0000000000165190

AUTHOR

Bianca Ackermann

showing 3 related works from this author

HSF1-controlled and age-associated chaperone capacity in neurons and muscle cells of C. elegans.

2010

Protein stability under changing conditions is of vital importance for the cell and under the control of a fine-tuned network of molecular chaperones. Aging and age-related neurodegenerative diseases are directly associated with enhanced protein instability. Employing C. elegans expressing GFP-tagged luciferase as a reporter for evaluation of protein stability we show that the chaperoning strategy of body wall muscle cells and neurons is significantly different and that both are differently affected by aging. Muscle cells of young worms are largely resistant to heat stress, which is directly mediated by the stress response controlled through Heat Shock Transcription Factor 1. During recover…

AgingProteomeGreen Fluorescent Proteinslcsh:MedicineBiologyBiochemistryBiochemistry/Protein FoldingAnimals Genetically ModifiedHeat shock proteinAnimalsMyocyteHeat shockCaenorhabditis elegansCaenorhabditis elegans ProteinsHSF1lcsh:ScienceDNA PrimersNeuronsMultidisciplinaryBase SequenceMuscleslcsh:RCell Biology/Cellular Death and Stress ResponsesMolecular biologyCell biologyHeat shock factorMicroscopy FluorescenceChaperone (protein)biology.proteinProtein foldinglcsh:QProtein stabilizationResearch ArticleMolecular ChaperonesTranscription FactorsPLoS ONE
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The Fumarate/Succinate Antiporter DcuB of Escherichia coli Is a Bifunctional Protein with Sites for Regulation of DcuS-dependent Gene Expression

2008

DcuB of Escherichia coli catalyzes C4-dicarboxylate/succinate antiport during growth by fumarate respiration. The expression of genes of fumarate respiration, including the genes for DcuB (dcuB) and fumarate reductase (frdABCD) is transcriptionally activated by C4-dicarboxylates via the DcuS-DcuR two-component system, comprising the sensor kinase DcuS, which contains a periplasmic sensing domain for C4-dicarboxylates. Deletion or inactivation of dcuB caused constitutive expression of DcuS-regulated genes in the absence of C4-dicarboxylates. The effect was specific for DcuB and not observed after inactivation of the homologous DcuA or the more distantly related DcuC transporter. Random and s…

AntiporterMutantlac operonBiologymedicine.disease_causePeptide MappingBiochemistryAntiportersFumaratesEscherichia colimedicineMolecular BiologyEscherichia coliDerepressionDicarboxylic Acid TransportersIon TransportEscherichia coli ProteinsMutagenesisSuccinatesGene Expression Regulation BacterialCell BiologyPeriplasmic spaceFumarate reductaseDNA-Binding ProteinsSuccinate DehydrogenaseAmino Acid SubstitutionBiochemistryGene Knockdown TechniquesMutagenesis Site-DirectedProtein KinasesTranscription FactorsJournal of Biological Chemistry
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Inhibition of myosin light chain kinase reduces brain edema formation after traumatic brain injury.

2010

The role of the endothelial contractile apparatus in the process of brain edema formation after brain trauma is not characterized. Phosphorylation of myosin light chains by myosin light chain kinases (MLCK) activates endothelial contractile elements and results in a rearrangement of the cytoskeleton. This may enhance post-traumatic blood-brain barrier dysfunction. In order to investigate the role of the MLCK on brain edema formation and blood-brain barrier permeability after brain injury, mice were anesthetized and subjected to a controlled cortical impact (CCI). MLCK expression is significantly up-regulated after CCI with a maximum 12 h post-injury. Specific inhibition of MLCK by ML-7 resu…

MaleMyosin light-chain kinaseMyosin Light ChainsTime FactorsEndotheliumIntracranial PressureTraumatic brain injuryCentral nervous systemBrain Edemamacromolecular substancesBrain damageNaphthalenesBlood–brain barrierBiochemistryNeuroprotectionDrug Administration ScheduleFunctional LateralityStatistics NonparametricCerebral edemaCellular and Molecular NeuroscienceMicemedicineAnimalsEnzyme InhibitorsMyosin-Light-Chain KinaseNeurologic Examinationbusiness.industryAzepinesmedicine.diseaseConstrictionCell biologyMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureGene Expression RegulationBlood-Brain BarrierBrain Injuriesmedicine.symptombusinessNeuroscienceEvans BlueJournal of neurochemistry
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