Search results for "binding proteins"

showing 10 items of 911 documents

Restoration of Clostridium difficile toxin-B-inhibited phospholipase D by phosphatidylinositol 4,5-bisphosphate.

1996

Receptor signalling to phospholipase D (PLD) in human embryonic kidney (HEK) cells stably expressing the m3 muscarinic acetylcholine receptor apparently involves Rho proteins. Since phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] has been recognized as an essential cofactor for PLD activity and since activated Rho proteins have been reported to stimulate the synthesis of PtdIns(4,5)P2, we studied whether in HEK cells PLD activity is regulated by PtdIns(4,5)P2 and, in particular, whether PtdIns(4,5)P2 can restore PLD activity inhibited by Clostridium difficile toxin B, which inactivates Rho proteins. Addition of MgATP to permeabilized HEK cells increased basal PLD activity and potentia…

Phosphatidylinositol 45-DiphosphateGTP'Bacterial ToxinsClostridium difficile toxin BBiologyBiochemistryCell Linechemistry.chemical_compoundBacterial ProteinsGTP-Binding ProteinsPhosphatidylcholineRhoB GTP-Binding ProteinPhospholipase DHumansPhosphatidylinositolEnzyme InhibitorsrhoB GTP-Binding ProteinPhospholipase DClostridioides difficileHEK 293 cellsCell MembraneMembrane ProteinsReceptors MuscarinicCell biologyEnzyme Activationenzymes and coenzymes (carbohydrates)chemistryPhosphatidylinositol 45-bisphosphateGuanosine 5'-O-(3-Thiotriphosphate)lipids (amino acids peptides and proteins)European journal of biochemistry
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Control of cellular phosphatidylinositol 4,5-bisphosphate levels by adhesion signals and Rho GTPases in NIH 3T3 fibroblasts

2000

The involvement of small GTPases of the Rho family in the control of phosphoinositide metabolism by adhesion signals was examined in NIH 3T3 fibroblasts. Abrogation of adhesion signals by detachment of cells from their substratum resulted in a time-dependent decrease in the cellular level of PtdIns(4,5)P2 by approximately 50%. This effect could be mimicked by treatment of adherent cells with Clostridium difficile toxin B and toxin B-1470, which inhibit specific subsets of Rho and Ras GTPases. Detachment of cells that had been pretreated with the clostridial toxins did not cause a further reduction in PtdIns(4,5)P2 levels, suggesting that the target GTPases are integrated into the control of…

Phosphatidylinositol 45-Diphosphaterac1 GTP-Binding Proteinrho GTP-Binding ProteinsBacterial ToxinsCellClostridium difficile toxin BRAC1GTPasePhospholipaseBiologyTransfectionBiochemistryMicechemistry.chemical_compoundPhosphoinositide Phospholipase CBacterial ProteinsCell AdhesionmedicineAnimalsPhosphorylationInositol phosphatechemistry.chemical_classificationPhospholipase CCytotoxinsPhosphoric Diester Hydrolases3T3 CellsMolecular biologyRecombinant ProteinsCell biologyKineticsPhosphotransferases (Alcohol Group Acceptor)medicine.anatomical_structurechemistryPhosphatidylinositol 45-bisphosphateType C PhospholipasesCalciumSignal TransductionEuropean Journal of Biochemistry
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Differential gene expression in p53-mediated G(1) arrest of human fibroblasts after gamma-irradiation or N-phosphoacetyl-L-aspartate treatment.

2000

In human fibroblasts, N:-phosphoacetyl-L-aspartate (PALA) and gamma-radiation induce reversible and irreversible p53-mediated G(1) cell cycle arrest, respectively. By coupling the premature chromosome condensation technique to fluorescence in situ hybridization, we found no evidence of DNA damage after PALA treatment. We used representational difference analysis (cDNA-RDA) to study changes in gene expression after PALA treatment and gamma-radiation in normal human fibroblasts. The mammary-derived growth inhibitor (MDGI) gene was expressed in PALA-treated cells. Ectopic MDGI expression arrested PALA-treated but not irradiated RKO cells. Expression of an antisense RNA against MDGI resulted in…

Phosphonoacetic AcidCancer ResearchTumor suppressor geneIn situ hybridizationBiologyFatty Acid-Binding ProteinsCell LineGene expressionHumansGeneIn Situ Hybridization FluorescenceMetaphaseSkinExpressed Sequence TagsExpressed sequence tagAspartic AcidCell CycleG1 PhaseChromosome MappingG0 phaseGeneral MedicineCell cycleFibroblastsMolecular biologyGrowth InhibitorsGene Expression RegulationGamma RaysKaryotypingRepresentational difference analysisTumor Suppressor Protein p53Carrier ProteinsCell Adhesion MoleculesFatty Acid Binding Protein 3Chromosomes Human Pair 7Carcinogenesis
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Identification of Novel Molecular Components of the Photoreceptor Connecting Cilium by Immunoscreens

2002

Abstract The connecting cilium of photoreceptor cells is the only intracellular link between the morphologically, functionally and biochemically different compartments of the inner and outer segments. The non-motile modified cilium plays an important role in the organization and the function of photoreceptor cells, namely in delivery and turnover of enzymes and substrates of the visual transduction cascade, and the photosensitive membranes of the outer segment. The protein components of the cilium participate in the intracellular transport through the cilium, in the outer segment disk morphogenesis and in the maintenance of discrete membrane domains. In order to identify yet unknown cytoske…

Photoreceptor Connecting CiliumAdenomatous Polyposis Coli ProteinXenopus ProteinsBiologyPhotoreceptor cellRats Sprague-DawleyMiceCellular and Molecular NeurosciencemedicineAnimalsDrosophila ProteinsCiliaCloning MolecularCytoskeletonMicrotubule-Associated Protein 4CytoskeletonGene LibraryRetinaCiliumCalcium-Binding ProteinsDynactin ComplexSensory SystemsRatsCell biologyMice Inbred C57BLOphthalmologymedicine.anatomical_structureCentrinsense organsMicrotubule-Associated ProteinsPhotoreceptor Cells VertebrateVisual phototransductionExperimental Eye Research
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Modulation of the Biological Activity of a Tobacco LTP1 by Lipid Complexation

2004

Plant lipid transfer proteins (LTPs) are small, cysteine-rich proteins secreted into the extracellular space. They belong to the pathogenesis-related proteins (PR-14) family and are believed to be involved in several physiological processes including plant disease resistance, although their precise biological function is still unknown. Here, we show that a recombinant tobacco LTP1 is able to load fatty acids and jasmonic acid. This LTP1 binds to specific plasma membrane sites, previously characterized as elicitin receptors, and is shown to be involved in the activation of plant defense. The biological properties of this LTP1 were compared with those of LTP1-linolenic and LTP1-jasmonic acid…

Phytophthora0106 biological sciences[SPI.GPROC] Engineering Sciences [physics]/Chemical and Process EngineeringCyclopentanesPlasma protein bindingBiologyFatty Acid-Binding ProteinsLigands01 natural sciencesMass SpectrometryFatty acid-binding proteinCell membrane03 medical and health scienceschemistry.chemical_compoundTobacco[SDV.IDA]Life Sciences [q-bio]/Food engineeringExtracellularmedicine[SDV.BV]Life Sciences [q-bio]/Vegetal Biology[SPI.GPROC]Engineering Sciences [physics]/Chemical and Process EngineeringOxylipinsMolecular BiologyComputingMilieux_MISCELLANEOUS030304 developmental biology0303 health sciencesDose-Response Relationship DrugCircular DichroismJasmonic acidCell MembraneFatty AcidsElicitinBiological activityArticlesCell Biology[SDV.IDA] Life Sciences [q-bio]/Food engineeringLipid MetabolismLipidsRecombinant Proteinsmedicine.anatomical_structureBiochemistrychemistryPHYTOPHTORA PARASITICACarrier ProteinsTRANSFERT LIPIDIQUEPlant lipid transfer proteinsChromatography LiquidProtein Binding010606 plant biology & botanyMolecular Biology of the Cell
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Mouse embryonic stem cells are hypersensitive to apoptosis triggered by the DNA damage O(6)-methylguanine due to high E2F1 regulated mismatch repair.

2007

Exposure of stem cells to genotoxins may lead to embryonic lethality or teratogenic effects. This can be prevented by efficient DNA repair or by eliminating genetically damaged cells. Using undifferentiated mouse embryonic stem (ES) cells as a pluripotent model system, we compared ES cells with differentiated cells, with regard to apoptosis induction by alkylating agents forming the highly mutagenic and killing DNA adduct O(6)-methylguanine. Upon treatment with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), ES cells undergo apoptosis at much higher frequency than differentiated cells, although they express a high level of the repair protein O(6)-methylguanine-DNA methyltransferase (MGMT). Apo…

Pluripotent Stem CellsMethylnitronitrosoguanidineDNA ComplementaryGuanineDNA damageDNA repairCellular differentiationApoptosisBiologyDNA Mismatch RepairModels BiologicalDNA AdductsMiceO(6)-Methylguanine-DNA MethyltransferaseDNA adductAnimalsMolecular BiologyEmbryonic Stem CellsSwiss 3T3 CellsBase SequenceCell DifferentiationCell BiologyDNA MethylationFibroblastsEmbryonic stem cellMolecular biologyDNA-Binding ProteinsMutS Homolog 2 ProteinDNA methylationDNA mismatch repairStem cellE2F1 Transcription FactorDNA DamageCell death and differentiation
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Demonstration of an endocrine signaling circuit for insulin in the sponge Geodia cydonium.

1989

Abstract The existence of an insulin-mediated cell-to-cell signaling in the sponge Geodia cydonium is demonstrated in this study by molecular biological and immunological techniques. The sequence of a sponge cDNA clone encoding preproinsulin was analyzed for the first time and determined to comprise a high homology to human preproinsulin (60-80% homology). The predicted polypeptide of preproinsulin from sponge contains two disulfide bridges which link the A- to the B-chain. The intra-A chain disulfide bridge is absent. Applying immunological and electron microscopical techniques it is shown that insulin is produced in specialized cells (spherulous cells). Experimental evidence is presented …

PreproinsulinAnnexinsCellular differentiationBlotting WesternMolecular Sequence DataBiologyGeneral Biochemistry Genetics and Molecular BiologySequence Homology Nucleic AcidAnimalsHumansInsulinAmino Acid SequenceProtein PrecursorsReceptorMolecular BiologyPancreatic hormoneProinsulinGeneral Immunology and MicrobiologyBase SequenceGeneral NeuroscienceCalcium-Binding ProteinsDNAImmunohistochemistryReceptor InsulinPoriferaMicroscopy ElectronBiochemistryGene Expression RegulationHormone receptorSignal transductionHormoneResearch ArticleProinsulinSignal Transduction
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Interaction of 68–kDa TAR RNA-binding protein and other cellular proteins with rpion protein-RNA stem-loop

1995

The RNA stem-loop structure of the trans-activating region TAR sequence of human immunodeficiency virus-1 mRNA is the binding site for a number of host cell proteins. A virtually identical set of proteins from HeLa nuclear extracts was found to bind to the predicted RNA hairpin element of prion protein (PrP) mRNA, as demonstrated in UV cross-linking/RNase protection and Northwestern assays. We show that the cellular TAR loop-binding protein, p68, is among those proteins which associate with PrP RNA. Competition experiments with various TAR RNA mutants revealed that binding of partially purified p68 to PrP RNA stem-loop occurs sequence-specifically. The 100-kDa 2-5A synthetase which is invol…

PrionsBlotting WesternMolecular Sequence DataRNA-dependent RNA polymeraseReceptors Cell SurfaceRNA-binding proteinBiologyBinding CompetitiveCellular and Molecular NeuroscienceVirology2'5'-Oligoadenylate SynthetaseHumansLymphocytesHIV Long Terminal RepeatBase SequenceRNA-Binding ProteinsRNABlotting NorthernNon-coding RNAMolecular biologyRNA silencingNeurologyMutagenesisRNA editingeIF4ANucleic Acid ConformationNeurology (clinical)Small nuclear RNAHeLa CellsJournal of Neurovirology
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Pro-inflammatory T helper 17 directly harms oligodendrocytes in neuroinflammation.

2021

Significance Multiple sclerosis (MS) is a neuroinflammatory, demyelinating disease that represents one of the most frequent causes of irreversible disability in young adults. Treatment options to halt disability are limited. We discovered that T helper (Th)17 cells in contact with oligodendrocytes produce higher levels of glutamate and induce significantly greater oligodendrocyte damage than their Th2 counterpart. Blockade of CD29, which is linked to glutamate release pathways and expressed in high levels on Th17 cells, preserved human oligodendrocyte processes from Th17-mediated injury. Our data thus provide evidence for the direct and deleterious attack of Th17 cells on the myelin compart…

Programmed cell deathEncephalomyelitis Autoimmune ExperimentalCentral nervous systemFreund's AdjuvantoligodendrocytesMice Transgenicglutamate03 medical and health sciencesMyelinMice0302 clinical medicineImmunology and Inflammationintravital microscopymedicineAnimalsNeuroinflammation030304 developmental biologyInflammationMice Knockout0303 health sciencesMultidisciplinaryChemistryMultiple sclerosisGlutamate receptorMembrane ProteinsCD29Biological SciencesCD29 blockademedicine.disease420Oligodendrocyte3. Good healthCell biologyDNA-Binding ProteinsMice Inbred C57BLOligodendrogliamedicine.anatomical_structurePertussis ToxinTh17 CellsMyelin-Oligodendrocyte Glycoprotein030217 neurology & neurosurgeryProceedings of the National Academy of Sciences of the United States of America
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Loss of ATM sensitizes against O6-methylguanine triggered apoptosis, SCEs and chromosomal aberrations.

2003

A critical pre-cytotoxic and -apoptotic DNA lesion induced by methylating carcinogens and chemotherapeutic drugs is O6-methylguanine (O6MeG). The mechanism by which O6MeG causes cell death via apoptosis is only partially understood. The current model ascribes a role to DNA replication and mismatch repair, which converts O6MeG into a critical distal lesion (presumably a DNA double-strand break) that is finally responsible for genotoxicity and apoptosis. Here we analysed whether the PI3-like kinase ATM is involved in this process. ATM is a major player in recognizing and signaling DNA breaks, but most reports are limited to ionizing radiation. Comparing mouse ATM knockout fibroblasts (ATM-/-)…

Programmed cell deathGuanineDNA damageApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsBiologyProtein Serine-Threonine Kinasesmedicine.disease_causeBiochemistryMicemedicineCytotoxic T cellAnimalsMolecular BiologyChromosome AberrationsMice KnockoutTumor Suppressor ProteinsCell BiologyTransfectionMolecular biologyDNA-Binding ProteinsCell killingApoptosisDNA mismatch repairSister Chromatid ExchangeGenotoxicityDNA repair
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