Search results for "p38 Mitogen-Activated Protein Kinases"

showing 10 items of 145 documents

Nuclear protein kinases: still enigmatic components in plant cell signalling

2010

International audience; Plants constantly face changing conditions in their environment. Unravelling the transduction mechanisms from signal perception at the plasma membrane level down to gene expression in the nucleus is a fascinating challenge. Protein phosphorylation, catalysed by protein kinases, is one of the major posttranslational modifications involved in the specificity, kinetic(s) and intensity of a signal transduction pathway. Although commonly assumed, the involvement of nuclear protein kinases in signal transduction is often poorly characterized. In particular, both their regulation and mode of action remain to be elucidated and may lead to the unveiling of new original mechan…

0106 biological sciencesPhysiologyp38 mitogen-activated protein kinasesPROTEIN KINASENUCLEAR TRANSLOCATIONPlant ScienceBiology01 natural sciencesSecond Messenger Systems03 medical and health sciencesNCK1Protein phosphorylationNuclear proteinNUCLEUS030304 developmental biologyPROTEIN (DE)PHOSPHORYLATION0303 health sciencesGRB10SIGNAL TRANSDUCTIONNuclear ProteinsAutophagy-related protein 13PlantsCell biology[SDV.BV.PEP]Life Sciences [q-bio]/Vegetal Biology/Phytopathology and phytopharmacyBiochemistryCDC37Mitogen-activated protein kinasebiology.proteinProtein Kinases010606 plant biology & botany
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Selective p38α MAP kinase/MAPK14 inhibition in enzymatically modified LDL-stimulated human monocytes: implications for atherosclerosis.

2016

The first ATP-competitive p38α MAPK/MAPK14 inhibitor with excellent in vivo efficacy and selectivity, skepinone-L, is now available. We investigated the impact of selective p38α MAPK/MAPK14 inhibition on enzymatically modified LDL (eLDL) stimulated human monocytes with its implications for atherosclerosis. Among the different p38 MAPK isoforms, p38α/MAPK14 was the predominantly expressed and activated isoform in isolated human peripheral blood monocytes. Moreover, eLDL colocalized with macrophages positive for p38α MAPK/MAPK14 in human carotid endarterectomy specimens. Using the human leukemia cell line THP-1 and/or primary monocyte-derived macrophages, skepinone-L inhibited eLDL-induced ac…

0301 basic medicineAdultMaleChemokineMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesCD36CCL4Dibenzocycloheptenes030204 cardiovascular system & hematologyBiochemistryGene Expression Regulation EnzymologicMonocytesMitogen-Activated Protein Kinase 1403 medical and health sciences0302 clinical medicineCell Line TumorGeneticsHumansInterleukin 8Molecular BiologyFoam cellMAPK14AgedAged 80 and overCaspase 7biologyChemistryCaspase 3Cholesterol LDLAtherosclerosisMolecular biology030104 developmental biologyBiochemistryMitogen-activated protein kinasebiology.proteinFemaleBiotechnologyFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Oxidative stress preconditioning of mouse perivascular myogenic progenitors selects a subpopulation of cells with a distinct survival advantage in vi…

2018

AbstractCell engraftment, survival and integration during transplantation procedures represent the crux of cell-based therapies. Thus, there have been many studies focused on improving cell viability upon implantation. We used severe oxidative stress to select for a mouse mesoangioblast subpopulation in vitro and found that this subpopulation retained self-renewal and myogenic differentiation capacities while notably enhancing cell survival, proliferation and migration relative to unselected cells. Additionally, this subpopulation of cells presented different resistance and recovery properties upon oxidative stress treatment, demonstrating select advantages over parental mesoangioblasts in …

0301 basic medicineCancer ResearchCellular differentiationCellstem cells; oxidative stress; clone isolation/dk/atira/pure/subjectarea/asjc/2800/2804Mice SCIDp38 Mitogen-Activated Protein KinasesMiceCell MovementProtein IsoformsMuscular Dystrophy/dk/atira/pure/subjectarea/asjc/2400/2403Settore BIO/06 - Anatomia Comparata E Citologiaeducation.field_of_studylcsh:CytologyStem CellsSettore BIO/13Cell DifferentiationSkeletalCell biologymedicine.anatomical_structureMuscleMatrix Metalloproteinase 2Animals; Cell Cycle Checkpoints; Cell Differentiation; Cell Line; Cell Movement; Cell Survival; Hydrogen Peroxide; Matrix Metalloproteinase 2; Mice; Mice SCID; Muscle Skeletal; Muscular Dystrophy Animal; Oxidative Stress; Protein Isoforms; Reactive Oxygen Species; Sarcoglycans; Stem Cell Transplantation; Stem Cells; p38 Mitogen-Activated Protein Kinases/dk/atira/pure/subjectarea/asjc/1300/1306/dk/atira/pure/subjectarea/asjc/1300/1307Cell SurvivalPopulationImmunologyBiologySCIDArticleCell Line03 medical and health sciencesCellular and Molecular NeuroscienceIn vivoSarcoglycansmedicineAnimalsProgenitor celllcsh:QH573-671educationMuscle Skeletaloxidative streMesoangioblastAnimalCell BiologyCell Cycle CheckpointsHydrogen PeroxideMuscular Dystrophy Animalclone isolationTransplantationstem cellOxidative Stress030104 developmental biologyCell cultureReactive Oxygen SpeciesStem Cell TransplantationCell Death & Disease
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Polyphenols from Pennisetum glaucum grains induce MAP kinase phosphorylation and cell cycle arrest in human osteosarcoma cells

2019

Abstract Osteosarcoma is the most common bone tumor with a high prevalence among children and adolescents. Polyphenols are widely investigated for their chemopreventive and chemotherapeutic proprieties. In the present study, we explored the pro-apoptotic effects of pearl millet, Pennisetum glaucum, phenolic compounds (PGPC) on osteosarcoma U-2OS cells. Our results show that PGPC induced U-2OS cells death, in a dose dependent manner, with an IC50 of 80 μg/mL. Annexin-V and 7-AAD staining show that PGPC induced cell death mainly through caspase-dependent apoptosis as shown by a decrease in cell death when co-treated with pan-caspase inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketon…

0301 basic medicineCell signalingProgrammed cell deathCell cycle checkpointp38 mitogen-activated protein kinases[SDV]Life Sciences [q-bio]Medicine (miscellaneous)Pearl milletCell cycle arrest03 medical and health sciences0404 agricultural biotechnologyTX341-641Intracellular calciumProtein kinase BPI3K/AKT/mTOR pathwayCaspase030109 nutrition & dieteticsNutrition and DieteticsbiologyNutrition. Foods and food supplyChemistryCyclin-dependent kinase 2Polyphenols04 agricultural and veterinary sciencesU-2OS cells040401 food scienceMolecular biology3. Good healthApoptosisbiology.proteinFood Science
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SGLT-2 (Sodium-Glucose Cotransporter 2) Inhibition Reduces Ang II (Angiotensin II)-Induced Dissecting Abdominal Aortic Aneurysm in ApoE (Apolipoprote…

2019

Objective: Abdominal aortic aneurysm (AAA) is a pathological condition of permanent vessel dilatation that predisposes to the potentially fatal consequence of aortic rupture. SGLT-2 (sodium-glucose cotransporter 2) inhibitors have emerged as powerful pharmacological tools for type 2 diabetes mellitus treatment. Beyond their glucose-lowering effects, recent studies have shown that SGLT-2 inhibitors reduce cardiovascular events and have beneficial effects on several vascular diseases such as atherosclerosis; however, the potential effects of SGLT-2 inhibition on AAA remain unknown. This study evaluates the effect of oral chronic treatment with empagliflozin—an SGLT-2 inhibitor—on dissecting …

0301 basic medicineDissecting Abdominal Aortic AneurysmApolipoprotein EMalemedicine.medical_specialtyInflammation030204 cardiovascular system & hematologyp38 Mitogen-Activated Protein Kinases03 medical and health sciencesMice0302 clinical medicineApolipoproteins EGlucosidesInternal medicinemedicineAnimalsHumansBenzhydryl CompoundsAortic ruptureSodium-Glucose Transporter 2 InhibitorsCells CulturedNeovascularization Pathologicbusiness.industryAngiotensin IINF-kappa Bmedicine.diseaseAngiotensin IIAbdominal aortic aneurysmMatrix MetalloproteinasesMice Inbred C57BLAortic Dissection030104 developmental biologyEndocrinologySodium/Glucose Cotransporter 2Knockout mousemedicine.symptomChemokinesCardiology and Cardiovascular MedicinebusinessAortic Aneurysm AbdominalArteriosclerosis, thrombosis, and vascular biology
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Role of the DNA repair glycosylase OGG1 in the activation of murine splenocytes

2017

OGG1 (8-oxoguanine-DNA glycosylase) is the major DNA repair glycosylase removing the premutagenic DNA base modification 8-oxo-7,8-dihydroguanine (8-oxoG) from the genome of mammalian cells. In addition, there is accumulating evidence that OGG1 and its substrate 8-oxoG might function in the regulation of certain genes, which could account for an attenuated immune response observed in Ogg1-/- mice in several settings. Indications for at least two different mechanisms have been obtained. Thus, OGG1 could either act as an ancillary transcription factor cooperating with the lysine-specific demethylase LSD1 or as an activator of small GTPases. Here, we analysed the activation by lipopolysaccaride…

0301 basic medicineGuanineDNA RepairDNA repairp38 mitogen-activated protein kinasesBiologyBiochemistryDNA GlycosylasesMice03 medical and health sciencesAnimalsMolecular BiologyTranscription factorTumor Necrosis Factor-alphaKinaseActivator (genetics)MacrophagesDNACell BiologyBase excision repairMolecular biology030104 developmental biologyGene Expression RegulationDNA glycosylaseTumor necrosis factor alphaSpleenDNA DamageTranscription FactorsDNA Repair
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The analysis of estrogen receptor-α positive breast cancer stem-like cells unveils a high expression of the serpin proteinase inhibitor PI-9: Possibl…

2016

Abstract Breast cancer stem cells seem to play important roles in breast tumor recurrence and endocrine therapy resistance, although the underlying mechanisms have not been well established. Moreover, in some tumor systems the immunosurveillance failure against cancer cells has been related to the presence of the granzyme B inhibitor PI-9. This study explored the status of PI-9 in tumorspheres isolated from estrogen receptor-α positive (ERα+) breast cancer MCF7 cells. Studies were performed in tertiary tumorspheres which possess high levels of stemness markers (Nanog, Oct3/4 and Sox2) and self-renewal ability. The exposure to estrogens (17-β estradiol and genistein) increased the number and…

0301 basic medicineHomeobox protein NANOGReceptors CXCR4Cancer Researchmedicine.medical_specialtyEstrogen receptorBreast NeoplasmsBiologyp38 Mitogen-Activated Protein KinasesGranzymes03 medical and health sciences0302 clinical medicineBreast cancerSOX2Internal medicineserpin proteinase inhibitor 9 breast cancer stem-like cells breast cancer estrogen receptorsSettore BIO/10 - BiochimicamedicineHumansSerpinsCell ProliferationEstrogen Receptor alphaCancermedicine.diseaseGenisteinGene Expression Regulation NeoplasticImmunosurveillance030104 developmental biologyEndocrinologyOncology030220 oncology & carcinogenesisCancer cellMCF-7 CellsNeoplastic Stem CellsCancer researchFemaleNeoplasm Recurrence LocalStem cellSignal Transduction
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Loss of cellular FLICE-inhibitory protein promotes acute cholestatic liver injury and inflammation from bile duct ligation.

2017

Cholestatic liver injury results from impaired bile flow or metabolism and promotes hepatic inflammation and fibrogenesis. Toxic bile acids that accumulate in cholestasis induce apoptosis and contribute to early cholestatic liver injury, which is amplified by accompanying inflammation. The aim of the current study was to evaluate the role of the antiapoptotic caspase 8-homolog cellular FLICE-inhibitory (cFLIP) protein during acute cholestatic liver injury. Transgenic mice exhibiting hepatocyte-specific deletion of cFLIP (cFLIP−/−) were used for in vivo and in vitro analysis of cholestatic liver injury using bile duct ligation (BDL) and the addition of bile acids ex vivo. Loss of cFLIP in h…

0301 basic medicineLiver CirrhosisTime FactorsPhysiologyCASP8 and FADD-Like Apoptosis Regulating ProteinInflammationApoptosisp38 Mitogen-Activated Protein KinasesHepatitisBile Acids and Salts03 medical and health sciencesNecrosisCholestasisPhysiology (medical)medicineHepatic Stellate CellsAnimalsASK1Genetic Predisposition to DiseaseLigationCells CulturedTumor Necrosis Factor alpha-Induced Protein 3chemistry.chemical_classificationLiver injuryCommon Bile DuctMice KnockoutReactive oxygen speciesHepatologyBile duct ligationGastroenterologyTranscription Factor RelAmedicine.diseaseOxidative Stress030104 developmental biologyCholedocholithiasisPhenotypechemistryLiverNeutrophil InfiltrationApoptosisFLICE Inhibitory ProteinCancer researchHepatocytesCytokinesmedicine.symptomInflammation MediatorsSignal TransductionAmerican journal of physiology. Gastrointestinal and liver physiology
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Time-course of thiol oxidation of protein phosphatases during cerulein-induced acute pancreatitis

2018

Acute pancreatitis (AP) is an acute inflammatory process of the pancreatic gland. The aim of this work was to evaluate the role of thiol oxidation of key proteins that can be involved in the regulation of the inflammatory process during AP. AP was induced in C57BL/6 mice by 7 hourly subcutaneous injections of cerulein (50 ug/kg bw). Animals were sacrificed after 1, 3, 5 and 7 injections of cerulein. One hour after the first injection, hyperoxidation of peroxiredoxin 1–4 was detected coinciding with a H2O2 peak. Three hours later, a marked up-regulation of mRNA and protein expression of sulfiredoxin, partially mediated by Nrf-2, takes place. The up-regulation of sulfiredoxin seems to be resp…

0301 basic medicineMessenger RNA030102 biochemistry & molecular biologyChemistryp38 mitogen-activated protein kinasesThiol oxidationPhosphataseProtein phosphatase 2Pharmacologymedicine.diseaseBiochemistry03 medical and health sciencesSulfiredoxin0302 clinical medicine030220 oncology & carcinogenesisPhysiology (medical)medicineAcute pancreatitisPeroxiredoxinFree Radical Biology and Medicine
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Activation of microglia synergistically enhances neurodegeneration caused by MPP+ in human SH-SY5Y cells

2019

While MPP+ may not directly activate microglia, the initial neuronal damage inflicted by the toxin may trigger microglia, possibly leading to synergistic pro-apoptotic interaction between neuro-inflammation and toxin-induced neurotoxicity, which may further aggravate neurodegeneration. However, what molecular targets are synergistically up or downregulated during this interaction is not well understood. Here, we addressed this by co-culturing fully differentiated human SH-SY5Y cells treated with parkinsonian toxin 1-Methyl-4-phenylpyridinium (MPP+), with endotoxin-activated microglial cell line EOC 20 to determine how this interaction affects pro-apoptotic (p38, JNK, and bax:bcl2 ratios) an…

0301 basic medicinePharmacologySH-SY5YMicrogliaChemistryp38 mitogen-activated protein kinasesNeurodegenerationNeurotoxicityInflammationmedicine.diseaseCell biology03 medical and health sciences030104 developmental biology0302 clinical medicinemedicine.anatomical_structureApoptosismedicineViability assaymedicine.symptom030217 neurology & neurosurgeryEuropean Journal of Pharmacology
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