Search results for "P3"

showing 10 items of 786 documents

A novel regulatory mechanism of MAP kinases activation and nuclear translocation mediated by PKA and the PTP-SL tyrosine phosphatase

1999

Protein tyrosine phosphatase PTP-SL retains mitogen-activated protein (MAP) kinases in the cytoplasm in an inactive form by association through a kinase interaction motif (KIM) and tyrosine dephosphorylation. The related tyrosine phosphatases PTP-SL and STEP were phosphorylated by the cAMP-dependent protein kinase A (PKA). The PKA phosphorylation site on PTP-SL was identified as the Ser231 residue, located within the KIM. Upon phosphorylation of Ser231, PTP-SL binding and tyrosine dephosphorylation of the MAP kinases extracellular signal–regulated kinase (ERK)1/2 and p38α were impaired. Furthermore, treatment of COS-7 cells with PKA activators, or overexpression of the Cα catalytic subunit …

Cytoplasmanimal structuresRecombinant Fusion ProteinsCèl·lulesAmino Acid MotifsNerve Tissue ProteinsProtein tyrosine phosphataseSH2 domainTransfectionenvironment and public healthModels Biologicalp38 Mitogen-Activated Protein KinasesReceptor tyrosine kinaseSH3 domainCell LinePhosphoserinetyrosine phosphatasesAnimalsHumansProtein phosphorylationPKAReceptor-Like Protein Tyrosine Phosphatases Class 7PhosphorylationPTP-SLCell NucleusMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3biologyBrief ReportIntracellular Signaling Peptides and ProteinsBiological TransportCell BiologyProtein Tyrosine Phosphatases Non-ReceptorCyclic AMP-Dependent Protein KinasesEnzyme Activationenzymes and coenzymes (carbohydrates)MAP kinasesBiochemistryMitogen-activated protein kinaseCOS CellsMutationbiology.proteinPhosphorylationMitogen-Activated Protein KinasesProtein Tyrosine PhosphatasesEnzimssignal transductionProto-oncogene tyrosine-protein kinase Src
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FOXP3 Inhibitory Peptide P60 Increases Efficacy of Cytokine-induced Killer Cells Against Renal and Pancreatic Cancer Cells

2019

Background/aim Cytokine-induced killer (CIK) cells are ex vivo expanded major histocompatibility complex (MHC)-unrestricted cytotoxic cells with promising effects against a variety of cancer types. Regulatory T-cells (T-reg) have been shown to reduce the effectiveness of CIK cells against tumor cells. Peptide P60 has been shown to inhibit the immunosuppressive functions of T-regs. This study aimed at examining the effect of p60 on CIK cells efficacy against renal and pancreatic cancer cells. Materials and methods The effect of P60 on CIK cytotoxicity was examined using flow cytometry, WST-8-based cell viability assay and interferon γ (IFNγ) ELISA. Results P60 treatment resulted in a signifi…

Cytotoxicity ImmunologicCancer ResearchFOXP3Cell SurvivalImmunotherapy.KidneyMajor histocompatibility complexT-Lymphocytes RegulatoryInterferon-gamma03 medical and health sciencesCytokine-Induced Killer Cells0302 clinical medicineCytokine-induced killer (CIK) cellCell Line TumorPancreatic cancermedicineHumansCytotoxic T cellViability assayCytotoxicityPancreasCancerCytokine-induced killer cellbiologyChemistryFOXP3Forkhead Transcription FactorsGeneral Medicinemedicine.diseaseCoculture TechniquesKidney NeoplasmsPancreatic NeoplasmsOncologyCell culture030220 oncology & carcinogenesisAdoptive cell transferCancer researchbiology.proteinCytokinesPeptidesAnticancer Research
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Coordinated induction of drug transporters and phase I and II metabolism in human liver slices

2008

Although regulation of phase I drug metabolism in human liver is relatively well studied, the regulation of phase II enzymes and of drug transporters is incompletely characterized. Therefore, we used human liver slices to investigate the PXR, CAR and AhR-mediated induction of drug transporters and phase I and II metabolic enzymes. Precision-cut human liver slices were incubated for 5 or 24 h with prototypical inducers: phenobarbital (PB) (50 mu M) for CAR, beta-naphthoflavone (BNF) (25 mu M) for AhR, and rifampicin (RIF) (10 mu M) for PXR, and gene expression of the phase I enzymes CYP1A1, 1A2, 3A4, 3A5, 2136, 2A6, the phase II enzymes UGT1A1 and 1A6, and the transporters MRP2, MDR1, BSEP, …

DIFFERENTIAL REGULATIONQUANTITATIVE RT-PCRRAT-LIVERGene ExpressionPharmaceutical Sciencedrug transportersIn Vitro TechniquesPharmacologydigestive systemCytochrome P-450 Enzyme SystemUDP-GLUCURONOSYLTRANSFERASE 1A1Constitutive androstane receptorHumansSTELLATE CELL ACTIVATIONEnzyme inducerinductionliver slicesCONSTITUTIVE ANDROSTANE RECEPTORchemistry.chemical_classificationPregnane X receptorbiologyCYP3A4Multidrug resistance-associated protein 2TransporterPRIMARY HUMAN HEPATOCYTESMetabolic Detoxication Phase IIdrug metabolismEnzymeLiverPharmaceutical PreparationsBiochemistrychemistryEnzyme Inductionbiology.proteinMetabolic Detoxication Phase IPREGNANE-X-RECEPTORCarrier ProteinsPROTOTYPICAL INDUCERSDrug metabolismBILE-ACIDEuropean Journal of Pharmaceutical Sciences
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"Table 54" of "Tuning and test of fragmentation models based on identified particles and precision event shape data."

1996

XP distribution for DEL++ production.. Data read from plot.

DN/DXInclusiveE+ E- --> DELTA(1232P33)++ XE+ E- Scattering91.2Single Differential Distribution
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Ultraviolet light-induced apoptotic death is impaired by the HMG-CoA reductase inhibitor lovastatin.

2003

HMG-CoA reductase inhibitors (i.e., statins) attenuate C-terminal isoprenylation of Rho GTPases, thereby inhibiting UV-C-induced activation of c-Jun-N-terminal kinases/stress-activated protein kinases (JNKs/SAPKs). Inhibition of UV-C-triggered JNK/SAPK activation by lovastatin is due to inhibition of Rac-SEK1/MKK4-mediated phosphorylation of JNKs/SAPKs at Thr183/Tyr185. UV-C-stimulated phosphorylation of p38 kinase (Thr180/Tyr182) is also impaired by lovastatin. Cell killing provoked by UV-C irradiation was significantly inhibited by lovastatin. This was paralleled by a reduced frequency of chromosomal aberrations, accelerated recovery from UV-C-induced transient replication blockage, inhib…

DNA ReplicationUltraviolet Raysp38 mitogen-activated protein kinasesBiophysicsApoptosisCHO CellsBiochemistryp38 Mitogen-Activated Protein KinasesCricetinaemedicineUltraviolet lightAnimalsMitogen-Activated Protein Kinase 8LovastatinMolecular BiologyCaspasebiologyKinaseCell BiologyCell biologyrac GTP-Binding ProteinsEnzyme ActivationCell killingApoptosisCaspasesHMG-CoA reductasebiology.proteinLovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsMitogen-Activated Protein Kinasesmedicine.drugBiochemical and biophysical research communications
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NLRP3 controls ATM activation in response to DNA damage

2020

The DNA damage response (DDR) is essential to preserve genomic integrity and acts as a barrier to cancer. The ATM pathway orchestrates the cellular response to DNA double strand breaks (DSBs), and its attenuation is frequent during tumorigenesis. Here, we show that NLRP3, a Pattern Recognition Receptor known for its role in the inflammasome complex formation, interacts with the ATM kinase to control the early phase of DDR, independently of its inflammasome activity. NLRP3 down-regulation in human bronchial epithelial cells impairs ATM pathway activation as shown by an altered ATM substrate phosphorylation profile, and due to impaired p53 activation, confers resistance to acute genomic stres…

DNA damage[SDV]Life Sciences [q-bio]medicine.disease_cause03 medical and health sciencesSubstrate-level phosphorylationchemistry.chemical_compound0302 clinical medicineDNA Damage Signalingmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular Biology[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyCancer0303 health sciencesInnate immune systemintegumentary systemChemistryNLRP3 receptorPattern recognition receptorInflammasome3. Good healthCell biology[SDV] Life Sciences [q-bio]030220 oncology & carcinogenesisCarcinogenesisInflammasome complexDNAmedicine.drug
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Vip3C, a novel class of vegetative insectidal proteins from Bacillus thuringiensis

2012

Three vip3 genes were identified in two Bacillus thuringiensis Spanish collections. Sequence analysis revealed a novel Vip3 protein class (Vip3C). Preliminary bioassays of larvae from 10 different lepidopteran species indicated that Vip3Ca3 caused more than 70% mortality in four species after 10 days at 4 οg/cm 2. © 2012, American Society for Microbiology.

DNA BacterialBioquímicaSequence analysisMolecular Sequence DataBiotecnologia agrícolaBacillus thuringiensisBiologyApplied Microbiology and BiotechnologyLepidoptera genitaliaBacterial proteinPlagues ControlBacterial ProteinsPhylogeneticsBacillus thuringiensisBotanyPlaguicidesInvertebrate MicrobiologyAnimalsBioassayGenePhylogenyLarvaSequence Homology Amino AcidEcologyfungiSequence Analysis DNAbiology.organism_classificationSurvival AnalysisVip3 genesLepidopteraSpainLarvaProteïnesFood ScienceBiotechnology
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Contribution of CYP3A5 to the in vitro hepatic clearance of tacrolimus.

2005

Abstract Background: Tacrolimus is metabolized predominantly to 13-O-demethyltacrolimus in the liver and intestine by cytochrome P450 3A (CYP3A). Patients with high concentrations of CYP3A5, a CYP3A isoenzyme polymorphically produced in these organs, require higher doses of tacrolimus, but the exact mechanism of this association is unknown. Methods: cDNA-expressed CYP3A enzymes and a bank of human liver microsomes with known CYP3A4 and CYP3A5 content were used to investigate the contribution of CYP3A5 to the metabolism of tacrolimus to 13-O-demethyltacrolimus as quantified by liquid chromatography–tandem mass spectrometry. Results: Demethylation of tacrolimus to 13-O-demethyltacrolimus was …

DNA ComplementaryCYP3AClinical BiochemistryPharmacologyBiologyIn Vitro Techniques030226 pharmacology & pharmacyTacrolimus03 medical and health sciences0302 clinical medicinePharmacokineticsCytochrome P-450 Enzyme SystemCytochrome P-450 CYP3AHumansCYP3A7030304 developmental biologyDemethylation0303 health sciencesCYP3A4Biochemistry (medical)MetabolismTacrolimusMicrosomeMicrosomes LiverBaculoviridaeImmunosuppressive AgentsClinical chemistry
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Structure of SNX9 SH3 in complex with a viral ligand reveals the molecular basis of its unique specificity for alanine-containing class I SH3 motifs

2021

Class I SH3 domain-binding motifs generally comply with the consensus sequence [R/K]x0PxxP, the hydrophobic residue 0 being proline or leucine. We have studied the unusual 0 = Ala-specificity of SNX9 SH3 by determining its complex structure with a peptide present in eastern equine encephalitis virus (EEEV) nsP3. The structure revealed the length and composition of the n-Src loop as important factors determining specificity. We also compared the affinities of EEEV nsP3 peptide, its mutants, and cellular ligands to SNX9 SH3. These data suggest that nsP3 has evolved to minimize reduction of conformational entropy upon binding, hence acquiring stronger affinity, enabling takeover of SNX9. The R…

DYNAMICSPROLINE-RICH PEPTIDESviruksetPROTEINSvirusesHTLV-1 GagLigandsEVOLUTIONARY CONSERVATIONalfaviruksetsrc Homology DomainsHIGH-AFFINITYretroviruksetDOMAINStructural BiologyBINDINGAnimalsHorsesMolecular Biologysoluviestintä11832 Microbiology and virologyAlanineBinding SitesPXXP MOTIFSisothermal titration calorimetrySH3solution NMR spectroscopyEEEV nsP3HIV-11182 Biochemistry cell and molecular biologyproteiinitCHEMICAL-SHIFTS3111 BiomedicinePeptidesSNX9Protein Binding
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Smadzeņu viļņus analizējošas programmatūras izstrāde

2018

Piekļuve personālajām EEG ierīcēm pēdējos gados ir strauji augusi, radot interesi par to potenciālo pietietojumu smadzeņu – datora interfeisa izveidē. Šī pētniecības darba mērķis ir apkopot informāciju par to kā smadzenēs ģenerētu signālu ir iespējams pārveidot komandās ar kurām iespējams vadīt dažāda veida programmatūru. Darbā tiek pētīts kādus smadzeņu signālus ir iespējams pārvērst vadības komandās, kādi ir populārākie algoritmi šo signālu pārveidošanai un kādi smadzeņu – datora interfeisa veidi šobrīd ir pieejami programmatūras izstrādei. Tiek pievērsta uzmanība arī tam kāda ir personālo EEG ierīču kvalitāte un vai tā ir piemērota kvalitatīvai programmatūras vadībai.

Datorzinātnesmadzeņu - datora interfeissEEGalfa viļņiP300
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