0000000000087379

AUTHOR

Alireza Pouya

showing 3 related works from this author

TOX3 regulates neural progenitor identity

2016

The human genomic locus for the transcription factor TOX3 has been implicated in susceptibility to restless legs syndrome and breast cancer in genome-wide association studies, but the physiological role of TOX3 remains largely unknown. We found Tox3 to be predominantly expressed in the developing mouse brain with a peak at embryonic day E14 where it co-localizes with the neural stem and progenitor markers Nestin and Sox2 in radial glia of the ventricular zone and intermediate progenitors of the subventricular zone. Tox3 is also expressed in neural progenitor cells obtained from the ganglionic eminence of E15 mice that express Nestin, and it specifically binds the Nestin promoter in chromati…

0301 basic medicineNeurogenesisBiophysicsNotch signaling pathwaySubventricular zoneMice TransgenicBiologyBiochemistryMice03 medical and health sciences0302 clinical medicineNeural Stem CellsSOX2PregnancyStructural BiologyGeneticsmedicineAnimalsRNA Small InterferingProgenitor cellMolecular BiologyCells Culturedreproductive and urinary physiologyNeuronsNeurogenesisGene Expression Regulation DevelopmentalNestinEmbryo MammalianMolecular biologyNeural stem cellMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurenervous systemembryonic structuresTrans-ActivatorsFemaleStem cellApoptosis Regulatory ProteinsReceptors Progesterone030217 neurology & neurosurgeryBiochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms
researchProduct

Mitochondrial function and energy metabolism in neuronal HT22 cells resistant to oxidative stress

2014

Background and Purpose The hippocampal cell line HT22 is an excellent model for studying the consequences of endogenous oxidative stress. Extracellular glutamate depletes cellular glutathione by blocking the glutamate/cystine antiporter system xc−. Glutathione depletion induces a well-defined programme of cell death characterized by an increase in reactive oxygen species and mitochondrial dysfunction. Experimental Approach We compared the mitochondrial shape, the abundance of mitochondrial complexes and the mitochondrial respiration of HT22 cells, selected based on their resistance to glutamate, with those of the glutamate-sensitive parental cell line. Key Results Glutamate-resistant mitoch…

PharmacologyOligomycinATP synthaseCellular respirationOxidative phosphorylationMitochondrionBiologymedicine.disease_causechemistry.chemical_compoundMitochondrial permeability transition poreBiochemistrychemistrymedicinebiology.proteinATP–ADP translocaseOxidative stressBritish Journal of Pharmacology
researchProduct

The thiol switch C684 in Mitofusin-2 mediates redox-induced alterations of mitochondrial shape and respiration

2017

Mitofusin-2 (MFN2) is a GTPase in the outer mitochondrial membrane involved in the regulation of mitochondrial fusion and bioenergetics. MFN2 also plays a role in mitochondrial fusion induced by changes in the intracellular redox state. Adding oxidized glutathione (GSSG), the core cellular stress indicator, to mitochondrial preparations stimulates mitochondrial fusion by inducing disulphide bond-mediated oligomer formation of MFN2 and its homolog MFN1 which involve cysteine 684 (C684) of MFN2. Mitochondrial hyperfusion represents an adaptive stress response that confers transient protection by increasing mitochondrial ATP production but how this depends on the thiol switch C684 in MFN2 has …

Mice Knockout0301 basic medicineCell RespirationMFN2Cell BiologyOxidative phosphorylationMitochondrionBiologyMitochondrial apoptosis-induced channelGTP PhosphohydrolasesMitochondriaCell biologyMice03 medical and health sciencesCellular and Molecular NeuroscienceMitofusin-2030104 developmental biologymitochondrial fusionAnimalsMFN1Sulfhydryl CompoundsATP–ADP translocaseCell ShapeOxidation-ReductionCells CulturedNeurochemistry International
researchProduct