Search results for "ACTIVATOR"

showing 10 items of 488 documents

Redox signaling in acute pancreatitis

2015

Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On th…

NecrosisGSH reduced glutathioneSTAT3 signal transducer and activator of transcription 3ERK extracellular signal-regulated kinasesClinical BiochemistryCCK cholecystokininTRAFs TNF receptor associated factorsReview ArticleIκB kinasePharmacologymedicine.disease_causeBiochemistrySHP small heterodimer partnerSTIM1 stromal interaction molecule 1chemistry.chemical_compoundHATs histone acetyltransferasesMedicineASK1GCL glutamate cysteine ligaseTNF-α tumor necrosis factor alphaIKK IκB kinaseNOS nitric oxide synthaseAcute inflammationHIF hypoxia inducible factorlcsh:QH301-705.5NF-κB nuclear factor kappa BDAMPs damage-associated molecular pattern moleculeslcsh:R5-920biologyGSSG oxidized glutathioneNF-kappa BNLRs nucleotide-binding oligomerization domain (NOD) like receptorsTRADD tumor necrosis factor receptor type 1-associated DEATH domain proteinTRPC3 transient receptor potential channel 3VEGF vascular endothelial growth factorGlutathioneTNFR tumor necrosis factor receptorHMGB1 high-mobility group Box 1 proteinIP3R inositol 145-trisphosphate receptor type 3VCAM-1 Vascular Cell adhesion protein 1Acute DiseaseJNK c-Jun N-terminal kinaseAcute pancreatitisTLRs toll-like receptorsmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionAP-1 activator protein-1Signal TransductionmRNA messenger ribonucleic acidHMGB1ASC apoptosis-associated speck-like protein containing a carboxy-terminal CARDRNS reactive nitrogen speciesPTPs protein tyrosine phosphatasesROS reactive oxygen speciesNADH nicotinamide adenine dinucleotidepHe extracellular pHFAEE fatty acid ethyl estersAP acute pancreatitisHumansXanthine oxidaseCBP CREB-binding proteinRyR endoplasmic reticulum membrane ryanodine receptorsMDA malondialdehydeNO nitric oxideXO xanthine oxidaseASK1 apoptosis signal-regulating kinase-1business.industryOrganic ChemistryAutophagyNADPH nicotinamide adenine dinucleotide phosphateHDACs histone deacetylasesmedicine.diseaseCARS compensatory anti-inflammatory response syndromeXDH xanthine dehydrogenaseIL interleukinIκB inhibitor of kappa BAcute pancreatitisETC Electron transport chainPancreatitisMKPs MAPK phosphatasesSAP severe acute pancreatitischemistrylcsh:Biology (General)DTT dithiothreitolOxidative stressNAC N-acetyl cysteineImmunologybiology.proteinCalciumLysosomesReactive Oxygen SpeciesbusinessMAPK mitogen-activated protein kinaseOxidative stressERCP endoscopic retrograde cholangiopancreatographyRedox Biology
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Junctophilin-1 is a modifier gene of GDAP1-related Charcot-Marie-Tooth disease.

2014

Mutations in the GDAP1 gene cause different forms of Charcot-Marie-Tooth (CMT) disease, and the primary clinical expression of this disease is markedly variable in the dominant inheritance form (CMT type 2K; CMT2K), in which carriers of the GDAP1 p.R120W mutation can display a wide range of clinical severity. We investigated the JPH1 gene as a genetic modifier of clinical expression variability because junctophilin-1 (JPH1) is a good positional and functional candidate. We demonstrated that the JPH1-GDAP1 cluster forms a paralogon and is conserved in vertebrates. Moreover, both proteins play a role in Ca(2+) homeostasis, and we demonstrated that JPH1 is able to restore the store-operated Ca…

Nerve Tissue ProteinsDiseaseMitochondrionBiologyCell LineEvolution MolecularMiceCharcot-Marie-Tooth DiseaseGeneticsAnimalsHumansGenetic Predisposition to DiseaseStromal Interaction Molecule 1Molecular BiologyGeneGenetics (clinical)PhylogenyGenes ModifierActivator (genetics)Endoplasmic reticulumMembrane ProteinsSTIM1General MedicinePhenotypeMolecular biologyMitochondriaNeoplasm ProteinsMutationCalciumHomeostasisHuman molecular genetics
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Sporogen, S14-95, and S-curvularin, three inhibitors of human inducible nitric-oxide synthase expression isolated from fungi.

2003

The induction of human inducible nitric-oxide synthase (iNOS) expression depends (among other factors) on activation of the signal transducer and activator of transcription 1 (STAT1) pathway. Therefore, the STAT1 pathway may be an appropriate target for the development of inhibitors of iNOS expression. HeLa S3 cells transiently transfected with a gamma-activated site (GAS)/interferon-stimulated response element-driven reporter gene construct were used as the primary screening system. Using this system, three novel inhibitors of interferon-gamma-dependent gene expression, namely, sporogen, S14-95, and S-curvularin, were isolated from different Penicillium species. These three compounds also …

Nitric Oxide Synthase Type IIINitric Oxide Synthase Type IIGene expressionHumansRNA MessengerEnzyme InhibitorsPromoter Regions GeneticCells CulturedNitritesPharmacologyRegulation of gene expressionReporter genebiologyPenicilliumNitric Oxide Synthase Type IIITransfectionCurvularinMolecular biologyNitric oxide synthaseDNA-Binding ProteinsSTAT1 Transcription FactorGene Expression Regulationbiology.proteinSTAT proteinTrans-ActivatorsMolecular MedicineEpoxy CompoundsZearalenoneNitric Oxide SynthaseCell DivisionMolecular pharmacology
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Association of low-penetrance alleles with male breast cancer risk and clinicopathological characteristics: results from a multicenter study in Italy

2013

It is well-known that male breast cancer (MBC) susceptibility is mainly due to high-penetrance BRCA1/2 mutations. Here, we investigated whether common low-penetrance breast cancer (BC) susceptibility alleles may influence MBC risk in Italian population and whether variant alleles may be associated with specific clinicopathological features of MBCs. In the frame of the Italian Multicenter Study on MBC, we genotyped 413 MBCs and 745 age-matched male controls at 9 SNPs annotating known BC susceptibility loci. By multivariate logistic regression models, we found a significant increased MBC risk for 3 SNPs, in particular, with codominant models, for rs2046210/ESR1 (OR = 1.71; 95 % CI: 1.43–2.05;…

OncologyAdultMaleCancer Researchmedicine.medical_specialtyMultivariate analysisSettore MED/06 - Oncologia MedicaClinicopathological characteristicBRCA1/2; Clinicopathological characteristics; ER/PR status; Low-penetrance breast cancer alleles; Male breast cancer; SNPsSingle-nucleotide polymorphismPolymorphism Single NucleotideER/PR statuBreast Neoplasms MaleBreast cancerBRCA1/2Internal medicineGenotypemedicineHumansGenetic Predisposition to DiseaseAlleleReceptor Fibroblast Growth Factor Type 2Low-penetrance breast cancer alleleAllelesAgedAged 80 and overbusiness.industryEstrogen Receptor alphaHigh Mobility Group Proteinsclinicopathological characteristicsMiddle Agedmedicine.diseasePenetranceMale breast cancerer/pr statusOncologyTOX3ItalyReceptors EstrogenMale breast cancerCase-Control StudiesMultivariate AnalysisTrans-Activatorslow-penetrance breast cancer allelesbusinessApoptosis Regulatory ProteinsReceptors Progesteroneclinicopathological characteristics; er/pr status; male breast cancer; brca1/2; snps; low-penetrance breast cancer allelesSNPs
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Effects of p63 expression on survival in oral squamous cell carcinoma

2007

BACKGROUND: P63 is the protein codified by p63 gene, a p53 gene homolog, known for its pivotal role in cell cycle regulation, and involved in the tumor differentiation. Aims of the present study were to assess the frequency and pattern of p63 protein expression in oral squamous cell carcinoma (OSCC) in relation to the main tumour characteristics and to verify whether p63 can be considered a marker of prognosis in patients with OSCC. MATERIAL AND METHODS: In a retrospective study, a cohort of 64 OSCC patients was investigated for p63 protein expression and its cellular localization by immunohistochemistry (monoclonal mouse anti-human p63 protein-clone 4A4). After grouping by p63 expression, …

OncologyAdultMaleCancer Researchmedicine.medical_specialtyPathologySurvival rateBiologyOSCCInternal medicinemedicineBiomarkers TumorCox regression analysisHumansGrading (tumors)GeneSurvival rateCellular localizationAgedNeoplasm StagingCox regression analysis; OSCC; p53 family; p63; Survival rate;p63integumentary systemTumor Suppressor ProteinsRetrospective cohort studyGeneral MedicineMiddle AgedPrognosisSurvival Analysisp63 p53 family OSCC Survival rate Cox regression analysisDNA-Binding Proteinsstomatognathic diseasesOncologyCohortMonoclonalCarcinoma Squamous CellTrans-ActivatorsImmunohistochemistryFemaleMouth NeoplasmsOSCCsense organsp53 familyp53 familyCox regressionTranscription Factors
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Common Breast Cancer Susceptibility Alleles and the Risk of Breast Cancer for BRCA1 and BRCA2 Mutation Carriers: Implications for Risk Prediction

2010

Abstract The known breast cancer susceptibility polymorphisms in FGFR2, TNRC9/TOX3, MAP3K1, LSP1, and 2q35 confer increased risks of breast cancer for BRCA1 or BRCA2 mutation carriers. We evaluated the associations of 3 additional single nucleotide polymorphisms (SNPs), rs4973768 in SLC4A7/NEK10, rs6504950 in STXBP4/COX11, and rs10941679 at 5p12, and reanalyzed the previous associations using additional carriers in a sample of 12,525 BRCA1 and 7,409 BRCA2 carriers. Additionally, we investigated potential interactions between SNPs and assessed the implications for risk prediction. The minor alleles of rs4973768 and rs10941679 were associated with increased breast cancer risk for BRCA2 carrie…

OncologyCancer Researchendocrine system diseasesVesicular Transport ProteinsGene mutation0302 clinical medicineRisk FactorsGenotypeskin and connective tissue diseasesAged 80 and over0303 health sciencesBRCA1 ProteinHigh Mobility Group ProteinsMiddle Aged3. Good healthOncology030220 oncology & carcinogenesisFemaleBreast diseaseReceptors ProgesteroneAdultHeterozygotemedicine.medical_specialtyGenotypeBreast NeoplasmsSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideRisk AssessmentArticle03 medical and health sciencesBreast cancerSDG 3 - Good Health and Well-beingInternal medicinemedicineHumansGenetic Predisposition to DiseaseAllelesAged030304 developmental biologyBRCA2 ProteinHereditary cancer and cancer-related syndromes [ONCOL 1]Sodium-Bicarbonate SymportersHaplotypeCancergenome-wide association estrogen-receptor loci variantsmedicine.diseaseSurvival AnalysisTOX3MutationTrans-ActivatorsCancer researchApoptosis Regulatory Proteins
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Ki-67 as an independent prognostic factor in an unselected cohort of patients with ovarian cancer: results of an explorative, retrospective study.

2013

The identification of prognostic markers has clinical implications in epithelial ovarian carcinoma (EOC). Here, we studied markers for proliferation (Ki-67), endocrine regulation [progesterone receptor (PR), estrogen receptor (ER)], and invasion [urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor (PAI-1)]. All patients with available follow-up information and EOC tissue, who were treated at our institution between 1997 and 2004, were enrolled in the present study. Expression of Ki-67, PR and ER was determined by immunohistochemical analyses. uPA and PAI-1 antigen levels were determined using enzyme‑linked immunosorbent assays. One hundred and eight patients enter…

OncologyCancer Researchmedicine.medical_specialtyCarcinoma Ovarian EpithelialDisease-Free SurvivalCohort StudiesInternal medicineProgesterone receptorPlasminogen Activator Inhibitor 1medicineBiomarkers TumorHumansNeoplasms Glandular and EpithelialProspective cohort studyCell ProliferationRetrospective StudiesUrokinaseOvarian Neoplasmsbiologybusiness.industryProportional hazards modelHazard ratioCancerGeneral MedicineMiddle Agedmedicine.diseaseUrokinase-Type Plasminogen ActivatorTumor BurdenKi-67 AntigenOncologyReceptors EstrogenKi-67biology.proteinFemalebusinessOvarian cancerReceptors Progesteronemedicine.drugOncology reports
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Node-Negative Breast Cancer: Which Patients Should Be Treated?

2010

Adjuvant systemic therapy has led to markedly improved outcome in early-stage breast cancer. However, the absolute gains from chemotherapy might be modest in node-negative patients. Adjuvant chemotherapy is the only option for triple-negative breast cancer patients and should be used with trastuzumab in HER2-positive patients. Considering the large group of patients with some degree of endocrine responsiveness, adding chemotherapy according to risk is an option. At present, we guide our therapeutic decisions using clinicopathologic risk classifications like the St. Gallen risk category or Adjuvant! online. A downside of these risk estimations is a low specificity and consequently the risk f…

Oncologymedicine.medical_specialtyChemotherapybusiness.industrymedicine.medical_treatmentReview Articlemedicine.diseaseSystemic therapySurgeryClinical trialchemistry.chemical_compoundBreast cancerOncologychemistryTrastuzumabInternal medicinePlasminogen activator inhibitor-1medicineSurgerybusinessPlasminogen activatorAdjuvantmedicine.drugBreast care (Basel, Switzerland)
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Receptor activator of NF-kB (RANK) expression associates with bone metastasis in breast carcinomas.

2010

Oncologymedicine.medical_specialtyHistologyPhysiologyActivator (genetics)business.industryEndocrinology Diabetes and MetabolismInternal medicinemedicineBone metastasisbusinessmedicine.diseaseReceptorBone
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Plasmatic Plasminogen Activator Inhibitor Activity in Patients with Primary Breast Cancer

1997

Oncologymedicine.medical_specialtybusiness.industryInternal medicineMedicineIn patientHematologyPrimary breast cancerProspective cohort studybusinessPlasminogen activatorThrombosis and Haemostasis
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