Search results for "Peptide fragment"

showing 10 items of 356 documents

Chemokine stromal cell-derived factor-1alpha modulates VLA-4 integrin-dependent adhesion to fibronectin and VCAM-1 on bone marrow hematopoietic proge…

2001

Stromal cell-derived factor-1alpha (SDF-1alpha) is a potent chemoattractant for hematopoietic progenitor cells (HPC), suggesting that it could play an important role during their migration within or to the bone marrow (BM). The integrin VLA-4 mediates HPC adhesion to BM stroma by interacting with CS-1/fibronectin and VCAM-1. It is required during hematopoiesis and homing of HPC to the BM. As HPC migration in response to SDF-1alpha might require dynamic regulation of integrin function, we investigated if SDF-1alpha could modulate VLA-4 function on BM CD34(hi) cells.CD34(hi) BM cells and hematopoietic cell lines were tested for the effect of SDF-1alpha on VLA-4-dependent adhesion to CS-1/fibr…

Cancer ResearchIntegrinsReceptors CXCR4Stromal cellIntegrinCD34Receptors Lymphocyte HomingVascular Cell Adhesion Molecule-1Bone Marrow CellsIntegrin alpha4beta1Hematopoietic Cell Growth FactorsCell LineColony-Forming Units Assaychemistry.chemical_compoundMiceLeukemia Megakaryoblastic AcutePrecursor B-Cell Lymphoblastic Leukemia-LymphomaGeneticsCell AdhesionTumor Cells CulturedAnimalsHumansVCAM-1Cell adhesionMolecular BiologybiologyChemotaxisVLA-4Antibodies MonoclonalCell BiologyHematologyHematopoietic Stem CellsChemokine CXCL12Peptide FragmentsRecombinant ProteinsCell biologyFibronectinsFibronectinchemistryLiverbiology.proteinStromal CellsChemokines CXCHoming (hematopoietic)Signal TransductionExperimental hematology
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Nanofitins targeting heat shock protein 110: an innovative immunotherapeutic modality in cancer.

2021

The presence of an inactivating heat shock protein 110 (HSP110) mutation in colorectal cancers has been correlated with an excellent prognosis and with the ability of HSP110 to favor the formation of tolerogenic (M2-like) macrophages. These clinical and experimental results suggest a potentially powerful new strategy against colorectal cancer: the inhibition of HSP110. In this work, as an alternative to neutralizing antibodies, Nanofitins (scaffold ~7 kDa proteins) targeting HSP110 were isolated from the screening of a synthetic Nanofitin library, and their capacity to bind (immunoprecipitation, biolayer interferometry) and to inhibit HSP110 was analyzed in vitro and in vivo. Three Nanofiti…

Cancer ResearchMice03 medical and health sciencesLymphocytes Tumor-Infiltrating0302 clinical medicineImmune systemPeptide LibraryIn vivoCell Line TumorHeat shock proteinTumor MicroenvironmentmedicineAnimalsHumansCytotoxic T cellHSP110 Heat-Shock Proteinssmall peptide moleculesTumor microenvironmentanticancer targeted therapybiologyChemistryMacrophagesCancer[SDV.SP]Life Sciences [q-bio]/Pharmaceutical sciencesmedicine.diseaseXenograft Model Antitumor AssaysPeptide FragmentsIn vitro3. Good healthNanofitinsOncologyPositron-Emission Tomography030220 oncology & carcinogenesisbiology.proteinCancer researchFemaleAntibodyColorectal NeoplasmsHSP110
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Midregion PTHrP regulates Rip1 and caspase expression in MDA-MB231 breast cancer cells.

2007

It was previously reported that the midregion PTHrP domain (38-94)-amide restrains growth and invasion "in vitro", causes striking toxicity and accelerates death of some breast cancer cell lines, the most responsive being MDA-MB231 whose tumorigenesis was also attenuated "in vivo". In addition, we have demonstrated that midregion PTHrP is imported in the nucleoplasm of cultured MDA-MB231 cells, and that "in vitro" it can bind chromatin of metaphase spread preparations and also an isolated 20-mer oligonucleotide, thereby appearing endowed with a putative transcription factor-like DNA-binding ability. Here, we examined whether PTHrP (38-94)-amide was able to modulate the expression of genes e…

Cancer ResearchProgrammed cell deathbcl-X ProteinApoptosisBreast NeoplasmsPTHrP Rip1 caspase breast cancer cellsmedicine.disease_causeTransfectionCell MovementCell Line TumorGene expressionmedicineTranscriptional regulationHumansNeoplasm InvasivenessSettore BIO/06 - Anatomia Comparata E Citologiaskin and connective tissue diseasesCaspaseCell ProliferationNucleoplasmbiologyJNK Mitogen-Activated Protein KinasesParathyroid Hormone-Related ProteinRNA-Binding ProteinsOligonucleotides AntisenseMolecular biologyPeptide FragmentsChromatinCell biologyNuclear Pore Complex ProteinsSettore BIO/12 - Biochimica Clinica E Biologia Molecolare ClinicaOncologyApoptosisCaspasesbiology.proteinFemalebcl-Associated Death ProteinCarcinogenesisSignal TransductionBreast cancer research and treatment
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Partial tyrosinase-specific self tolerance by HLA-A*0201-restricted cytotoxic T lymphocytes in mice and man

2003

The human tyrosinase (hTyr) (369-377) cytotoxic T lymphocyte (CTL) epitope is presented by malignant melanoma and various nontransformed cells in association with human leukocyte antigen (HLA)-A*0201 (A2.1) and used for vaccination-based immunotherapy of melanoma patients. Its mouse homologue, mTyr (369-377), is naturally processed and bound by A2.1 with equivalent efficacy and thus enabled us to explore the effect of self tolerance on Tyr-specific T cells in different lines of A2.1 transgenic (Tg) mice and man. We found that self Tyr-reactive CTL in Tg mice and, importantly, in man were affected by partial tolerance resulting in only residual T lymphocytes of higher avidity for self Tyr al…

Cancer ResearchT-LymphocytesGenetic VectorsMice Transgenicchemical and pharmacologic phenomenaBiologyEpitopeImmune toleranceEpitopesMiceImmune systemAntigenAntigens CDAntigens NeoplasmHLA-A2 AntigenAnimalsHumansCytotoxic T cellCTLA-4 AntigenIL-2 receptorMelanomaAntigen PresentationHLA-A AntigensMonophenol MonooxygenaseVaccinationReceptors Interleukin-2hemic and immune systemsAntigens DifferentiationMolecular biologyPeptide FragmentsMice Inbred C57BLCTL*Self ToleranceOncologySelf ToleranceImmunologyImmunotherapyT-Lymphocytes CytotoxicInternational Journal of Cancer
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WIN 55,212-2, agonist of cannabinoid receptors, prevents amyloid β1-42 effects on astrocytes in primary culture

2015

Alzheimer's disease (AD), a neurodegenerative illness involving synaptic dysfunction with extracellular accumulation of Aβ1-42 toxic peptide, glial activation, inflammatory response and oxidative stress, can lead to neuronal death. Endogenous cannabinoid system is implicated in physiological and physiopathological events in central nervous system (CNS), and changes in this system are related to many human diseases, including AD. However, studies on the effects of cannabinoids on astrocytes functions are scarce. In primary cultured astrocytes we studied cellular viability using MTT assay. Inflammatory and oxidative stress mediators were determined by ELISA and Western-blot techniques both in…

Cannabinoid receptormedicine.medical_treatmentInterleukin-1betaNitric Oxide Synthase Type IIlcsh:Medicinemedicine.disease_causeReceptors CannabinoidWIN 55212-2Receptorlcsh:ScienceCerebral CortexMultidisciplinaryCalcium Channel BlockersSistema nerviós Malaltiesmedicine.symptomSignal transductionResearch ArticleSignal Transductionmedicine.drugmedicine.medical_specialtyCell SurvivalMorpholinesPrimary Cell CultureInflammationNaphthalenesBiologyNeurologiaFetusInternal medicinemedicineAnimalsViability assayCannabinoid Receptor AgonistsAmyloid beta-PeptidesSuperoxide DismutaseTumor Necrosis Factor-alphalcsh:RTranscription Factor RelAPeptide FragmentsBenzoxazinesRatsPPAR gammaOxidative StressEndocrinologyGene Expression RegulationCyclooxygenase 2Astrocyteslcsh:QFisiologia humanaCannabinoidOxidative stress
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Inhibitors of Rho-kinase modulate amyloid-β (Aβ) secretion but lack selectivity for Aβ42

2005

Certain non-steroidal anti-inflammatory drugs (NSAIDs) preferentially inhibit production of the amyloidogenic Abeta42 peptide, presumably by direct modulation of gamma-secretase activity. A recent report indicated that NSAIDs could reduce Abeta42 by inhibition of the small GTPase Rho, and a single inhibitor of Rho kinase (ROCK) mimicked the effects of Abeta42-lowering NSAIDs. To investigate whether Abeta42 reduction is a common property of ROCK inhibitors, we tested commercially available compounds in cell lines that were previously used to demonstrate the Abeta42-lowering activity of NSAIDs. Surprisingly, we found that two ROCK inhibitors reduced total Abeta secretion in a dose-dependent m…

Cell SurvivalMutantPeptideCHO CellsProtein Serine-Threonine KinasesPharmacologyBiochemistryAmyloid beta-Protein PrecursorCellular and Molecular NeuroscienceCricetulusCricetinaeEndopeptidasesmental disordersAmyloid precursor proteinAnimalsAspartic Acid EndopeptidasesSecretionSmall GTPaseEnzyme InhibitorsRho-associated protein kinasechemistry.chemical_classificationrho-Associated KinasesAmyloid beta-PeptidesbiologyAnti-Inflammatory Agents Non-SteroidalIntracellular Signaling Peptides and ProteinsIn vitro toxicologyProtein-Tyrosine KinasesPeptide Fragmentsnervous system diseasesBiochemistrychemistrybiology.proteinAmyloid Precursor Protein SecretasesSelectivityProtein Processing Post-TranslationalJournal of Neurochemistry
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Vitamin E transport, membrane incorporation and cell metabolism: Is α-tocopherol in lipid rafts an oar in the lifeboat?

2010

International audience; Vitamin E is composed of closely related compounds, including tocopherols and tocotrienols. Studies of the last decade provide strong support for a specific role of alpha-tocopherol in cell signalling and the regulation of gene expression. It produces significant effects on inflammation, cell proliferation and apoptosis that are not shared by other vitamin E isomers with similar antioxidant properties. The different behaviours of vitamin E isomers might relate, at least in part, to the specific effects they exert at the plasma membrane. alpha-Tocopherol is not randomly distributed throughout the phospholipid bilayer of biological membranes, and as compared with other…

Cell deathAntioxidant[ SDV.AEN ] Life Sciences [q-bio]/Food and Nutrition[SDV]Life Sciences [q-bio]medicine.medical_treatmentalpha-TocopherolSignal transductionBiologyAntioxidants03 medical and health scienceschemistry.chemical_compoundMembrane Microdomains0302 clinical medicineATP Binding Cassette Transporter Subfamily B Member 3medicineHumansVitamin ETocopherolATP Binding Cassette Transporter Subfamily B Member 2Protein PrecursorsLipid bilayerLipid raftLDL-Receptor Related Proteins030304 developmental biology0303 health sciencesTocopherolVitamin ECell MembraneBiological TransportBiological membraneLipid metabolismPeptide FragmentsCell biology[SDV] Life Sciences [q-bio]Lipid raftIntestinal AbsorptionLiverReceptors LDLBiochemistrychemistryATP-Binding Cassette Transporterslipids (amino acids peptides and proteins)Antioxidantalpha-Tocopherol[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgeryFood ScienceBiotechnologyMolecular Nutrition & Food Research
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PTHrP [67-86] regulates the expression of stress proteins in breast cancer cells inducing modifications in urokinase-plasminogen activator and MMP-1 …

2003

It was previously reported that a midregion domain of parathyroid hormone-related protein (PTHrP), that is, [67-86]-amide, is able to restrain growth and promote matrigel penetration by the 8701-BC cell line, derived from a biopsy fragment of a primary ductal infiltrating carcinoma of the human breast, and that cell invasion in vitro is drastically impaired by inactivation of urokinase-plasminogen activator (uPa). In this study we started a more detailed investigation of the possible effects on gene expression arising from the interaction between PTHrP [67-86]-amide and 8701-BC breast cancer cells by a combination of conventional-, differential display-and semi-quantitative multiplex-polyme…

CellBreast NeoplasmsBiologyHeat Shock Transcription FactorsDownregulation and upregulationCell Line TumorHeat shock proteinmedicineHumansNeoplasm InvasivenessHSP90 Heat-Shock ProteinsEnzyme InhibitorsHSF1Heat-Shock ProteinsMatrigelActivator (genetics)CarcinomaParathyroid Hormone-Related ProteinCell BiologyOligonucleotides AntisenseUrokinase-Type Plasminogen ActivatorMolecular biologyPeptide FragmentsProtein Structure TertiaryUp-RegulationDNA-Binding ProteinsGene Expression Regulation NeoplasticHeat shock factormedicine.anatomical_structureCell cultureCancer researchFemaleQuercetinMatrix Metalloproteinase 1Transcription FactorsJournal of Cell Science
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Rapid and Sensitive Identification of Major Histocompatibility Complex Class I-associated Tumor Peptides by Nano-LC MALDI MS/MS

2005

Identification of major histocompatibility complex (MHC)-associated peptides recognized by T-lymphocytes is a crucial prerequisite for the detection and manipulation of specific immune responses in cancer, viral infections, and autoimmune diseases. Unfortunately immunogenic peptides are less abundant species present in highly complex mixtures of MHC-extracted material. Most peptide identification strategies use microcapillary LC coupled to nano-ESI MS/MS in a challenging on-line approach. Alternatively MALDI PSD analysis has been applied for this purpose. We report here on the first off-line combination of nanoscale (nano) LC and MALDI TOF/TOF MS/MS for the identification of naturally proce…

CellsCellPeptideHuman leukocyte antigenMajor histocompatibility complexSensitivity and SpecificityBiochemistryEpitopeAnalytical ChemistryMajor Histocompatibility ComplexImmune systemCell Line TumormedicineHumansAmino Acid SequenceCarcinoma Renal CellMolecular Biologychemistry.chemical_classificationbiologyHistocompatibility Antigens Class IFlow CytometryMolecular biologyKidney NeoplasmsPeptide FragmentsNeoplasm Proteinsmedicine.anatomical_structurechemistrySpectrometry Mass Matrix-Assisted Laser Desorption-Ionizationbiology.proteinTime-of-flight mass spectrometryAntibodyMolecular & Cellular Proteomics
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NF-κB inducing kinase (NIK) is an essential post-transcriptional regulator of T-cell activation affecting F-actin dynamics and TCR signaling

2018

NF-κB inducing kinase (NIK) is the key protein of the non-canonical NF-κB pathway and is important for the development of lymph nodes and other secondary immune organs. We elucidated the specific role of NIK in T cells using T-cell specific NIK-deficient (NIKΔT) mice. Despite showing normal development of lymphoid organs, NIKΔT mice were resistant to induction of CNS autoimmunity. T cells from NIKΔT mice were deficient in late priming, failed to up-regulate T-bet and to transmigrate into the CNS. Proteomic analysis of activated NIK-/- T cells showed de-regulated expression of proteins involved in the formation of the immunological synapse: in particular, proteins involved in cytoskeleton dy…

Central Nervous System0301 basic medicineEncephalomyelitis Autoimmune ExperimentalT-LymphocytesT cellPrimary Cell CultureImmunologyReceptors Antigen T-CellPriming (immunology)Protein Serine-Threonine KinasesBiologyLymphocyte ActivationImmunological synapseMice03 medical and health sciences0302 clinical medicineImmune systemmedicineAnimalsImmunology and AllergyProtein kinase BAdaptor Proteins Signal TransducingMice KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3ZAP-70 Protein-Tyrosine KinasePhospholipase C gammaGene Expression ProfilingZAP70T-cell receptorMembrane ProteinsPhosphoproteinsActinsPeptide FragmentsCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureGene Expression Regulation030220 oncology & carcinogenesisMyelin-Oligodendrocyte GlycoproteinLymph NodesSignal transductionT-Box Domain ProteinsProto-Oncogene Proteins c-aktSpleenSignal TransductionJournal of Autoimmunity
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