Search results for "HSP72 Heat-Shock Proteins"

showing 7 items of 7 documents

BAG2 Interferes with CHIP-Mediated Ubiquitination of HSP72

2016

The maintenance of cellular proteostasis is dependent on molecular chaperones and protein degradation pathways. Chaperones facilitate protein folding, maturation, and degradation, and the particular fate of a misfolded protein is determined by the interaction of chaperones with co-chaperones. The co-factor CHIP (C-terminus of HSP70-inteacting protein, STUB1) ubiquitinates chaperone substrates and directs proteins to the cellular degradation systems. The activity of CHIP is regulated by two co-chaperones, BAG2 and HSPBP1, which are potent inhibitors of the E3 ubiquitin ligase activity. Here, we examined the functional correlation of HSP72, CHIP, and BAG2, employing human primary fibroblasts.…

0301 basic medicineTime FactorsUbiquitin-Protein LigasesImmunoblottingHSP72 Heat-Shock ProteinsUbiquitin-conjugating enzymeProtein degradationArticleCatalysisCell Linelcsh:ChemistryInorganic Chemistry03 medical and health sciencesUbiquitinddc:570Humansaging; BAG2; CHIP; HSP72; proteostasis; ubiquitinationPhysical and Theoretical ChemistryHSP72lcsh:QH301-705.5Molecular BiologyCellular SenescenceSpectroscopySTUB1proteostasisBAG2biologyCHIPagingOrganic ChemistryUbiquitinationGeneral MedicineComputer Science ApplicationsUbiquitin ligaseCell biology030104 developmental biologyProteostasislcsh:Biology (General)lcsh:QD1-999Chaperone (protein)biology.proteinRNA InterferenceProtein foldingMolecular ChaperonesInternational Journal of Molecular Sciences
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Hsp72 controls bortezomib-induced HepG2 cell death via interaction with pro-apoptotic factors.

2007

The proteasome inhibitor bortezomib is an efficacious inducer of apoptosis in the hepatoma HepG2 cell line. This study shows that bortezomib increased in these cells the level of the survival factor Hsp72 in a time- and dose-dependent manner. In a first phase of treatment, Hsp72 rapidly increased so that at 24 h of incubation with 50 nM bortezomib its level was approximately five-fold higher than the control. In this phase Hsp72 seemed to play a role in preventing HepG2 cell death, since it interacted with and sequestered the pro-apoptotic factors p53, AIF, Bax and Apaf-1. During a second day of treatment, although the nuclear levels of Hsp72, p53 and AIF increased, the interaction of Hsp72…

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularTime FactorsCellBlotting WesternApoptosisHSP72 Heat-Shock ProteinsAmino Acid Chloromethyl KetonesBortezomibCell Line TumormedicineHumansImmunoprecipitationProtease Inhibitorscardiovascular diseasesCaspasebcl-2-Associated X ProteinOncogenebiologyBortezomibReverse Transcriptase Polymerase Chain ReactionLiver NeoplasmsApoptosis Inducing Factorproteasome inhibitor hepatocarcinoma apoptosisGeneral MedicineCell cycleBoronic Acidsmedicine.anatomical_structureApoptotic Protease-Activating Factor 1OncologyApoptosisPyrazinesProteasome inhibitorCancer researchbiology.proteinTumor Suppressor Protein p53Apoptosis Regulatory Proteinsmedicine.drugProtein Binding
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The expression of HSP27 is associated with poor clinical outcome in intrahepatic cholangiocarcinoma.

2007

Abstract Background The heat shock proteins (HSPs) 27-kDa (HSP27) and 72-kDa (HSP72), are ubiquitous chaperone molecules inducible in cells exposed to different stress conditions. Increased level of HSPs are reported in several human cancers, and found to be associated with the resistance to some anticancer treatments and poor prognosis. However, there is no study of the relationship between HSPs expression and patient's prognosis in intrahepatic cholangiocarcinoma (IHCCA). In this exploratory retrospective study, we investigated the expressions of HSP27 and HSP72 as potential prognostic factors in IHCCA. Methods Thirty-one paraffin-embedded samples were analyzed by immunohistochemical meth…

MaleCancer ResearchHSP27 Heat-Shock ProteinsMitosisHSP72 Heat-Shock ProteinsBile Duct Neoplasmlcsh:RC254-282CholangiocarcinomaImmunoenzyme TechniquesNecrosisLymphocytes Tumor-InfiltratingHsp27Surgical oncologyHeat shock proteinGeneticsBiomarkers TumorMedicineHumansNeoplasm InvasivenessSurvival rateIntrahepatic CholangiocarcinomaHeat-Shock ProteinsAgedCell ProliferationRetrospective Studiesbiologybusiness.industryRetrospective cohort studyMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisNeoplasm ProteinsSurvival RateBile Ducts IntrahepaticOncologyBile Duct NeoplasmsImmunologybiology.proteinCancer researchFemaleStem cellbusinessMolecular ChaperonesResearch ArticleBMC cancer
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Chelation of synaptic zinc induces overexcitation in the hilar mossy cells of the rat hippocampus.

2004

Complete removal of synaptic zinc by the chelator dietyldithiocarbamate (DEDTC; 500 mg/kg i.p.) in rat was followed by convulsive behaviour including wet dog shakes alternating immobility. Histological analysis 1 day after DEDTC administration detected expression of heat shock protein in the hippocampus restricted to hilar cells. These cells colocalize the marker for neurons and the glutamate receptor GluR2/3 showing that they are excitatory neurons. Additionally, they projected to the contralateral dentate gyrus. Therefore, they correspond to hilar mossy cells. These data show that the synaptic zinc has a role in normal hippocampus avoiding overexcitation, that would impair functionality e…

medicine.medical_specialtyCentral nervous systemPresynaptic TerminalsWheat Germ Agglutinin-Horseradish Peroxidase ConjugateHippocampusAction PotentialsHSP72 Heat-Shock Proteinsc-FosHippocampusSynaptic TransmissionSeizuresInternal medicineNeural PathwaysmedicineAnimalsReceptors AMPAHeat-Shock ProteinsChelating AgentsbiologyGeneral NeuroscienceDentate gyrusGlutamate receptorColocalizationImmunohistochemistryRatsZincEndocrinologymedicine.anatomical_structurenervous systemDentate GyrusMossy Fibers Hippocampalbiology.proteinExcitatory postsynaptic potentialDitiocarbImmediate early geneProto-Oncogene Proteins c-fosNeuroscience letters
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Neural overexcitation and implication of NMDA and AMPA receptors in a mouse model of temporal lobe epilepsy implying zinc chelation.

2006

Summary: Purpose: Zinc chelation with diethyldithiocarbamate (DEDTC) during nondamaging kainic acid administration enhances excitotoxicity to the level of cell damage. The objective of this work was to study the developing of the lesion in this model of temporal lobe epilepsy and the implications of the different types of glutamate receptors. Methods: The antagonist of the N-methyl-d-aspartate (NMDA) receptor MK-801, and the antagonist of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor GYKI52466, were used concomitantly with intraperitoneal administration of kainic acid (15 mg/kg) followed by DEDTC (150 mg/kg) in mouse. The animals were killed at different times from 4 …

MaleKainic acidmedicine.medical_specialtyExcitotoxicityHippocampusKainate receptorHSP72 Heat-Shock ProteinsAMPA receptorBiologymedicine.disease_causeHippocampusReceptors N-Methyl-D-AspartateSynaptic Transmissionchemistry.chemical_compoundBenzodiazepinesMiceReceptors Kainic AcidInternal medicinemedicineAnimalsReceptors AMPACell damageChelating AgentsKainic AcidCell DeathGlutamate receptormedicine.diseaseDisease Models AnimalZincEndocrinologyNeuroprotective Agentsnervous systemNeurologychemistryEpilepsy Temporal LobeNMDA receptorNeurology (clinical)Dizocilpine MaleateDitiocarbProto-Oncogene Proteins c-fosEpilepsia
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Different Efficiency of Heat Shock Proteins (HSP) to Activate Human Monocytes and Dendritic Cells: Superiority of HSP60

2002

Abstract One essential immunoregulatory function of heat shock protein (HSP) is activation of the innate immune system. We investigated the activation of human monocytes and monocyte-derived dendritic cells (DC) by recombinant human HSP60, human inducible HSP72, and preparations of human gp96 and HSP70 under stringent conditions, in the absence of serum and with highly purified monocytes. HSP60 induced human DC maturation and activated human DC to secrete proinflammatory cytokines. HSP72 induced DC maturation to a lesser extent, but activated human monocytes and immature DC as efficiently as HSP60 to release proinflammatory cytokines. The independence of the effects of HSP60 and HSP72 from …

T-Lymphocytesmedicine.medical_treatmentImmunologyHSP72 Heat-Shock ProteinsPeptide bindingBiologyLymphocyte ActivationMonocytesProinflammatory cytokineAntigens NeoplasmHeat shock proteinmedicineHumansImmunology and AllergyHSP70 Heat-Shock ProteinsSecretionHeat-Shock ProteinsInnate immune systemCell DifferentiationChaperonin 60Dendritic CellsMolecular biologyCoculture TechniquesRecombinant ProteinsHsp70CytokineCytokinesHSP60Inflammation MediatorsSignal TransductionThe Journal of Immunology
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Oncolytic parvovirus H1 induces release of heat-shock protein HSP72 in susceptible human tumor cells but may not affect primary immune cells.

2003

Certain autonomous parvoviruses preferentially replicate in and kill in vitro-transformed cells and may reduce the incidence of spontaneous and implanted tumors in animals. Hence, these viruses and their derivatives are currently under evaluation as antitumor vectors. However, the mechanisms underlying their tumor-suppressing properties are not yet understood. We asked whether the lytic parvovirus H1 may enhance the immunogenicity of infected tumor cells. Out of human melanoma and gastrointestinal tumor cells, we selected the cell line SK29-Mel-1 being very susceptible to H1-induced apoptotic killing. Here, no upregulation of HLA class I and costimulatory molecules could be observed followi…

Cancer ResearchTime FactorsCell SurvivalGenetic VectorsApoptosisHSP72 Heat-Shock ProteinsVirusParvovirusImmune systemCell Line TumorHumansHSP70 Heat-Shock ProteinsTransgenesMolecular BiologyMelanomaCells CulturedHeat-Shock ProteinsbiologyParvovirusImmunogenicityHSC70 Heat-Shock Proteinsbiology.organism_classificationVirologyOncolytic virusUp-RegulationCell killingViral replicationCell cultureCancer researchMolecular MedicineCarrier ProteinsCancer gene therapy
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