0000000000087382

AUTHOR

Zsuzsa Kovacs

showing 2 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
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Protein kinase inhibitor β enhances the constitutive activity of G-protein-coupled zinc receptor GPR39.

2014

GPR39 is a G-protein-coupled zinc receptor that protects against diverse effectors of cell death. Its protective activity is mediated via constitutive activation of Gα13 and the RhoA pathway, leading to increased SRE (serum-response element)-dependent transcription; the zinc-dependent immediate activation of GPR39 involves Gq-mediated increases in cytosolic Ca2+ and Gs coupling leading to increased cAMP levels. We used the cytosolic and soluble C-terminus of GPR39 in a Y2H (yeast-2-hybrid) screen for interacting proteins, thus identifying PKIB (protein kinase A inhibitor β). Co-expression of GPR39 with PKIB increased the protective activity of GPR39 via the constitutive, but not the ligand-…

RHOAmedicine.drug_classG proteinCHO CellsBiochemistryCell LineReceptors G-Protein-CoupledMiceCricetulusTwo-Hybrid System TechniquesmedicineAnimalsHumansProtein kinase AReceptorMolecular BiologyProtein Kinase InhibitorsbiologyEffectorCell MembraneIntracellular Signaling Peptides and ProteinsCell BiologyProtein kinase inhibitorCyclic AMP-Dependent Protein KinasesProtein Kinase A InhibitorCytosolZincBiochemistrybiology.proteinHeLa CellsThe Biochemical journal
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