Search results for "Signal"

showing 10 items of 6924 documents

Dibutyl Phthalate (DBP)-Induced Apoptosis and Neurotoxicity are Mediated via the Aryl Hydrocarbon Receptor (AhR) but not by Estrogen Receptor Alpha (…

2016

Dibutyl phthalate (di-n-butyl phthalate, DBP) is one of the most commonly used phthalate esters. DBP is widely used as a plasticizer in a variety of household industries and consumer products. Because phthalates are not chemically bound to products, they can easily leak out to enter the environment. DBP can pass through the placental and blood–brain barriers due to its chemical structure, but little is known about its mechanism of action in neuronal cells. This study demonstrated the toxic and apoptotic effects of DBP in mouse neocortical neurons in primary cultures. DBP stimulated caspase-3 and LDH activities as well as ROS formation in a concentration (10 nM–100 µM) and time-dependent (3–…

0301 basic medicineTime Factorsgenetic structuresPPARγPeroxisome proliferator-activated receptorApoptosis010501 environmental sciencesToxicology01 natural sciencesDBPMicechemistry.chemical_compoundERβReceptorCells CulturedERαCerebral CortexNeuronschemistry.chemical_classificationbiologyCaspase 3General NeurosciencePhthalateDibutyl PhthalatePhthalateOriginal ArticleSignal transductioncirculatory and respiratory physiologymedicine.medical_specialtyCell SurvivalDibutyl phthalateNeuroscience(all)03 medical and health sciencesInternal medicinemedicineAnimalsEstrogen Receptor betaRNA Messengercardiovascular diseasesEstrogen receptor beta0105 earth and related environmental sciencesDose-Response Relationship DrugAhREstrogen Receptor alphaNeuronAryl hydrocarbon receptorPPAR gamma030104 developmental biologyEndocrinologyReceptors Aryl Hydrocarbonchemistrybiology.proteinReactive Oxygen SpeciesEstrogen receptor alphaNeurotoxicity Research
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Alternative Splice Forms of CYLD Mediate Ubiquitination of SMAD7 to Prevent TGFB Signaling and Promote Colitis

2018

Background & Aims The CYLD lysine 63 deubiquitinase gene (CYLD) encodes tumor suppressor protein that is mutated in familial cylindromatosus, and variants have been associated with Crohn disease (CD). Splice forms of CYLD that lack exons 7 and 8 regulate transcription factors and functions of immune cells. We examined the expression of splice forms of CYLD in colon tissues from patients with CD and their effects in mice. Methods We performed immunohistochemical analyses of colon tissues from patients with untreated CD and patients without inflammatory bowel diseases (controls). We obtained mice that expressed splice forms of CYLD (sCYLD mice) without or with SMAD7 (sCYLD/SMAD7 mice) from tr…

0301 basic medicineTranscription FactorBiopsyInbred C57BLTransgenicImmune RegulationSettore MED/12MiceRandom Allocation0302 clinical medicineCrohn DiseaseReference ValuesNeedleIntestinal Mucosaintegumentary systemChemistryBiopsy NeedleGastroenterologyT helper cellFlow CytometryPost-translational ModificationImmunohistochemistryDeubiquitinating Enzyme CYLDCysteine Endopeptidasesmedicine.anatomical_structure030211 gastroenterology & hepatologyTumor necrosis factor alphaSignal TransductionGenetically modified mouseRegulatory T cellTransgeneMice TransgenicSmad7 ProteinTransforming Growth Factor beta103 medical and health sciencesImmune systemmedicineAnimalsHumansCytokine SignalingHepatologyAnimalHEK 293 cellsUbiquitinationMolecular biologyMice Inbred C57BLDisease Models Animal030104 developmental biologyDisease ModelsCytokine Signaling; Immune Regulation; Post-translational Modification; Transcription Factor; Biopsy Needle; Crohn Disease; Cysteine Endopeptidases; Deubiquitinating Enzyme CYLD; Disease Models Animal; Flow Cytometry; Immunohistochemistry; Intestinal Mucosa; Mice Inbred C57BL; Mice Transgenic; Random Allocation; Reference Values; Signal Transduction; Smad7 Protein; Transforming Growth Factor beta1; UbiquitinationTransforming growth factorGastroenterology
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11q Deletion or ALK Activity Curbs DLG2 Expression to Maintain an Undifferentiated State in Neuroblastoma

2020

High-risk 11q deleted neuroblastomas typically display undifferentiated/poorly differentiated morphology. Neuroblastoma is thought to develop from Schwann cell precursors and undifferentiated neural crest (NC) derived cells. It is therefore vital to understand mechanisms involved in the block of differentiation. We identify an important role for oncogenic ALK-ERK1/2-SP1 signaling in maintenance of undifferentiated NC-derived progenitors via repression of DLG2, a tumor suppressor in neuroblastoma. DLG2 is expressed in the ‘bridge signature’ that represents the transcriptional transition state when neural crest cells or Schwann Cell Precursors become chromaffin cells of the adrenal gland. We …

0301 basic medicineTranscription GeneticCarcinogenesisChromaffin CellsRetinoic acidlaw.inventionNeuroblastomachemistry.chemical_compound0302 clinical medicinelawNerve Growth FactorMedicine and Health Sciencesretinoic acidAnaplastic Lymphoma Kinaselcsh:QH301-705.5NeuronsMice Inbred BALB CNeural crestCell DifferentiationPrognosisCandidate Tumor Suppressor GeneDLG2Up-RegulationCell biologyGene Expression Regulation NeoplasticERKPhenotypeTreatment Outcomemedicine.anatomical_structureFemaleChromosome Deletiontumor suppressorMAP Kinase Signaling SystemSp1 Transcription FactorSchwann cellGenetics and Molecular BiologyTretinoinBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesAdrenergic AgentsCell Line TumorNeuroblastomamedicineAnimalsHumansProgenitor cellGenePsychological repressionCell ProliferationChromosomes Human Pair 11Tumor Suppressor Proteinsmedicine.disease030104 developmental biologyALKlcsh:Biology (General)chemistryTrk receptorGeneral BiochemistrySuppressorSchwann CellsGuanylate Kinases030217 neurology & neurosurgerySSRN Electronic Journal
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NF-κB and Disease

2020

The role of NF-κB in all diseases characterized by an inflammatory process, from cancer to autoimmune diseases, is known, but—precisely because it is involved in many diseases—this transcriptional factor continues to attract scientific research and the new knowledge that emerges is fundamental in highlighting the therapeutic potential that this factor can have in the various diseases in which it is involved [...]

0301 basic medicineTranscriptional factorDiseaseCatalysislcsh:ChemistryInorganic Chemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineAnimalsHumansMolecular Targeted TherapyPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyNF-kB diseasebusiness.industryOrganic ChemistryNF-kappa BCancerNF-κBGeneral Medicinemedicine.diseaseComputer Science Applicationsn/aEditorial030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Gene Expression Regulationchemistry030220 oncology & carcinogenesisCancer researchDisease SusceptibilitybusinessBiomarkersSignal TransductionInternational Journal of Molecular Sciences
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Active Akt signaling triggers CLL toward Richter transformation via overactivation of Notch1

2021

Abstract Richter’s transformation (RT) is an aggressive lymphoma that occurs upon progression from chronic lymphocytic leukemia (CLL). Transformation has been associated with genetic aberrations in the CLL phase involving TP53, CDKN2A, MYC, and NOTCH1; however, a significant proportion of RT cases lack CLL phase–associated events. Here, we report that high levels of AKT phosphorylation occur both in high-risk CLL patients harboring TP53 and NOTCH1 mutations as well as in patients with RT. Genetic overactivation of Akt in the murine Eµ-TCL1 CLL mouse model resulted in CLL transformation to RT with significantly reduced survival and an aggressive lymphoma phenotype. In the absence of recurren…

0301 basic medicineTumor microenvironmentChronic lymphocytic leukemiaImmunologyNotch signaling pathwayMedizinAggressive lymphomaCell BiologyHematologyBiologymedicine.diseaseBiochemistrySomatic evolution in cancerLymphoma03 medical and health sciencesLeukemia030104 developmental biology0302 clinical medicineimmune system diseaseshemic and lymphatic diseasesmedicineCancer researchneoplasmsProtein kinase B030215 immunology
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Les lymphocytes Th9

2016

Th9 cells are CD4 T helper cells characterized by their ability to produce IL-9 and IL-21. These cells are obtained from naive CD4(+) T cells cultured in the presence of TGF-β and IL-4. Thus their differentiation results from the balance between the signaling pathways induced by IL-4 in one hand and the one induced by TGF-β in the other hand. These cells are inflammatory cells and were first described in the context of atopic and autoimmune diseases in which they have a pathogenic role. They are also involved in the defense against parasite infections. Recently, some reports defined Th9 anticancer properties through their cytokine secretion. Indeed, their high secretion of IL-9 and IL-21 in…

0301 basic medicineTumor microenvironmentmedicine.medical_treatmentGeneral MedicineImmunotherapyBiologyGeneral Biochemistry Genetics and Molecular Biology3. Good healthCell biology03 medical and health sciences030104 developmental biology0302 clinical medicineImmune systemmedicineCytotoxic T cellCytokine secretionSecretionInterleukin 9Signal transduction030215 immunologymédecine/sciences
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Impact of the Usher syndrome on olfaction

2015

Usher syndrome is a genetically and clinically heterogeneous disease in humans, characterized by sensorineural hearing loss, retinitis pigmentosa and vestibular dysfunction. This disease is caused by mutations in genes encoding proteins that form complex networks in different cellular compartments. Currently, it remains unclear whether the Usher proteins also form networks within the olfactory epithelium (OE). Here, we describe Usher gene expression at the mRNA and protein level in the OE of mice and showed interactions between these proteins and olfactory signaling proteins. Additionally, we analyzed the odor sensitivity of different Usher syndrome mouse models using electro-olfactogram re…

0301 basic medicineUsher syndromeCell Cycle ProteinsMice TransgenicNerve Tissue ProteinsOlfactionMyosinsBiologyCell LineMice03 medical and health sciencesOlfactory MucosaGene expressionRetinitis pigmentosaotorhinolaryngologic diseasesGeneticsmedicineAnimalsHumansCiliaMolecular BiologyGeneGenetics (clinical)GeneticsExtracellular Matrix ProteinsMessenger RNAGene Expression ProfilingEpithelial CellsGeneral MedicineCadherinsmedicine.diseaseeye diseasesSmellCytoskeletal ProteinsDisease Models Animal030104 developmental biologymedicine.anatomical_structureGene Expression RegulationMyosin VIIaMutationOdorantsSignal transductionCarrier ProteinsUsher SyndromesOlfactory epitheliumSignal TransductionHuman Molecular Genetics
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In silico pathway analysis in cervical carcinoma reveals potential new targets for treatment

2016

Abstract: An in silico pathway analysis was performed in order to improve current knowledge on the molecular drivers of cervical cancer and detect potential targets for treatment. Three publicly available Affymetrix gene expression data-sets (GSE5787, GSE7803, GSE9750) were retrieved, vouching for a total of 9 cervical cancer cell lines (CCCLs), 39 normal cervical samples, 7 CIN3 samples and 111 cervical cancer samples (CCSs). Predication analysis of microarrays was performed in the Affymetrix sets to identify cervical cancer biomarkers. To select cancer cell-specific genes the CCSs were compared to the CCCLs. Validated genes were submitted to a gene set enrichment analysis (GSEA) and Expre…

0301 basic medicineUterine Cervical NeoplasmMAPK3Uterine Cervical NeoplasmsBioinformaticsHeLa CellMitogen-Activated Protein Kinase0302 clinical medicineTransforming Growth Factor betaMedicineOligonucleotide Array Sequence AnalysisCancerCervical cancerABLCell CycleIn silico pathway analysiCell cycleGene Expression Regulation NeoplasticOncology030220 oncology & carcinogenesisFemaleDNA microarrayMitogen-Activated Protein KinasesTreatment targetResearch PaperHumanin silico pathway analysisMAP Kinase Signaling SystemIn silicoComputational biologytreatment targetsProto-Oncogene Proteins c-myc03 medical and health sciencesCell Line TumorBiomarkers TumorHumansComputer SimulationAmino Acid SequenceBiologyCervical carcinomabusiness.industryOligonucleotide Array Sequence AnalysiGene Expression ProfilingCancerComputational Biologymedicine.diseaseChromatin Assembly and DisassemblyGene expression profiling030104 developmental biologyHuman medicinebusinessHeLa CellsOncotarget
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Vitamin A Deficiency and the Lung.

2018

Vitamin A (all-trans-retinol) is a fat-soluble micronutrient which together with its natural derivatives and synthetic analogues constitutes the group of retinoids. They are involved in a wide range of physiological processes such as embryonic development, vision, immunity and cellular differentiation and proliferation. Retinoic acid (RA) is the main active form of vitamin A and multiple genes respond to RA signalling through transcriptional and non-transcriptional mechanisms. Vitamin A deficiency (VAD) is a remarkable public health problem. An adequate vitamin A intake is required in early lung development, alveolar formation, tissue maintenance and regeneration. In fact, chronic VAD has b…

0301 basic medicineVitamincollagenLung DiseasesEpithelial-Mesenchymal Transitionextracellular matrixRetinoic acidlcsh:TX341-641Reviewepithelial–mesenchymal transitionlungExtracellular matrix03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRisk Factorsretinoic acidMedicineAnimalsHumans030212 general & internal medicineVitamin AN-cadherinpulmonary diseaseNutrition and DieteticsLungbusiness.industryVitamin A DeficiencyRegeneration (biology)RetinolE-cadherinMicronutrientmedicine.diseaseVitamin A deficiency030104 developmental biologymedicine.anatomical_structureE-cadherin N-cadherin Vitamin A deficiency collagen epithelial–mesenchymal transition extracellular matrix lung pulmonary disease retinoic acid retinolchemistryImmunologyAirway Remodelingbusinesslcsh:Nutrition. Foods and food supplyFood ScienceretinolSignal Transduction
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C3 Drives Inflammatory Skin Carcinogenesis Independently of C5

2021

Nonmelanoma skin cancer such as cutaneous squamous cell carcinoma (cSCC) is the most common form of cancer and can occur as a consequence of DNA damage to the epithelium by UVR or chemical carcinogens. There is growing evidence that the complement system is involved in cancer immune surveillance; however, its role in cSCC remains unclear. Here, we show that complement genes are expressed in tissue from patients with cSCC, and C3 activation fragments are present in cSCC biopsies, indicating complement activation. Using a range of complement-deficient mice in a two-stage mouse model of chemically-induced cSCC, where a subclinical dose of 7,12-dimethylbenz[a]anthracene causes oncogenic mutatio…

0301 basic medicineWT wild typeSkin NeoplasmsComplement receptorComplement Membrane Attack Complexmedicine.disease_causeBiochemistrychemistry.chemical_compoundMice0302 clinical medicineCR complement receptorComplement ActivationSkinMice KnockoutcSCC cutaneous squamous cell carcinomaComplement C5Complement C3Receptors Complement030220 oncology & carcinogenesisCarcinoma Squamous CellDisease ProgressionTumor BiologyOriginal ArticleMAC membrane attack complexSignal TransductionHPV16 human papillomavirus type 16910-Dimethyl-12-benzanthraceneTPA 12-O-tetradecanoylphorbol-13-acetateMice TransgenicDermatologySettore MED/08 - Anatomia Patologica03 medical and health sciencesmedicineAnimalsHumansC3Molecular BiologyReceptor Anaphylatoxin C5aDMBA 712-dimethylbenz[a]anthracenebusiness.industry712-Dimethylbenz[a]anthraceneCancerCell BiologyNeoplasms Experimentalmedicine.diseaseComplement systemDisease Models Animal030104 developmental biologychemistryTumor progressionCancer researchCarcinogensTumor EscapeSkin cancerbusinessCarcinogenesisComplement membrane attack complexSkin carcinogenesis.EC epithelial cell
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