0000000000217269

AUTHOR

Thomas Wilhelm

0000-0002-0494-3984

showing 4 related works from this author

Neuronal inhibition of the autophagy nucleation complex extends life span in post-reproductive C. elegans

2017

Autophagy is a ubiquitous catabolic process that causes cellular bulk degradation of cytoplasmic components and is generally associated with positive effects on health and longevity. Inactivation of autophagy has been linked with detrimental effects on cells and organisms. The antagonistic pleiotropy theory postulates that some fitness-promoting genes during youth are harmful during aging. On this basis, we examined genes mediating post-reproductive longevity using an RNAi screen. From this screen, we identified 30 novel regulators of post-reproductive longevity, including pha-4. Through downstream analysis of pha-4, we identified that the inactivation of genes governing the early stages of…

0301 basic medicineAgingCytoplasmmedia_common.quotation_subjectLongevityVesicular Transport ProteinsContext (language use)Biology03 medical and health sciences0302 clinical medicinePleiotropyAutophagyGeneticsmedicineAnimalsGene SilencingCaenorhabditis elegansCaenorhabditis elegans ProteinsGenemedia_commonNeuronsGeneticsReproductionNeurodegenerationAutophagyLongevityGenetic Pleiotropymedicine.diseaseCell biology030104 developmental biologyCytoplasmSarcopeniaTrans-ActivatorsRNA InterferenceFunction and Dysfunction of the Nervous System030217 neurology & neurosurgerySignal TransductionResearch PaperDevelopmental BiologyGenes & Development
researchProduct

Investigation into mechanisms mediating the inhibitory effect of 1,4-benzodiazepines on mast cells by gene expression profiling.

2013

Abstract Aims This study aims to identify by a molecular genetic approach potential targets in mast cells at which 1,4-benzodiazepines may cause their inhibitory effect on mast cell activity. Main methods Gene expression analyses with microarray gene chip and/or quantitative PCR were performed using 1,4-benzodiazepine-treated human mast cell leukemia HMC-1.2 cells, promyelocytic leukemia HL-60 cells and human mast cells from healthy volunteers and patients with mast cell activation disease (MCAD). Pathway analysis was applied to search for enriched biological functions and canonical pathways within differentially regulated genes. Key findings Both neoplastic and normal human mast cells expr…

AdultMalegenetics [Mastocytosis]Gene ExpressionHL-60 CellsFlunitrazepamBiologyPolymerase Chain ReactionGeneral Biochemistry Genetics and Molecular BiologyClonazepamLYNddc:570medicineTranslocator proteinpharmacology [Flunitrazepam]HumansMast CellsGeneral Pharmacology Toxicology and Pharmaceuticsmethods [Polymerase Chain Reaction]Interleukin 5AgedRegulation of gene expressionBenzodiazepinonesGene Expression Profilingdrug effects [Gene Expression]General MedicineMiddle AgedMast cell leukemiamedicine.diseaseMast cellMicroarray Analysis4'-chlorodiazepamCell biologyInterleukin 33Gene expression profilingmedicine.anatomical_structuremethods [Microarray Analysis]biology.proteinpharmacology [Clonazepam]drug effects [Mast Cells]Femalepharmacology [Benzodiazepinones]Mastocytosismethods [Gene Expression Profiling]
researchProduct

Autophagy during ageing – from Dr Jekyll to Mr Hyde

2017

Autophagy is a ubiquitous catabolic process, which causes cellular bulk degradation through vesicular engulfment of obsolete, damaged or harmful cytoplasmic components. While autophagy regulates cellular homeostasis during development and in youth, there is mounting evidence that autophagy becomes increasingly dysfunctional with age. Recent work in Caenorhabditis elegans even suggests that late-life dysfunctional autophagy exhibits detrimental effects that drive the ageing process. Other studies link elevated autophagy closely to increased health and longevity. This review aims to put these apparently opposing views into perspective and define our current understanding of the role of autoph…

0301 basic medicineAgingmedia_common.quotation_subjectLongevityCellular homeostasisSaccharomyces cerevisiaeBiochemistry03 medical and health sciencesAutophagyAnimalsHumansCaenorhabditis elegansMolecular BiologyCaenorhabditis elegansmedia_commonbiologyAutophagyLongevityCell BiologyCatabolic Processbiology.organism_classificationCell biologyDrosophila melanogaster030104 developmental biologyAgeingSignal TransductionThe FEBS Journal
researchProduct

Neuronal inhibition of the autophagy nucleation complex extends lifespan in post-reproductive C. elegans

2017

AbstractAutophagy is a ubiquitous catabolic process, which causes cellular bulk degradation of cytoplasmic components and thereby regulates cellular homeostasis. Inactivation of autophagy has been linked with detrimental effects to cells and organisms. The antagonistic pleiotropy theory postulates that fitness promoting genes during youth are harmful during aging (Williams 1957). On this basis we examined genes mediating post-reproductive longevity using an RNA interference screen. From this screen we identified 30 novel regulators of post-reproductive longevity including pha-4. Through downstream analysis of pha-4 we identify that genes governing the early stages of autophagy up until the …

0303 health sciencesmedia_common.quotation_subjectNeurodegenerationAutophagyLongevityCellular homeostasisContext (language use)Biologymedicine.diseaseCell biology03 medical and health sciences0302 clinical medicineRNA interferencePleiotropymedicineGene030217 neurology & neurosurgery030304 developmental biologymedia_common
researchProduct