Search results for " Mitogen"

showing 10 items of 202 documents

Cabut, a C2H2 zinc finger transcription factor, is required during Drosophila dorsal closure downstream of JNK signaling.

2005

AbstractDuring dorsal closure, the lateral epithelia on each side of the embryo migrate dorsally over the amnioserosa and fuse at the dorsal midline. Detailed genetic studies have revealed that many molecules are involved in this epithelial sheet movement, either with a signaling function or as structural or motor components of the process. Here, we report the characterization of cabut (cbt), a new Drosophila gene involved in dorsal closure. cbt is expressed in the yolk sac nuclei and in the lateral epidermis. The Cbt protein contains three C2H2-type zinc fingers and a serine-rich domain, suggesting that it functions as a transcription factor. cbt mutants die as embryos with dorsal closure …

animal structuresMorphogenesisBiologyCabutZinc fingerMorphogenesismedicineAnimalsDrosophila ProteinsDorsal closureYolk sacMolecular BiologyTranscription factorYolk nucleiCytoskeletonGeneticsZinc fingerEpidermis (botany)C2H2 Zinc FingerJNK Mitogen-Activated Protein KinasesZinc FingersCell BiologyDorsal closureCell biologymedicine.anatomical_structureDrosophila melanogasterEpidermal Cellsembryonic structuresMutationJNK cascadeDrosophilaJNKDevelopmental BiologySignal TransductionTranscription FactorsDevelopmental biology
researchProduct

A frozen analogue approach to aminopyridinylimidazoles leading to novel and promising p38 MAP kinase inhibitors.

2012

In this study we report the design, synthesis, and biological evaluation of constrained aminopyridinylimidazoles as p38α MAP kinase inhibitors. The frozen analogue approach focused on the pyridinyl unit, using purine bioisosteres as constrained structure analogues. The identification of the most potent bioisostere was followed by a further derivatization to address hydrophobic region II. In combination with C-2 modifications of the imidazole core, we were able to design highly active inhibitors on the p38α MAP kinase. The inhibitor design presented herein represents a promising and highly efficient advancement of recent stages of development in this class of p38 MAP kinase inhibitors. In co…

biologyChemistryStereochemistryPyridinesp38 mitogen-activated protein kinasesEntropyImidazolesMolecular ConformationCombinatorial chemistryp38 Mitogen-Activated Protein KinasesMolecular conformationMolecular Docking Simulationchemistry.chemical_compoundStructure-Activity RelationshipPurinesMitogen-activated protein kinaseDrug DesignDrug Discoverybiology.proteinMolecular MedicineStructure–activity relationshipBioisostereBiological evaluationJournal of medicinal chemistry
researchProduct

p38 MAPK: A dual role in hepatocyte proliferation through reactive oxygen species

2013

p38 MAPKs are important mediators of signal transduction that respond to a wide range of extracellular stressors such as UV radiation, osmotic shock, hypoxia, pro-inflammatory cytokines, and oxidative stress. The most abundant family member is p38α, which helps to couple cell proliferation and growth in response to certain damaging stimuli. In fact, increased proliferation and impaired differentiation are hallmarks of p38α-deficient cells. It has been reported that reactive oxygen species (ROS) play a critical role in cytokine-induced p38α activation. Under physiological conditions, p38α can function as a mediator of ROS signaling and either activate or suppress cell cycle progression depen…

chemistry.chemical_classificationMAPK/ERK pathwayReactive oxygen speciesMAP Kinase Signaling SystemCell growthp38 mitogen-activated protein kinasesCell Growth ProcessesGeneral MedicineCell cycleBiologymedicine.disease_causep38 Mitogen-Activated Protein KinasesBiochemistryLiver regenerationCell biologychemistryHepatocytesmedicineAnimalsHumansSignal transductionReactive Oxygen SpeciesOxidative stressFree Radical Research
researchProduct

Integrin α2β1 Mediates Isoform-Specific Activation of p38 and Upregulation of Collagen Gene Transcription by a Mechanism Involving the α2 Cytoplasmic…

1999

Two collagen receptors, integrins alpha1beta1 and alpha2beta1, can regulate distinct functions in cells. Ligation of alpha1beta1, unlike alpha2beta1, has been shown to result in recruitment of Shc and activation of the Ras/ERK pathway. To identify the downstream signaling molecules activated by alpha2beta1 integrin, we have overexpressed wild-type alpha2, or chimeric alpha2 subunit with alpha1 integrin cytoplasmic domain in human osteosarcoma cells (Saos-2) lacking endogenous alpha2beta1. The chimeric alpha2/alpha1 chain formed a functional heterodimer with beta1. In contrast to alpha2/alpha1 chimera, forced expression of alpha2 integrin resulted in upregulation of alpha1 (I) collagen gene …

collagenIntegrinsReceptors CollagenTranscription GeneticintegrinIntegrincytoplasmic domainCDC42Biologyp38 MAPKTransfectionCD49cp38 Mitogen-Activated Protein KinasesCollagen receptorTumor Cells CulturedHumansProtein IsoformsCell BiologyMolecular biologyCell biologyUp-RegulationEnzyme ActivationIntegrin alpha Mbiology.proteinIntegrin beta 6Original ArticleSignal transductionMitogen-Activated Protein KinasesITGA6Signal TransductionThe Journal of Cell Biology
researchProduct

Resveratrol post-transcriptionally regulates pro-inflammatory gene expression via regulation of KSRP RNA binding activity

2014

Resveratrol shows beneficial effects in inflammation-based diseases like cancer, cardiovascular and chronic inflammatory diseases. Therefore, the molecular mechanisms of the anti-inflammatory resveratrol effects deserve more attention. In human epithelial DLD-1 and monocytic Mono Mac 6 cells resveratrol decreased the expression of iNOS, IL-8 and TNF-α by reducing mRNA stability without inhibition of the promoter activity. Shown by pharmacological and siRNA-mediated inhibition, the observed effects are SIRT1-independent. Target-fishing and drug responsive target stability experiments showed selective binding of resveratrol to the RNA-binding protein KSRP, a central post-transcriptional regul…

endocrine system diseasesMRNA destabilizationRNA Stabilityp38 mitogen-activated protein kinasesGene ExpressionRNA-binding proteinResveratrolBiologyp38 Mitogen-Activated Protein KinasesMicechemistry.chemical_compoundCell Line TumorStilbenesGene expressionGeneticsAnimalsHumansddc:610RNA Messengerskin and connective tissue diseasesMice KnockoutMessenger RNAGene knockdownExosome Multienzyme Ribonuclease Complexorganic chemicalsAnti-Inflammatory Agents Non-SteroidalGene regulation Chromatin and EpigeneticsRNA-Binding Proteinsfood and beveragesMolecular biology3. Good healthCell biologychemistryResveratrolMutationTrans-ActivatorsPhosphorylationInflammation Mediatorshormones hormone substitutes and hormone antagonistsNucleic Acids Research
researchProduct

PET Imaging of the Impact of Extracellular pH and MAP Kinases on the p-Glycoprotein (Pgp) Activity

2012

The functional activity of p-glycoprotein (Pgp) can be increased in vitro by an extracellular acidosis via activation of MAP kinases (p38, ERK1/2). In order to study these effects in vivo a new (68)Ga-labeled PET tracer was developed which serves as a substrate of the Pgp and therefore indirectly mirrors the Pgp activity. For in vivo studies, experimental tumors were imaged under acidic conditions (inspiratory hypoxia, injection of lactic acid) and during inhibition of MAP kinases in a μ-PET system. In vitro, [(68)Ga]MFL6.MZ showed an accumulation within the cells of about 20% which was increased to 30% by Pgp inhibition. In solid tumors a marked tracer uptake was observed showing spatial h…

integumentary systembiologyKinasep38 mitogen-activated protein kinasesIn vitroBiochemistryIn vivobiology.proteinExtracellularBiophysicsmedicinemedicine.symptomPreclinical imagingP-glycoproteinAcidosis
researchProduct

Complement Protein C1q Binds to Hyaluronic Acid in the Malignant Pleural Mesothelioma Microenvironment and Promotes Tumor Growth

2017

C1q is the first recognition subcomponent of the complement classical pathway, which acts towards the clearance of pathogens and apoptotic cells. C1q is also known to modulate a range of functions of immune and non-immune cells, including their involvement in placental development and sensorial synaptic pruning. We have recently shown that C1q can promote tumour by encouraging their adhesion, migration and proliferation in addition to angiogenesis and metastasis. In this study, we have examined the role of C1q in the microenvironment of malignant pleuric mesothelioma (MPM), a rare form of cancer commonly associated with exposure to asbestos. We found that C1q was highly expressed in all MPM…

lcsh:Immunologic diseases. Allergy0301 basic medicineComplement system; Malignant pleural mesothelioma; Hyaluronic acid; Mesothelioma cells; C1q; CancerAngiogenesisMPMp38 mitogen-activated protein kinasesImmunologyHAchemical and pharmacologic phenomenaBiologyMetastasisMesothelioma cell03 medical and health sciencesClassical complement pathwaychemistry.chemical_compound0302 clinical medicineImmune systemhyaluronic acidHyaluronic acidmedicinemalignant pleural mesotheliomacancerImmunology and AllergyCell adhesioncomplement systemC1qcomplement system; MPM; HA; Mesothelioma cells; C1q and cancerOriginal ResearchC1q and cancermedicine.diseaseComplement system030104 developmental biologyC1q; Cancer; Complement system; Hyaluronic acid; Malignant pleural mesothelioma; Mesothelioma cells; Immunology and Allergy; Immunologychemistrymesothelioma cells030220 oncology & carcinogenesisImmunologyCancer researchlcsh:RC581-607Frontiers in Immunology
researchProduct

eIF2α confers cellular tolerance to S. aureus α-toxin

2015

We report on the role of conserved stress-response pathways for cellular tolerance to a pore forming toxin. First, we observed that small molecular weight inhibitors including of eIF2α-phosphatase, jun-N-terminal kinase (JNK), and PI3-kinase sensitized normal mouse embryonal fibroblasts (MEFs) to the small pore forming S. aureus α-toxin. Sensitization depended on expression of mADAM10, the murine ortholog of a proposed high-affinity receptor for α-toxin in human cells. Similarly, eIF2α (S51A/S51A) MEFs, which harbor an Ala knock-in mutation at the regulated Ser51 phosphorylation site of eukaryotic translation initiation factor 2α, were hyper-sensitive to α-toxin. Inhibition of translation w…

lcsh:Immunologic diseases. AllergyMAPK/ERK pathwayImmunologyeIF2αBiologyCycloheximide03 medical and health scienceschemistry.chemical_compoundCellular toleranceImmunology and AllergyInitiation factorpore forming toxinsReceptorOriginal Research030304 developmental biologyGenetics0303 health sciencesKinase030302 biochemistry & molecular biologyJNK Mitogen-Activated Protein KinasesADAM10Translation (biology)MAPKCell biologyEIF2AK4chemistryPhosphorylationCytolysinS. aureus α-toxinlcsh:RC581-607Frontiers in Immunology
researchProduct

Amphiregulin activates human hepatic stellate cells and is upregulated in non alcoholic steatohepatitis

2015

AbstractAmphiregulin (AR) involvement in liver fibrogenesis and hepatic stellate cells (HSC) regulation is under study. Non-alcoholic fatty liver disease (NAFLD) and its more severe form non-alcoholic steatohepatitis (NASH) may progress to cirrhosis and hepatocellular cancer (HCC). Our aim was to investigate ex vivo the effect of AR on human primary HSC (hHSC) and verify in vivo the relevance of AR in NAFLD fibrogenesis. hHSC isolated from healthy liver segments were analyzed for expression of AR and its activator, TNF-α converting enzyme (TACE). AR induction of hHSC proliferation and matrix production was estimated in the presence of antagonists. AR involvement in fibrogenesis was also ass…

medicine.medical_specialtyBiopsyGene ExpressionADAM17 ProteinBiologyAmphiregulinSeverity of Illness Indexp38 Mitogen-Activated Protein Kinasesdigestive systemArticleMicePhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineDownregulation and upregulationAmphiregulinGrowth factor receptorNon-alcoholic Fatty Liver DiseaseInternal medicineHepatic Stellate CellsmedicineAnimalsHumansProtein Kinase CPI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biology0303 health sciencesMultidisciplinaryFatty livernutritional and metabolic diseasesmedicine.diseaseFibrosisActinsdigestive system diseases3. Good healthEnzyme ActivationErbB ReceptorsADAM ProteinsDisease Models AnimalEndocrinologyHepatic stellate cellCancer research030211 gastroenterology & hepatologyTumor necrosis factor alphaCollagenSteatohepatitisSignal TransductionScientific Reports
researchProduct

Dual specificity phosphatase 1 knockout mice show enhanced susceptibility to anaphylaxis but are sensitive to glucocorticoids.

2007

Dual specificity phosphatase DUSP1 (otherwise known as mitogen-activated phosphatase 1 or MKP-1) dephosphorylates MAPKs, particularly p38, and negatively regulates innate immunity. Recent studies have shown that the DUSP1 gene is transcriptionally up-regulated by glucocorticoids (GCs) and that the antiinflammatory action of GCs is impaired in DUSP1-/- mice. Here we show that GC-mediated dephosphorylation of ERK-1 and ERK-2 activated by IgE receptor cross-linking is unimpaired in bone marrow-derived mast cells (BMMCs) of DUSP1-/- mice. Dephosphorylation of phospho-p38 MAPK is impaired but only at early times of GC treatment. Proinflammatory cytokine and chemokine gene expression (CCL2, IL-6,…

medicine.medical_specialtyChemokinePhosphataseImmunoglobulin Ep38 Mitogen-Activated Protein KinasesProinflammatory cytokineDephosphorylationMiceEndocrinologyInternal medicineSepsisDual-specificity phosphatasemedicineAnimalsGenetic Predisposition to DiseaseMolecular BiologyAnaphylaxisGlucocorticoidsMice KnockoutMitogen-Activated Protein Kinase 1Mice Inbred C3HMitogen-Activated Protein Kinase 3biologyInterleukin-6Tumor Necrosis Factor-alphaDegranulationDual Specificity Phosphatase 1General MedicineMice Inbred C57BLEndocrinologyGene Expression RegulationMice Inbred DBAbiology.proteinCytokinesTumor necrosis factor alphaMolecular endocrinology (Baltimore, Md.)
researchProduct