Search results for "Growth factor"

showing 10 items of 1300 documents

Proteomic Analyses Reveal an Acidic Prime Side Specificity for the Astacin Metalloprotease Family Reflected by Physiological Substrates

2011

Astacins are secreted and membrane-bound metalloproteases with clear associations to many important pathological and physiological processes. Yet with only a few substrates described their biological roles are enigmatic. Moreover, the lack of knowledge of astacin cleavage site specificities hampers assay and drug development. Using PICS (proteomic identification of protease cleavage site specificity) and TAILS (terminal amine isotopic labeling of substrates) degradomics approaches >3000 cleavage sites were proteomically identified for five different astacins. Such broad coverage enables family-wide determination of specificities N- and C-terminal to the scissile peptide bond. Remarkably, me…

KeratinocytesModels MolecularProteomicsVascular Endothelial Growth Factor AProteasesmedicine.medical_treatmentProteolysisMolecular Sequence DataBiologyCleavage (embryo)BiochemistryCell LineSubstrate SpecificityAnalytical Chemistry03 medical and health sciencesTandem Mass SpectrometrymedicineHumansAmino Acid SequenceMolecular BiologyPeptide sequencePhylogeny030304 developmental biologyEnzyme Precursors0303 health sciencesProteaseStaining and LabelingEdman degradationmedicine.diagnostic_testResearch030302 biochemistry & molecular biologyTioproninMetalloendopeptidasesTerminal amine isotopic labeling of substratesRecombinant ProteinsKineticsBiochemistryProteolysisKallikreinsAstacinPeptidesSequence AlignmentChromatography LiquidMolecular & Cellular Proteomics
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Pore-forming Staphylococcus aureus alpha-toxin triggers epidermal growth factor receptor-dependent proliferation.

2006

Staphylococcal alpha-toxin is an archetypal killer protein that homo-oligomerizes in target cells to create small transmembrane pores. The membrane-perforating beta-barrel motif is a conserved attack element of cytolysins of Gram-positive and Gram-negative bacteria. Following the recognition that nucleated cells can survive membrane permeabilization, a profile of abundant transcripts was obtained in transiently perforated keratinocytes. Several immediate early genes were found to be upregulated, reminiscent of the cellular response to growth factors. Cell cycle analyses revealed doubling of S + G2/M phase cells 26 h post toxin treatment. Determination of cell counts uncovered that after an …

KeratinocytesStaphylococcus aureusSrc Homology 2 Domain-Containing Transforming Protein 1ImmunologyCellBacterial ToxinsBlotting WesternFluorescent Antibody TechniqueTransfectionMicrobiologyCell LineHemolysin ProteinsDownregulation and upregulationNucleated cellVirologymedicineHumansGrowth factor receptor inhibitorEpidermal growth factor receptorStaphylococcus aureus alpha toxinAdaptor Proteins Signal TransducingCell Line TransformedCell ProliferationbiologyCytotoxinsReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingCell CycleCell cycleFlow CytometryTransmembrane proteinCell biologyErbB Receptorsmedicine.anatomical_structureShc Signaling Adaptor Proteinsbiology.proteinMitogensSignal TransductionCellular microbiology
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The Neuronal Nitric Oxide Synthase Is Upregulated in Mouse Skin Repair and in Response to Epidermal Growth Factor in Human HaCaT Keratinocytes

2004

Expression of nNOS mRNA was found in normal human and mouse skin tissue. Upon wounding, we observed a rapid downregulation of nNOS mRNA and protein in wounds of mice; however, when repair continued, nNOS mRNA was strongly upregulated and nNOS protein expression peaked at late stages of healing. Immunohistochemistry revealed wound keratinocytes as the cellular source of nNOS. In line with the in vivo situation, we found a basal expression of nNOS in the human keratinocyte cell line HaCaT. A marked stimulation of nNOS expression in the cells was achieved with epidermal growth factor receptor (EGFR) ligands such as epidermal growth factor (EGF), heparin-binding EGF, transforming growth factor-…

Keratinocytesinorganic chemicalsReceptor ErbB-3Receptor ErbB-2medicine.medical_treatmentwound healingNitric Oxide Synthase Type IDermatologyBiochemistryGene Expression Regulation EnzymologicCell LineMiceDownregulation and upregulationnitric oxideEpidermal growth factormedicineAnimalsHumansRNA MessengerEpidermal growth factor receptorMolecular BiologySkinMice Inbred BALB CEpidermal Growth Factorintegumentary systembiologyGrowth factorgrowth factorCell BiologyUp-RegulationCell biologyErbB Receptorsbody regionsNitric oxide synthaseHaCaTmedicine.anatomical_structurenervous systemImmunologycardiovascular systembiology.proteinNeuregulinNitric Oxide SynthaseKeratinocyteSignal TransductionJournal of Investigative Dermatology
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Resistance of keratinocytes to TGFbeta-mediated growth restriction and apoptosis induction accelerates re-epithelialization in skin wounds.

2002

The pleiotropic growth factor TGFβ plays an important role in regulating responses to skin injury. TGFβ targets many different cell types and is involved in all aspects of wound healing entailing inflammation,re-epithelialization, matrix formation and remodeling. To elucidate the role of TGFβ signal transduction in keratinocytes during cutaneous wound healing, we have used transgenic mice expressing a dominant negative type II TGFβ receptor exclusively in keratinocytes. We could demonstrate that this loss of TGFβ signaling in keratinocytes led to an accelerated re-epithelialization of full thickness excisional wounds accompanied by an increased proliferation in keratinocytes at the wound ed…

Keratinocytesmedicine.medical_treatmentEGR1InflammationApoptosisMice TransgenicBiologyImmediate early proteinCell LineImmediate-Early ProteinsMiceDownregulation and upregulationTransforming Growth Factor betamedicineAnimalsTranscription factorEarly Growth Response Protein 1Wound Healingintegumentary systemGrowth factorGene Expression ProfilingCell BiologyCell biologyDNA-Binding ProteinsEpidermal CellsImmunologymedicine.symptomSignal transductionEpidermisWound healingCell DivisionTranscription FactorsJournal of cell science
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Genome-Wide Association Analysis in Primary Sclerosing Cholangitis

2010

Background & Aims We aimed to characterize the genetic susceptibility to primary sclerosing cholangitis (PSC) by means of a genome-wide association analysis of single nucleotide polymorphism (SNP) markers. Methods A total of 443,816 SNPs on the Affymetrix SNP Array 5.0 (Affymetrix, Santa Clara, CA) were genotyped in 285 Norwegian PSC patients and 298 healthy controls. Associations detected in this discovery panel were re-examined in independent case-control panels from Scandinavia (137 PSC cases and 368 controls), Belgium/The Netherlands (229 PSC cases and 735 controls), and Germany (400 cases and 1832 controls). Results The strongest associations were detected near HLA-B at chromosome 6p21…

LOCIMacrophage Stimulating 1 (Hepatocyte Growth Factor-Like)Genome-wide association studySUSCEPTIBILITYGene FrequencyHLA AntigensRisk FactorsHEPATOCELLULAR-CARCINOMAOdds RatioBileBiliary TractINCREASED RISKOligonucleotide Array Sequence AnalysisGastroenterologyMULTIPLE-SCLEROSISCROHNS-DISEASEEuropePhenotypeULCERATIVE-COLITISInflammation MediatorsSNP arrayCholangitis SclerosingSingle-nucleotide polymorphismLocus (genetics)Human leukocyte antigenBiologyPolymorphism Single NucleotideRisk AssessmentCell LinePrimary sclerosing cholangitisGlypicansGenetic predispositionmedicineHumansGenetic Predisposition to DiseaseGene SilencingACID RECEPTOR TGR5Genetic associationInflammationChi-Square DistributionHepatologyGene Expression ProfilingGlypican 6medicine.diseaseGENEG-Protein-Coupled Bile Acid Receptor 1Case-Control StudiesImmunologyColitis UlcerativeGenome-Wide Association StudyINFLAMMATORY-BOWEL-DISEASEGastroenterology
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Increased expression of leptin and the leptin receptor as a marker of breast cancer progression: possible role of obesity-related stimuli.

2006

Abstract Purpose: Recent in vitro studies suggested that the autocrine leptin loop might contribute to breast cancer development by enhancing cell growth and survival. To evaluate whether the leptin system could become a target in breast cancer therapy, we examined the expression of leptin and its receptor (ObR) in primary and metastatic breast cancer and noncancer mammary epithelium. We also studied whether the expression of leptin/ObR in breast cancer can be induced by obesity-related stimuli, such as elevated levels of insulin, insulin-like growth factor-I (IGF-I), estradiol, or hypoxic conditions. Experimental Design: The expression of leptin and ObR was examined by immunohistochemistry…

LeptinCancer ResearchER-BETAmedicine.medical_treatmentHYPOXIA-INDUCIBLE FACTOR-1NeoplasmsTumor Cells CulturedBreastInsulin-Like Growth Factor Iskin and connective tissue diseasesReceptorAged 80 and overEstradiolIGF-I RECEPTORCELL-LINEReverse Transcriptase Polymerase Chain ReactionLeptindigestive oral and skin physiologyCarcinoma Ductal BreastMiddle AgedMetastatic breast cancerINSULINCell HypoxiaESTROGENOncologyDisease ProgressionIGF-I RECEPTOR; HYPOXIA-INDUCIBLE FACTOR-1; OB GENE; GROWTH-FACTOR; CELL-LINE; ER-BETA; ESTROGEN; ALPHA; INSULIN; MCF-7Receptors LeptinFemaleOB GENEhormones hormone substitutes and hormone antagonistsAdultmedicine.medical_specialtyGROWTH-FACTORBreast NeoplasmsReceptors Cell SurfaceBreast cancerInternal medicinemedicineBiomarkers TumorHumansObesityAutocrine signallingAgedLeptin receptorbusiness.industryInsulinmedicine.diseaseALPHAEndocrinologyTumor progressionCase-Control StudiesMCF-7business
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Effect of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) on Hormones of Energy Balance in a TCDD-Sensitive and a TCDD-Resistant Rat Strain

2014

One of the hallmarks of the acute toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a drastically reduced feed intake by an unknown mechanism. To further elucidate this wasting syndrome, we followed the effects of a single large dose (100 μg/kg) of TCDD on the serum levels of several energy balance-influencing hormones, clinical chemistry variables, and hepatic aryl hydrocarbon receptor (AHR) expression in two rat strains that differ widely in their TCDD sensitivities, for up to 10 days. TCDD affected most of the analytes in sensitive Long-Evans rats, while there were few alterations in the resistant Han/Wistar strain. However, analyses of feed-restricted unexposed Long-Evans rats i…

LeptinFOOD-INTAKETCDDFGF21Polychlorinated Dibenzodioxinsmedicine.medical_treatmentAHRwasting syndromeacute toxicity413 Veterinary science8-tetrachlorodibenzo-p-dioxinlcsh:Chemistry2378-tetrachlorodibenzo-<i>p</i>-dioxin; TCDD; wasting syndrome; energy balance; hormones; acute toxicity; strain differences; AHRPPAR-ALPHAInsulinMESSENGER-RNA EXPRESSIONInsulin-Like Growth Factor Ita315Receptorlcsh:QH301-705.5AH RECEPTORSpectroscopyenergiatasebiologyChemistryLeptinGeneral MedicineCENTRAL LEPTIN INFUSIONstrain differencesComputer Science ApplicationsLiverGhrelinAdiponectinARYL-HYDROCARBON RECEPTOR7medicine.medical_specialty3education2GlucagonCatalysisArticleInorganic ChemistrySpecies SpecificityInternal medicinemedicineAnimals2378-tetrachlorodibenzo-p-dioxinRats Long-EvansRNA MessengerPhysical and Theoretical ChemistryRats WistarCARBOXYKINASE PEPCK ACTIVITYMolecular BiologyI IGF-IhormonesGrowth factorOrganic ChemistryBody WeightAryl hydrocarbon receptorGlucagonenergy balancehormonitRatsFibroblast Growth FactorsEndocrinologylcsh:Biology (General)lcsh:QD1-999Receptors Aryl Hydrocarbonbiology.proteinGROWTH-FACTOR 21Energy MetabolismHormoneInternational Journal of Molecular Sciences
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Physical fitness, hormonal, and immunological responses during prolonged military field training

2018

Physical fitness is crucial to warfighters’ performance in the battlefield. Previous studies have shown negative changes in their hormonal and neuromuscular responses induced by military field training (MFT). The purpose of this study was to investigate the changes in hormonal and immunological values and body composition during a prolonged MFT and to find out how warfighters’ physical condition influences these changes. Conscripts (n = 49, age 20 1 years, height 179 9 cm, body mass 73.8 7.8 kg, fat 12.6 3.7% and BMI 23 kg/m²) were measured before, during, after MFT, and after a 4-day recovery period. Serum insulin-like growth factor-1 (IGF-1), tumor necrosis factor alpha (TNF-a), interleuk…

LeptinMalefyysinen rasitusImmunologywarfighterfyysinen toimintakykyPhysical performanceYoung AdultMetabolism and RegulationHumansimmuniteettisotilaatInsulin-Like Growth Factor IMuscle SkeletalCreatine KinaseExerciseOriginal ResearchAdiposityHormonalInterleukin-6Tumor Necrosis Factor-alphaEndurance and PerformanceBody Weightphysical performancehormonalhormonitimmunologicalMilitary PersonnelPhysical Fitnessstrengthfyysinen aktiivisuus
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Metabolic parameters and adipokine profile during GH replacement therapy in children with GH deficiency

2007

Objective: GH replacement therapy in children with GH deficiency (GHD) mainly promotes linear growth. Not only have very few studies fully analyzed the metabolic consequences of GH therapy, but also the question as to whether GH may affect adipokine secretion has been insufficiently investigated. Our aim was to study the effects of GH replacement therapy on auxological data, lipid and glycemic profiles, insulin homeostasis (HOMA-IR) and serum adipokines in children. Methods: This was a 1-year prospective study. Thirty-four GHD children (11.6 ± 2.6 years) and thirty healthy matched controls were enrolled. Children affected by GHD were studied both before beginning continuous GH replacement t…

LeptinMalemedicine.medical_specialtyTime FactorsAdolescentHormone Replacement TherapyEndocrinology Diabetes and Metabolismmedicine.medical_treatmentAdipokineBiologyBody Mass IndexSettore MED/13 - Endocrinologiachemistry.chemical_compoundEndocrinologyInternal medicinemedicineHumansInsulinInsulin-Like Growth Factor IChildGrowth DisordersTriglyceridesGlycemicmedicine.diagnostic_testAdiponectinHuman Growth HormoneCholesterolLeptinInsulinBody WeightCholesterol LDLGeneral MedicineBody HeightTreatment OutcomeEndocrinologychemistryTransgender hormone therapyFemaleAdiponectinLipid profileGH METABOLISM ADIPOKINESEuropean Journal of Endocrinology
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Expression of angiogenic regulators, VEGF and leptin, is regulated by the EGF/PI3K/STAT3 pathway in colorectal cancer cells.

2009

Both leptin and vascular endothelial growth factor (VEGF) are growth and angiogenic cytokines that are upregulated in different types of cancer and have been implicated in neoplastic progression. Here we investigated the molecular mechanism by which leptin and VEGF expression are regulated in colon cancer by epidermal growth factor (EGF). In colon cancer cell line HT-29, EGF induced the binding of signal transducer and activator transcription 3 (STAT3) to STAT3 consensus motifs within the VEGF and leptin promoters and stimulated leptin and VEGF mRNA and protein synthesis. All these EGF effects were significantly blocked when HT-29 cells were treated with an inhibitor of the phosphoinositide…

LeptinSTAT3 Transcription FactorVascular Endothelial Growth Factor ASmall interfering RNAPhysiologyColorectal cancerClinical BiochemistryNeovascularization PhysiologicEGF/PI3K/STAT3colorectal cancerchemistry.chemical_compoundPhosphatidylinositol 3-KinasesEpidermal growth factormedicineHumansLY294002Gene SilencingRNA MessengerSTAT3Promoter Regions GeneticPI3K/AKT/mTOR pathwayCell NucleusbiologyEpidermal Growth FactorChemistryLeptinangiogenic regulators VEGF leptinCell Biologymedicine.diseaseUp-RegulationVascular endothelial growth factorGene Expression Regulation NeoplasticCancer researchbiology.proteinColorectal NeoplasmsHT29 Cellshormones hormone substitutes and hormone antagonistsProtein Binding
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