0000000000326937

AUTHOR

David Kaul

showing 2 related works from this author

Expression of Toll-Like Receptors in the Developing Brain

2012

Toll-like receptors (TLR) are key players of the innate and adaptive immune response in vertebrates. The original protein Toll in Drosophila melanogaster regulates both host defense and morphogenesis during development. Making use of real-time PCR, in situ hybridization, and immunohistochemistry we systematically examined the expression of TLR1-9 and the intracellular adaptor molecules MyD88 and TRIF during development of the mouse brain. Expression of TLR7 and TLR9 in the brain was strongly regulated during different embryonic, postnatal, and adult stages. In contrast, expression of TLR1-6, TLR8, MyD88, and TRIF mRNA displayed no significant changes in the different phases of brain develop…

AgingGene Expressionlcsh:MedicineMiceMolecular Cell BiologyMorphogenesislcsh:ScienceReceptorImmune ResponseRegulation of gene expressionMultidisciplinaryNeocortexToll-Like ReceptorsBrainGene Expression Regulation DevelopmentalAcquired immune systemInnate ImmunityCell biologyInfectious Diseasesmedicine.anatomical_structureMedicineResearch ArticleImmunologyCentral nervous systemMorphogenesisIn situ hybridizationBiologyMolecular GeneticsImmune ActivationDevelopmental NeuroscienceGeneticsmedicineAnimalsHumansRNA MessengerBiologyImmunity to Infectionslcsh:RImmunityComputational BiologyImmune DefenseAxonsHEK293 CellsTRIFImmune SystemCellular NeuroscienceImmunologyClinical Immunologylcsh:QTranscriptomeDevelopmental BiologyNeurosciencePLoS ONE
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An unconventional role for miRNA: let-7 activates Toll-like receptor 7 and causes neurodegeneration

2011

Activation of innate immune receptors by host-derived factors exacerbates CNS damage, but the identity of these factors remains elusive. We uncovered an unconventional role for the microRNA let-7, a highly abundant regulator of gene expression in the CNS, in which extracellular let-7 activates the RNA-sensing Toll-like receptor (TLR) 7 and induces neurodegeneration through neuronal TLR7. Cerebrospinal fluid (CSF) from individuals with Alzheimer’s disease contains increased amounts of let-7b, and extracellular introduction of let-7b into the CSF of wild-type mice by intrathecal injection resulted in neurodegeneration. Mice lacking TLR7 were resistant to this neurodegenerative effect, but thi…

Cell signalingApoptosisElectrophoretic Mobility Shift AssayBiologyReal-Time Polymerase Chain ReactionMiceAlzheimer DiseasemicroRNAExtracellularmedicineAnimalsHumansReceptorIn Situ HybridizationMice KnockoutNeuronsToll-like receptorMembrane GlycoproteinsMicroscopy ConfocalInnate immune systemGeneral NeuroscienceNeurodegenerationBrainvirus diseasesTLR7medicine.diseaseImmunohistochemistryMice Inbred C57BLMicroRNAsHEK293 CellsToll-Like Receptor 7Nerve DegenerationCancer researchSignal TransductionNature Neuroscience
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