0000000000643613

AUTHOR

Randy A. Hall

showing 4 related works from this author

International Union of Basic and Clinical Pharmacology. XCIV. Adhesion G Protein–Coupled Receptors

2015

The Adhesion family forms a large branch of the pharmacologically important superfamily of G protein-coupled receptors (GPCRs). As Adhesion GPCRs increasingly receive attention from a wide spectrum of biomedical fields, the Adhesion GPCR Consortium, together with the International Union of Basic and Clinical Pharmacology Committee on Receptor Nomenclature and Drug Classification, proposes a unified nomenclature for Adhesion GPCRs. The new names have ADGR as common dominator followed by a letter and a number to denote each subfamily and subtype, respectively. The new names, with old and alternative names within parentheses, are: ADGRA1 (GPR123), ADGRA2 (GPR124), ADGRA3 (GPR125), ADGRB1 (BAI1…

Models MolecularSocieties ScientificSubfamilyComputational biologyBiologyGPR110PharmacologyLigandsGPR113Second Messenger SystemsReceptors G-Protein-CoupledCell MovementTerminology as TopicCell AdhesionCyclic AMPAnimalsHumansProtein IsoformsReceptorNomenclatureG protein-coupled receptorPharmacologyCell MembraneInternational AgenciesAdhesionQPGPR56Pharmacology ClinicalIUPHAR Nomenclature ReportsMolecular MedicineQP517Cell Adhesion MoleculesSignal TransductionPharmacological Reviews
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PTEN recruitment controls synaptic and cognitive function in Alzheimer's models

2016

Dyshomeostasis of amyloid-β peptide (Aβ) is responsible for synaptic malfunctions leading to cognitive deficits ranging from mild impairment to full-blown dementia in Alzheimer's disease. Aβ appears to skew synaptic plasticity events toward depression. We found that inhibition of PTEN, a lipid phosphatase that is essential to long-term depression, rescued normal synaptic function and cognition in cellular and animal models of Alzheimer's disease. Conversely, transgenic mice that overexpressed PTEN displayed synaptic depression that mimicked and occluded Aβ-induced depression. Mechanistically, Aβ triggers a PDZ-dependent recruitment of PTEN into the postsynaptic compartment. Using a PTEN kno…

0301 basic medicinePrimary Cell CulturePDZ DomainsMice TransgenicMolecular neuroscienceBiologyNeurotransmissionSynaptic TransmissionMice03 medical and health sciences0302 clinical medicineAlzheimer DiseasePostsynaptic potentialmedicineAnimalsPTENGene Knock-In TechniquesAmyloid beta-PeptidesGeneral NeurosciencePTEN PhosphohydrolaseLong-term potentiationmedicine.diseaseRatsDisease Models Animal030104 developmental biologySynaptic fatigueSynaptic plasticitybiology.proteinAlzheimer's diseaseCognition DisordersNeuroscience030217 neurology & neurosurgeryNature Neuroscience
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New functions and signaling mechanisms for the class of adhesion G protein-coupled receptors

2014

The class of adhesion G protein-coupled receptors (aGPCRs), with 33 human homologs, is the second largest family of GPCRs. In addition to a seven-transmembrane α-helix-a structural feature of all GPCRs-the class of aGPCRs is characterized by the presence of a large N-terminal extracellular region. In addition, all aGPCRs but one (GPR123) contain a GPCR autoproteolysis-inducing (GAIN) domain that mediates autoproteolytic cleavage at the GPCR autoproteolysis site motif to generate N- and a C-terminal fragments (NTF and CTF, respectively) during protein maturation. Subsequently, the NTF and CTF are associated noncovalently as a heterodimer at the plasma membrane. While the biological function …

History and Philosophy of ScienceStructural biologyGeneral NeuroscienceExtracellularSignal transductionBiologyCell adhesionReceptorProtein maturationGeneral Biochemistry Genetics and Molecular BiologyFunction (biology)G protein-coupled receptorCell biologyAnnals of the New York Academy of Sciences
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The expanding functional roles and signaling mechanisms of adhesion G protein-coupled receptors.

2019

The adhesion class of G protein-coupled receptors (GPCRs) is the second largest family of GPCRs (33 members in humans). Adhesion GPCRs (aGPCRs) are defined by a large extracellular N-terminal region that is linked to a C-terminal seven transmembrane (7TM) domain via a GPCR-autoproteolysis inducing (GAIN) domain containing a GPCR proteolytic site (GPS). Most aGPCRs undergo autoproteolysis at the GPS motif, but the cleaved fragments stay closely associated, with the N-terminal fragment (NTF) bound to the 7TM of the C-terminal fragment (CTF). The NTFs of most aGPCRs contain domains known to be involved in cell-cell adhesion, while the CTFs are involved in classical G protein signaling, as well…

0301 basic medicineG proteinGeneral Science & TechnologyArticleGeneral Biochemistry Genetics and Molecular BiologyReceptors G-Protein-Coupledimmunology03 medical and health sciencesG-Protein-Coupled0302 clinical medicineHistory and Philosophy of ScienceReceptorsExtracellularAnimalsHumanscancerstructural biologymechanosensationReceptordevelopmentG protein-coupled receptorChemistryGeneral NeuroscienceneurobiologySciences bio-médicales et agricolesTransmembrane proteinCell biology030104 developmental biologyStructural biologyGeneric health relevanceSignal transductionadhesion G protein-coupled receptor030217 neurology & neurosurgeryIntracellularsignal transductionSignal Transduction
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