Y) PCSK9-D374Y mediated LDLR degradatio…

0301 basic medicineSmall peptidesmedia_common.quotation_subject030204 cardiovascular system & hematologyDecoy strategyPCSK903 medical and health sciences0302 clinical medicineHumansInternalizationCells Culturedmedia_commonExpression vectorEpidermal Growth FactorChemistryPCSK9PCSK9 InhibitorsTransfectionProprotein convertasePCSK9 inhibitionIn vitroCell biologyEGF-A domain030104 developmental biologyLDLRReceptors LDLLDL receptorMutationKexinlipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular MedicineAtherosclerosis
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Polymorphisms in TRAIL receptor genes and risk of breast cancer in Spanish women

2007

TRAIL is a potent inducer of apoptosis in malignant but not in normal cells. TRAIL binds to the proapoptotic death receptor DR4 and DR5 as well as to the decoy receptors DcR1 and DcR2. To evaluate the involvement of TRAIL receptor genes in breast cancer, we carried out a case-control study of eight selected polymorphisms in a large sample of Spanish women. Three of the eight selected SNPs (626G/C and 1322G/A in DR4 and 2699A/G in DcR2) showed some evidence of different genotype distributions in a random selection of 535 cases and 480 controls and were therefore studied in our entire sample (1008 cases and 768 controls). For the two DR4 polymorphisms, no differences in genotype or haplotype …

AdultUntranslated regionCancer ResearchLinkage disequilibriumBreast NeoplasmsSingle-nucleotide polymorphismBiologyPolymerase Chain ReactionPolymorphism Single NucleotideBreast cancerGenotypeGeneticsmedicineHumansDecoy receptorsskin and connective tissue diseasesReceptorAgedHaplotypeAge FactorsGeneral MedicineMiddle Agedmedicine.diseaseReceptors TNF-Related Apoptosis-Inducing LigandOncologySpainImmunologyFemaleCancer Biomarkers
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Tuning inflammation in tuberculosis: the role of decoy receptors

2009

Decoy receptors are "silent scavengers" of CC chemokines and cytokines, which play a key role in damping inflammation and tissue damage. In this review we discuss on recent findings demonstrating that these receptors set the balance between antimicrobial resistance, immune activation and inflammatory response in Mycobacterium tuberculosis infection.

ChemokineDecoy receptormedicine.medical_treatmentImmunologyInflammationMycobacterium tuberculosiImmunopathologyMicrobiologyMycobacterium tuberculosisMiceImmune systemmedicineAnimalsHumansTuberculosisDecoy receptorsReceptors CytokineReceptorCytokineDecoy receptors; TIR8/SIGIRR; D6; Mycobacterium tuberculosis; Cytokines; Chemokines; Immunopathology; InflammationInflammationSettore MED/04 - Patologia GeneraleAntiinfective agentbiologyMycobacterium tuberculosisbiology.organism_classificationTIR8/SIGIRRInfectious DiseasesCytokineChemokineImmunologybiology.proteinmedicine.symptomD6
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Role of the chemokine decoy receptor D6 in balancing inflammation, immune activation, and antimicrobial resistance in Mycobacterium tuberculosis infe…

2008

D6 is a decoy and scavenger receptor for inflammatory CC chemokines. D6-deficient mice were rapidly killed by intranasal administration of low doses of Mycobacterium tuberculosis. The death of D6(-/-) mice was associated with a dramatic local and systemic inflammatory response with levels of M. tuberculosis colony-forming units similar to control D6-proficient mice. D6-deficient mice showed an increased numbers of mononuclear cells (macrophages, dendritic cells, and CD4 and CD8 T lymphocytes) infiltrating inflamed tissues and lymph nodes, as well as abnormal increased concentrations of CC chemokines (CCL2, CCL3, CCL4, and CCL5) and proinflammatory cytokines (tumor necrosis factor alpha, int…

Chemokinedecoy receptor inflammation Mycobacterium tuberculosis infectionmedicine.medical_treatmentInterleukin-1betaImmunologyMice TransgenicInflammationReceptors CCR10BiologyModels BiologicalArticleCCL5Proinflammatory cytokineInterferon-gammaMiceImmune systemAnti-Infective AgentsDrug Resistance BacterialmedicineAnimalsImmunology and AllergyInterferon gammaInflammationTumor Necrosis Factor-alphaArticlesMycobacterium tuberculosisPhenotypeCytokineImmune SystemImmunologybiology.proteinTumor necrosis factor alphaLymph Nodesmedicine.symptommedicine.drug
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Differential inhibition of TRAIL-mediated DR5-DISC formation by decoy receptors 1 and 2.

2006

International audience; Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family that induces cancer cell death by apoptosis with some selectivity. TRAIL-induced apoptosis is mediated by the transmembrane receptors death receptor 4 (DR4) (also known as TRAIL-R1) and DR5 (TRAIL-R2). TRAIL can also bind decoy receptor 1 (DcR1) (TRAIL-R3) and DcR2 (TRAIL-R4) that fail to induce apoptosis since they lack and have a truncated cytoplasmic death domain, respectively. In addition, DcR1 and DcR2 inhibit DR4- and DR5-mediated, TRAIL-induced apoptosis and we demonstrate here that this occurs through distinct mechanisms. While DcR1 prevents the assembly of the…

MESH : Hela CellsMESH: Membrane GlycoproteinsMESH: Membrane MicrodomainsDecoy Receptor 1ApoptosisMESH : Membrane GlycoproteinsReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing LigandJurkat Cells0302 clinical medicineMESH : Tumor Necrosis Factor Decoy ReceptorsMESH: Jurkat CellsDecoy receptorsReceptorCells CulturedMESH : Jurkat CellsMESH : Tumor Necrosis Factor-alpha0303 health sciencesMembrane GlycoproteinsMESH : Protein BindingArticlesMESH : Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsTumor Necrosis Factor Receptor-Associated Peptides and ProteinsCell biology030220 oncology & carcinogenesisCaspasesDeath-inducing signaling complexApoptosis/drug effects; Apoptosis Regulatory Proteins/antagonists & inhibitors; Apoptosis Regulatory Proteins/pharmacology; Caspases/metabolism; Cells Cultured; Death Domain Receptor Signaling Adaptor Proteins; Enzyme Activation/drug effects; GPI-Linked Proteins; HeLa Cells; Humans; Jurkat Cells; Membrane Glycoproteins/antagonists & inhibitors; Membrane Glycoproteins/pharmacology; Membrane Microdomains/drug effects; Protein Binding/drug effects; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor/metabolism; TNF-Related Apoptosis-Inducing Ligand; Tumor Necrosis Factor Decoy Receptors; Tumor Necrosis Factor Receptor-Associated Peptides and Proteins/metabolism; Tumor Necrosis Factor-alpha/antagonists & inhibitors; Tumor Necrosis Factor-alpha/pharmacologyMESH : Apoptosis Regulatory ProteinsMESH: TNF-Related Apoptosis-Inducing LigandProtein BindingMESH: Cells CulturedDeath Domain Receptor Signaling Adaptor ProteinsMESH: Enzyme ActivationBiologyMESH: Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsGPI-Linked Proteins03 medical and health sciencesMembrane MicrodomainsCell surface receptorMESH : Cells Cultured[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyReceptors Tumor Necrosis Factor Member 10cHumansMESH: Protein Binding[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing LigandMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyDeath domainMESH: CaspasesMESH: HumansTumor Necrosis Factor-alphaMESH: Apoptosis Regulatory ProteinsMESH: ApoptosisMESH : HumansCell BiologyMESH: Receptors Tumor Necrosis FactorMESH: Tumor Necrosis Factor Decoy ReceptorsMESH : Receptors Tumor Necrosis FactorEnzyme ActivationMESH: Hela CellsReceptors TNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor Decoy ReceptorsApoptosisMESH: Tumor Necrosis Factor-alphaMESH : Membrane MicrodomainsMESH : CaspasesApoptosis Regulatory ProteinsMESH : Enzyme ActivationMESH : ApoptosisMESH : Death Domain Receptor Signaling Adaptor ProteinsTumor Necrosis Factor Decoy ReceptorsHeLa CellsMESH: Death Domain Receptor Signaling Adaptor Proteins
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Chemotherapy overcomes TRAIL-R4-mediated TRAIL resistance at the DISC level

2011

International audience; TNF-related apoptosis-inducing ligand or Apo2L (Apo2L/TRAIL) is a promising anti-cancer drug owing to its ability to trigger apoptosis by binding to TRAIL-R1 or TRAIL-R2, two membrane-bound receptors that are often expressed by tumor cells. TRAIL can also bind non-functional receptors such as TRAIL-R4, but controversies still exist regarding their potential to inhibit TRAIL-induced apoptosis. We show here that TRAIL-R4, expressed either endogenously or ectopically, inhibits TRAIL-induced apoptosis. Interestingly, the combination of chemotherapeutic drugs with TRAIL restores tumor cell sensitivity to apoptosis in TRAIL-R4-expressing cells. This sensitization, which ma…

MESH: CASP8 and FADD-Like Apoptosis Regulating ProteinMESH : Antineoplastic Combined Chemotherapy ProtocolsCASP8 and FADD-Like Apoptosis Regulating ProteinTRAILApoptosisMESH : Models BiologicalMitochondrionMESH : RNA Small InterferingMESH: Caspase 8TNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing LigandMESH : Tumor Necrosis Factor Decoy Receptors0302 clinical medicineRNA interferenceNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsMESH: RNA Small InterferingMESH: NeoplasmsRNA Small InterferingReceptorSensitizationCaspase 80303 health sciencesMESH : Caspase 8MESH: Drug Resistance Neoplasm3. Good healthCell biologyMESH: Antineoplastic Combined Chemotherapy ProtocolsMESH : Drug Resistance Neoplasmmedicine.anatomical_structure030220 oncology & carcinogenesisRNA InterferenceMESH : GPI-Linked ProteinsMESH: TNF-Related Apoptosis-Inducing LigandDeath Domain Receptor Signaling Adaptor ProteinsProgrammed cell deathMESH: Cell Line Tumorc-FLIPMESH: RNA InterferenceBiologyGPI-Linked ProteinsCaspase 8Models Biological03 medical and health sciencesCell Line TumorReceptors Tumor Necrosis Factor Member 10cmedicineTRAIL-R4HumanscancerChemotherapy[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing Ligand[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMolecular Biology030304 developmental biologyOriginal PaperMESH: HumansMESH : Cell Line TumorMESH: ApoptosisMESH : HumansMESH: Models BiologicalMESH : CASP8 and FADD-Like Apoptosis Regulating ProteinCell BiologyMESH: Tumor Necrosis Factor Decoy ReceptorsMESH : NeoplasmsReceptors TNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor Decoy ReceptorsDrug Resistance NeoplasmApoptosisMESH : RNA InterferenceMESH: GPI-Linked ProteinsMESH : ApoptosisMESH : Death Domain Receptor Signaling Adaptor ProteinsMESH: Death Domain Receptor Signaling Adaptor ProteinsTumor Necrosis Factor Decoy Receptors
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TRAIL-R4 promotes tumor growth and resistance to apoptosis in cervical carcinoma HeLa cells through AKT.

2011

International audience; BACKGROUND: TRAIL/Apo2L is a pro-apoptotic ligand of the TNF family that engages the apoptotic machinery through two pro-apoptotic receptors, TRAIL-R1 and TRAIL-R2. This cell death program is tightly controlled by two antagonistic receptors, TRAIL-R3 and TRAIL-R4, both devoid of a functional death domain, an intracellular region of the receptor, required for the recruitment and the activation of initiator caspases. Upon TRAIL-binding, TRAIL-R4 forms a heteromeric complex with the agonistic receptor TRAIL-R2 leading to reduced caspase-8 activation and apoptosis. METHODOLOGY/PRINCIPAL FINDINGS: We provide evidence that TRAIL-R4 can also exhibit, in a ligand independent…

Proliferation indexlcsh:MedicineTNF-Related Apoptosis-Inducing LigandHeLaMicePhosphatidylinositol 3-Kinases0302 clinical medicineMolecular Cell BiologyBasic Cancer ResearchMembrane Receptor SignalingEnzyme Inhibitorslcsh:SciencePhosphoinositide-3 Kinase Inhibitors0303 health sciencesMultidisciplinaryCell Deathbiologyapoptosis3. Good healthCell biologyOncology030220 oncology & carcinogenesisMedicineFemaleSignal transductionResearch ArticleSignal TransductionProgrammed cell deathMorpholinesproliferationBlotting WesternMice Nude03 medical and health sciencesTRAIL-R4[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyBiology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biologyCell growthAktCell Membranelcsh:RPTEN PhosphohydrolaseNeoplasms Experimentalbiology.organism_classificationTumor Necrosis Factor Decoy ReceptorsChromonesApoptosislcsh:QProto-Oncogene Proteins c-aktHeLa Cells
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