Search results for "Sarcoplasmic Reticulum Calcium-Transporting ATPases"

showing 6 items of 6 documents

SERCA and P-glycoprotein inhibition and ATP depletion are necessary for celastrol-induced autophagic cell death and collateral sensitivity in multidr…

2019

Multidrug resistance (MDR) represents an obstacle in anti-cancer therapy. MDR is caused by multiple mechanisms, involving ATP-binding cassette (ABC) transporters such as P-glycoprotein (P-gp), which reduces intracellular drug levels to sub-therapeutic concentrations. Therefore, sensitizing agents retaining effectiveness against apoptosis- or drug-resistant cancers are desired for the treatment of MDR cancers. The sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA) pump is an emerging target to overcome MDR, because of its continuous expression and because the calcium transport function is crucial to the survival of tumor cells. Previous studies showed that SERCA inhibitors exhibit anti-c…

0301 basic medicineProgrammed cell deathSERCALung NeoplasmsCell SurvivalAntineoplastic AgentsAutophagy-Related Protein 7Sarcoplasmic Reticulum Calcium-Transporting ATPases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAdenosine TriphosphateCell Line TumorAutophagyAnimalsHumansATP Binding Cassette Transporter Subfamily B Member 1P-glycoproteinPharmacologybiologyDose-Response Relationship DrugChemistryAutophagyXenograft Model Antitumor AssaysDrug Resistance MultipleTriterpenesMultiple drug resistanceMice Inbred C57BL030104 developmental biologyCelastrolApoptosisDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer cellbiology.proteinCancer researchHepatocytesPentacyclic TriterpenesPharmacological research
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Oxidative modification impairs SERCA activity in Drosophila and human cell models of Parkinson's disease

2021

DJ-1 is a causative gene for familial Parkinson's disease (PD) with different functions, standing out its role against oxidative stress (OS). Accordingly, PD model flies harboring a mutation in the DJ-1β gene (the Drosophila ortholog of human DJ-1) show high levels of OS markers like protein carbonylation, a common post-translational modification that may alter protein function. To increase our understanding of PD pathogenesis as well as to discover potential therapeutic targets for pharmacological intervention, we performed a redox proteomic assay in DJ-1β mutant flies. Among the proteins that showed increased carbonylation levels in PD model flies, we found SERCA, an endoplasmic reticulum…

0301 basic medicineSERCAProteomeProtein CarbonylationProtein Deglycase DJ-1MutantOxidative phosphorylationmedicine.disease_causeSarcoplasmic Reticulum Calcium-Transporting ATPasesAnimals Genetically ModifiedProtein CarbonylationNeuroblastoma03 medical and health sciences0302 clinical medicinemedicineAnimalsDrosophila ProteinsHumansMolecular BiologyMutationActivator (genetics)ChemistryEndoplasmic reticulumfungiParkinson DiseaseCell biologyDisease Models AnimalOxidative StressDrosophila melanogasterPhenotype030104 developmental biologyMutationMolecular MedicineCalciumOxidation-Reduction030217 neurology & neurosurgeryOxidative stressBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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Ca2+ signalling plays a role in celastrol‐mediated suppression of synovial fibroblasts of rheumatoid arthritis patients and experimental arthritis in…

2019

Background and purpose Celastrol exhibits anti-arthritic effects in rheumatoid arthritis (RA), but the role of celastrol-mediated Ca2+ mobilization in treatment of RA remains undefined. Here, we describe a regulatory role for celastrol-induced Ca2+ signalling in synovial fibroblasts of RA patients and adjuvant-induced arthritis (AIA) in rats. Experimental approach We used computational docking, Ca2+ dynamics and functional assays to study the sarcoplasmic/endoplasmic reticulum Ca2+ ATPase pump (SERCA). In rheumatoid arthritis synovial fibroblasts (RASFs)/rheumatoid arthritis fibroblast-like synoviocytes (RAFLS), mechanisms of Ca2+ -mediated autophagy were analysed by histological, immunohis…

0301 basic medicinemusculoskeletal diseasesMaleProgrammed cell deathSERCAArthritisSarcoplasmic Reticulum Calcium-Transporting ATPasesArthritis RheumatoidRats Sprague-Dawley03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBAPTAmedicineAutophagyAnimalsHumansCalcium SignalingCells CulturedPharmacologyMice KnockoutGene knockdownbiologyChemistrySynovial MembraneCalpainFibroblastsmedicine.diseaseResearch PapersArthritis ExperimentalTriterpenesCalcineurin030104 developmental biologyGene Expression RegulationCelastrolbiology.proteinCancer researchPentacyclic Triterpenes030217 neurology & neurosurgeryResearch PaperBritish Journal of Pharmacology
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Tracking Ca

2019

We characterize thus-far elusive domain rearrangements of a calcium-transporting ATPase in the native membrane.

Ion TransportProtein ConformationBiophysicsQuantitative Structure-Activity RelationshipSciAdv r-articlesMolecular Dynamics SimulationCrystallography X-RaySarcoplasmic Reticulum Calcium-Transporting ATPasesKineticsStructural BiologyCalciumProtein Interaction Domains and MotifsResearch ArticlesProtein BindingResearch ArticleScience advances
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Effects of sulindac sulfide on the membrane architecture and the activity of gamma-secretase.

2007

gamma-Secretase is a membrane-embedded multi-protein complex that catalyzes the final cut of the Alzheimer's disease-related amyloid precursor protein (APP) to amyloid-beta peptides of variable length (37-43 amino acids) via an unusual intramembrane cleavage. Recent findings propose that some commonly used non-steroidal anti-inflammatory drugs (NSAIDs) have the ability to modulate specifically gamma-secretase activity without inhibiting the enzyme as a whole. These drugs may shift the processing of APP from the longer amyloid-beta 42 peptide towards shorter, less fibrillogenic and less toxic amyloid-beta species. We hypothesize that gamma-secretase activity, as an enzyme that is strictly as…

Protein subunitBlotting WesternPeptideCHO CellsSarcoplasmic Reticulum Calcium-Transporting ATPasesCellular and Molecular NeuroscienceAmyloid beta-Protein PrecursorCricetulusMembrane MicrodomainsSulindacCricetinaemental disordersAmyloid precursor proteinPresenilin-1AnimalsHumansLipid raftCells CulturedPharmacologychemistry.chemical_classificationbiologyAnti-Inflammatory Agents Non-SteroidalCell MembraneP3 peptideAmino acidMembraneBiochemistrychemistrybiology.proteinBiophysicsAmyloid Precursor Protein SecretasesAmyloid precursor protein secretaseNeuropharmacology
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Synthesis, computational docking and biological evaluation of celastrol derivatives as dual inhibitors of SERCA and P-glycoprotein in cancer therapy.

2021

Abstract A series of eleven celastrol derivatives was designed, synthesized, and evaluated for their in vitro cytotoxic activities against six human cancer cell lines (A549, HepG2, HepAD38, PC3, DLD-1 Bax-Bak WT and DKO) and three human normal cells (LO2, BEAS-2B, CCD19Lu). To our knowledge, six derivatives were the first example of dipeptide celastrol derivatives. Among them, compound 3 was the most promising derivative, as it exhibited a remarkable anti-proliferative activity and improved selectivity in liver cancer HepAD38 versus human normal hepatocytes, LO2. Compound 6 showed higher selectivity in liver cancer cells against human normal lung fibroblasts, CCD19Lu cell line. The Ca2+ mob…

SERCAAntineoplastic AgentsApoptosisPharmacologySarcoplasmic Reticulum Calcium-Transporting ATPaseschemistry.chemical_compoundStructure-Activity RelationshipCell Line TumorDrug DiscoverymedicineCytotoxic T cellHumansATP Binding Cassette Transporter Subfamily B Member 1P-glycoproteinCell ProliferationPharmacologyBinding SitesbiologyOrganic ChemistryCancerGeneral Medicinemedicine.diseaseMolecular Docking SimulationchemistryApoptosisDocking (molecular)CelastrolCell cultureDrug Resistance NeoplasmDrug Designbiology.proteinDrug Screening Assays AntitumorPentacyclic TriterpenesEuropean journal of medicinal chemistry
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