Search results for "CA2+"

showing 10 items of 101 documents

Modulation of neuronal phospholipase D activity under depolarizing conditions

1999

Neuronal phospholipase D (PLD) activity was hypothesized to be involved in vesicle trafficking and endocytosis and, possibly, transmitter release. We here report that prolonged depolarization of rat hippocampal slices by potassium chloride (KCl) or 4-aminopyridine inhibited PLD activity. Similarly, PLD activity in rat cortical synaptosomes was significantly inhibited by depolarizing agents including veratridine and ouabain. Inhibition of calcium/calmodulin kinase II (CaMKII) which positively modulates synaptosomal PLD activity [Sarri et al. (1998) FEBS Lett. 440, 287-290] by KN-62 caused a further reduction of PLD activity in depolarized synaptosomes. Depolarization-induced inhibition of PL…

Phosphatidylinositol 45-DiphosphateTime FactorsBiophysicschemistry.chemical_elementCalciumHippocampusBiochemistryOuabainMembrane PotentialsPotassium Chloridechemistry.chemical_compoundStructural BiologyCa2+/calmodulin-dependent protein kinaseSynaptosomeElectrochemistryPhospholipase DGeneticsmedicineAnimalsPhospholipase D activityEnzyme InhibitorsRats WistarMolecular BiologyProtein Kinase CProtein Synthesis InhibitorsSynaptosomePhospholipase DCalcium/calmodulin-dependent protein kinase IINeomycinDepolarizationPhosphatidylinositol-45-bisphosphateCell BiologyRatsCell biologyenzymes and coenzymes (carbohydrates)chemistryCalcium-Calmodulin-Dependent Protein KinasesDepolarizationlipids (amino acids peptides and proteins)VeratridineSynaptosomesmedicine.drugFEBS Letters
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Polymorphonuclear leukocyte membrane fluidity and cytosolic Ca2+ content in young adults with acute myocardial infarction. Evaluation at the initial …

2004

Our aim was to examine two aspects of polymorphonuclear leukocyte (PMN) rheology (membrane fluidity and cytosolic Ca2+ content), at baseline and after in vitro activation, in a group of young adults with acute myocardial infarction (AMI) at the initial stage and after 12 months. We enrolled 21 AMI subjects aged < or = 45 years (mean age 41.1 +/- 3.5 years) and evaluated PMN membrane fluidity, labelling intact PMN cells with the fluorescent probe 1,4-(trimethylamino)-phenyl-4-phenylhexatriene and the PMN cytosolic Ca2+ content marking PMN cells with the fluorescent probe Fura 2-AM, at baseline and after in vitro activation with 4-phorbol 12-myristate 13-acetate (PMA) and N-formyl-methionyl-l…

Polymorphonuclear leukocyte Ca2+ contentPolymorphonuclear leukocyte activationAcute myocardial infarction in young peoplePolymorphonuclear leukocyte membrane fluidity
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Brca2/Xrcc2 dependent HR, but not NHEJ, is required for protection against O6-methylguanine triggered apoptosis, DSBs and chromosomal aberrations by …

2008

Abstract O 6 -methylguanine (O 6 MeG) is a highly critical DNA adduct induced by methylating carcinogens and anticancer drugs such as temozolomide, streptozotocine, procarbazine and dacarbazine. Induction of cell death by O 6 MeG lesions requires mismatch repair (MMR) and cell proliferation and is thought to be dependent on the formation of DNA double-strand breaks (DSBs) or, according to an alternative hypothesis, direct signaling by the MMR complex. Given a role for DSBs in this process, either homologous recombination (HR) or non-homologous end joining (NHEJ) or both might protect against O 6 MeG. Here, we compared the response of cells mutated in HR and NHEJ proteins to temozolomide and…

Programmed cell deathGuanineKu80DNA RepairDown-RegulationFluorescent Antibody TechniqueApoptosisCHO CellsBiologyTransfectionBiochemistryMiceO(6)-Methylguanine-DNA MethyltransferaseCricetulusCricetinaeDNA adductTemozolomideAnimalsDNA Breaks Double-StrandedMolecular BiologyBRCA2 ProteinChromosome AberrationsRecombination GeneticCell DeathCell growthCell BiologyTransfectionCell cycleMolecular biologyDNA-Binding ProteinsDacarbazineApoptosisMutationCancer researchHomologous recombinationSister Chromatid ExchangeDNA Repair
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Two distinct Ca2+ influx pathways activated by the bradykinin B2 receptor.

1996

The hormone-induced depletion of cellular Ca stores provides a signal for the Ca2+ influx into electrically non-excitable cells; however, the underlying molecular mechanisms remain elusive. Therefore, we analyzed bradykinin-activated Ca2+ influx into human foreskin fibroblast cells, HF-15, by fura-2 and 45Ca labeling to discriminate between Ca2+ influx into the fura-sensitive compartment and Ca uptake into fura-insensitive Ca stores. Bradykinin-activated CaZt influx into the fura-sensitive compartment was blocked by inhibitors of NO synthases. These inhibitors also suppressed bradykinin-activated increases in cGMP, indicating that the NO-dependent increase in cGMP is involved in the activat…

Receptor Bradykinin B2BradykininBradykininNitric OxideBiochemistryNitric oxideCell Linechemistry.chemical_compoundmedicineCyclic GMP-Dependent Protein KinasesHumansFibroblastCyclic GMPInterphaseFluorescent DyesIon TransportCell growthChemistryKinaseReceptors BradykininCa2 influxCompartment (chemistry)Calcium Channel BlockersCell biologymedicine.anatomical_structureBiochemistryCytoplasmCalciumFura-2Cell DivisionEuropean journal of biochemistry
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Association of recurrent mutations in BRCA1, BRCA2, RAD51C, PALB2, and CHEK2 with the risk of borderline ovarian tumor.

2021

Abstract Background There are several genes associated with ovarian cancer risk. Molecular changes in borderline ovarian tumor (BOT) indicate linkage of this disease to type I ovarian tumors (low-grade ovarian carcinomas). This study determined the prevalence and association of mutations in BRCA1, BRCA2, PALB2, RAD51C, and CHEK2 with the risk of BOTs. Methods The study group consisted of 102 patients with histologically confirmed BOT and 1743 healthy controls. In addition, 167 cases with ovarian cancer G1 were analyzed. The analyses included genotyping of 21 founder and recurrent mutations localized in 5 genes (BRCA1, BRCA2, PALB2, RAD51C, and CHEK2). The risk for developing BOT and low-gra…

Recurrent mutationsBorderline ovarian tumorRAD51COncologyPALB2Low-grade ovarian cancerBRCA1BRCA2CHEK2Genetics (clinical)Hereditary cancer in clinical practice
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Phases transitions in complexe oxides with perovskite structure : case system (1-x)Na0,5Bi0,5TiO3 - xCaTiO3

2015

The solid solutions (1-x)Na0,5Bi0,5TiO3 (NBT) – xCaTiO3 (CT) were studied by X-ray diffraction, Raman spectroscopy, scanning electron microscopy, impedance spectroscopy and DSC. These materials have a perovskite crystalline structure. This study reveals not only the complexity but also the richness of physical phenomena in these compounds: phases transitions sequences, the Ca2+ effect on the physical-chemistry properties and the relation between dielectric properties and crystalline structure. Thereby, (1-x)NBT – xCT solid solutions (0 ≤ x ≤ 1.00) were synthesized by chemical solid route, then they were sintered by a particular procedure in order to avoid sodium and bismuth volatilization. …

Relaxor[CHIM.MATE] Chemical Sciences/Material chemistryDielectric5TiO3 (NBT) – xCaTiO3Phases transitionPerovskiteCa2+ dopingFerroélectriques[PHYS.PHYS.PHYS-CHEM-PH] Physics [physics]/Physics [physics]/Chemical Physics [physics.chem-ph]Solution solide (1-x)Na0Hystérésis thermique5Bi0Transitions de phasesThermal hysteresis5TiO3 (NBT) – xCaTiO3 (CT) solid solutionDiélectriques(1-x)Na0Dopant Ca2+FerroelectricPérovskiteRelaxeurs
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Differential expression pattern of the novel serine/threonine kinase, STK33, in mice and men

2005

Serine/threonine kinase 33 (STK33/Stk33) is a recently discovered gene whose inferred amino acid sequence translation displays characters typical for a calcium/calmodulin dependent kinase (CAMK). In this study we analysed the STK33/Stk33 RNA and protein distribution and the localization of the protein. The STK33/Stk33 expression pattern resembles those of some related members of the CAMK group. STK33/Stk33 displays a nonubiquitous and, in most tissues, low level of expression. It is highly expressed in testis, particularly in cells from the spermatogenic epithelia. Moreover, significant expression is detected in lung epithelia, alveolar macrophages, horizontal cells in the retina and in emb…

Serine/threonine-specific protein kinaseGSK-3Ca2+/calmodulin-dependent protein kinaseAKT1Cell Biologyc-RafBiologyMolecular BiologyBiochemistryMolecular biologyCAMKAKT3MAP2K7FEBS Journal
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Identification and Characterization of BRCA1 and BRCA2 Founder Mutations

2012

A large number of cancer predisposing BRCA1/BRCA2 mutations have been reported, with a wide variety among populations. In some restricted groups, specific germline mutations in these tumor suppressor genes have been found with high predominance, due to a founder effect. We focused our review on the Italian founder mutations. The first Italian BRCA1 founder mutation, 5083del19, was found in Calabria: the presence of common allele in all carriers of this mutation (also in families with Calabrian origin living in other parts of Italy) confirmed its founder effect. The same BRCA1 mutation was identified in the Sicilian population, but only the haplotype analysis can reveal the common ancestor o…

Settore MED/06 - Oncologia Medicabusiness.industryObstetrics and GynecologyMedicineIdentification (biology)Computational biologyBRCA1; BRCA2; Founder mutationBRCA1Founder mutationbusinessBRCA2Current Women's Health Reviews
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Implementation of preventive and predictive BRCA testing in patients with breast, ovarian, pancreatic, and prostate cancer: a position paper of Itali…

2022

Constitutional BRCA1/BRCA2 pathogenic or likely pathogenic variants (PVs) are associated with an increased risk for developing breast and ovarian cancers. Current evidence indicates that BRCA1/2 PVs are also associated with pancreatic cancer, and that BRCA2 PVs are associated with prostate cancer risk. The identification of carriers of constitutional PVs in the BRCA1/2 genes allows the implementation of individual and family prevention pathways, through validated screening programs and risk-reducing strategies. According to the relevant and increasing therapeutic predictive implications, the inclusion of BRCA testing in the routine management of patients with breast, ovarian, pancreatic and…

Societies ScientificMaleOvarian NeoplasmsCancer Researchgenetic counselingBRCABRCA testing; BRCA-related cancer; BRCA1; BRCA2; PARP inhibitors; genetic counseling; pancreatic ductal adenocarcinomaProstatic Neoplasmspancreatic ductal adenocarcinomaScientificSettore MED/03 - GENETICA MEDICABRCA testing; BRCA-related cancer; BRCA1; BRCA2; PARP inhibitors; genetic counseling; pancreatic ductal adenocarcinoma; Female; Humans; Italy; Male; Societies Scientific; Ovarian Neoplasms; Pancreatic Neoplasms; Prostatic NeoplasmsBRCA1BRCA2BRCA-related cancerPancreatic NeoplasmsBRCA testingPARP inhibitorOncologyItalyHumansFemaleSocietiesPARP inhibitors
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Stable expression in HEK-293 cells of the rat alpha3/beta4 subtype of neuronal nicotinic acetylcholine receptor.

1996

The alpha3/beta4 subtype of neuronal nicotinic acetylcholine receptor (nAChR) was stably expressed in human embryonic kidney (HEK) 293 cells that co-expressed a voltage-gated Ca2+ channel. alpha3/beta4-nAChR-expressing clones were identified using the fura-2 Ca2+ imaging technique, and were further characterised by single-cell and whole-cell patch-clamp studies. Acetylcholine (ACh) induced fast activating currents which showed desensitisation and inward rectification. The conductance of the ACh-activated channel was 29 pS. The order of potency of the nicotinic agonists tested was cytisine approximately = nicotine > acetylcholine. The EC50 value for ACh was 145 microM; the Hill coefficient w…

Stable expressionPatch-Clamp Techniquesα3/β4 nAChRBiophysicsNicotinic AntagonistsPharmacologyReceptors NicotinicTransfectionBiochemistryCell LineGanglionic nAChRCa2+ imagingGanglion type nicotinic receptorStructural BiologyMuscarinic acetylcholine receptorGeneticsmedicineAnimalsHumansNicotinic AgonistsNicotinic AntagonistHEK cellMolecular BiologyNeuronsurogenital systemChemistryMuscarinic acetylcholine receptor M3Cell BiologyAcetylcholineRecombinant ProteinsRatsNicotinic acetylcholine receptorNicotinic agonistCalciumCalcium ChannelsAlpha-4 beta-2 nicotinic receptorAcetylcholinemedicine.drugFEBS letters
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