0000000000628573

AUTHOR

Anja Voigt

showing 2 related works from this author

A binary genetic approach to characterize TRPM5 cells in mice

2015

International audience; Transient receptor potential channel subfamily M member 5 (TRPM5) is an important downstream signaling component in a subset of taste receptor cells making it a potential target for taste modulation. Interestingly, TRPM5 has been detected in extra-oral tissues; however, the function of extra-gustatory TRPM5-expressing cells is less well understood. To facilitate visualization and manipulation of TRPM5-expressing cells in mice, we generated a Cre knock-in TRPM5 allele by homologous recombination. We then used the novel TRPM5-IRES-Cre mouse strain to report TRPM5 expression by activating a tau GFP transgene. To confirm faithful coexpression of tau GFP and TRPM5 we gene…

MalePhysiologytaste papillaegene targetingBehavioral NeuroscienceMice0302 clinical medicineTaste receptor[SDV.IDA]Life Sciences [q-bio]/Food engineeringGene Knock-In TechniquesIn Situ Hybridization Fluorescence0303 health sciencestaste budsiresGene targetingrosa26ImmunohistochemistrySensory SystemsCell biologyknock inmedicine.anatomical_structuretrpm5taste receptor cellsFemaleGenotypeTransgeneCre recombinaseTRPM Cation ChannelsMice TransgenicBiologyAntibodiestgfpseptal organ of masera03 medical and health sciencesOlfactory MucosaTonguemicrovillar cellsPhysiology (medical)Gene knockinmedicineAnimals[SPI.GPROC]Engineering Sciences [physics]/Chemical and Process EngineeringTRPM5cre recombinaseAlleles030304 developmental biologyPalateMice Inbred C57BLvomeronasal organolfactory epitheliumgastrointestinal tractHomologous recombinationOlfactory epithelium030217 neurology & neurosurgery
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The Friedreich's Ataxia protein frataxin modulates DNA base excision repair in prokaryotes and mammals

2010

DNA-repair mechanisms enable cells to maintain their genetic information by protecting it from mutations that may cause malignant growth. Recent evidence suggests that specific DNA-repair enzymes contain ISCs (iron–sulfur clusters). The nuclearencoded protein frataxin is essential for the mitochondrial biosynthesis of ISCs. Frataxin deficiency causes a neurodegenerative disorder named Friedreich's ataxia in humans. Various types of cancer occurring at young age are associated with this disease, and hence with frataxin deficiency. Mice carrying a hepatocyte-specific disruption of the frataxin gene develop multiple liver tumours for unresolved reasons. In the present study, we show that frata…

Iron-Sulfur ProteinsDNA Repairmedicine.disease_causeBiochemistryDNA Glycosylases8-oxoG 78-dihydro-8-oxoguanineMice0302 clinical medicineIron-Binding Proteinsoxidative stressBER base excision repairCells CulturedMammalsMice Knockout0303 health sciencesfrataxinDMEM Dulbecco's modified Eagle's mediumbiologyLiver NeoplasmsSalmonella entericairon–sulfur clusterLife SciencesIron-binding proteinsTransfection3. Good healthLB Luria–BertaniOGG1 8-oxoguanine DNA glycosylase 1ISC iron–sulfur clusterFpg formamido-pyrimidine DNA glycosylaseHPRT hypoxanthine phosphoribosyltransferaseResearch ArticleDNA damageDNA repairSSB DNA single-strand breakTransfectionCell Line03 medical and health sciencesFRDA Friedreich's ataxiaROS reactive oxygen speciesmedicineAnimalsHumansMUTYH human mutY homologue (Escherichia coli)Molecular BiologyGene030304 developmental biologyFriedreich's ataxiaCell BiologyFibroblastsMolecular biologytumorigenesisProkaryotic CellsFriedreich AtaxiaDNA base excision repairDNA glycosylaseMutationHepatocytesFrataxinbiology.proteinInstitut für ErnährungswissenschaftCarcinogenesisMAPK mitogen-activated protein kinase030217 neurology & neurosurgeryDNA Damage
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