G-protein diseases furnish a model for the turn-on switch.
about
Interaction of Galpha 12 and Galpha 13 with the cytoplasmic domain of cadherin provides a mechanism for beta -catenin releaseStructure of the small G protein Rap2 in a non-catalytic complex with GTPThe crystal structure of a self-activating G protein alpha subunit reveals its distinct mechanism of signal initiation.A Constitutively Active Gα Subunit Provides Insights into the Mechanism of G Protein ActivationA Conserved Phenylalanine as a Relay between the 5 Helix and the GDP Binding Region of Heterotrimeric Gi Protein SubunitStructural determinants involved in the formation and activation of G protein betagamma dimers.Dna2 mutants reveal interactions with Dna polymerase alpha and Ctf4, a Pol alpha accessory factor, and show that full Dna2 helicase activity is not essential for growthDifferential activity of the G protein beta5 gamma2 subunit at receptors and effectors.Posttranslational modification of Galphao1 generates Galphao3, an abundant G protein in brainStructure of Galpha(i1) bound to a GDP-selective peptide provides insight into guanine nucleotide exchangeAntigenically distinct conformations of CXCR4.Mutant G protein alpha subunit activated by Gbeta gamma: a model for receptor activation?Implications of non-canonical G-protein signaling for the immune systemThe differential effects of the gonadotropin receptors on aromatase expression in primary cultures of immature rat granulosa cells are highly dependent on the density of receptors expressed and the activation of the inositol phosphate cascade.Homology model of the CB1 cannabinoid receptor: sites critical for nonclassical cannabinoid agonist interaction.Mechanism of the receptor-catalyzed activation of heterotrimeric G proteins.RETRACTED: Structural basis for nucleotide exchange on G alpha i subunits and receptor coupling specificity.Pivotal role of extended linker 2 in the activation of Gα by G protein-coupled receptor.A Gsalpha mutant designed to inhibit receptor signaling through Gs.A mutation in the heterotrimeric stimulatory guanine nucleotide binding protein alpha-subunit with impaired receptor-mediated activation because of elevated GTPase activity.Structural and dynamical changes in an alpha-subunit of a heterotrimeric G protein along the activation pathway.Essential hypertension: genes and dreams.Computational methods in drug design: modeling G protein-coupled receptor monomers, dimers, and oligomersTherapeutic effects of cell-permeant peptides that activate G proteins downstream of growth factors.Recent advances in drug action and therapeutics: relevance of novel concepts in G-protein-coupled receptor and signal transduction pharmacology.Mechanistic diversity of cytokine receptor signaling across cell membranes.Mapping allosteric connections from the receptor to the nucleotide-binding pocket of heterotrimeric G proteinsDimerization of the class A G protein-coupled neurotensin receptor NTS1 alters G protein interaction.Signaling states of rhodopsin in rod disk membranes lacking transducin βγ-complex.Human G(salpha) mutant causes pseudohypoparathyroidism type Ia/neonatal diarrhea, a potential cell-specific role of the palmitoylation cycleSignal transfer from rhodopsin to the G-protein: evidence for a two-site sequential fit mechanismConversion of agonist site to metal-ion chelator site in the beta(2)-adrenergic receptor.State-selective binding peptides for heterotrimeric G-protein subunits: novel tools for investigating G-protein signaling dynamics.Abscisic acid regulation of guard-cell K+ and anion channels in Gbeta- and RGS-deficient Arabidopsis linesPrediction of the Risk for Essential Hypertension among Carriers of C825T Genetic Polymorphism of G Protein β3 (GNB3) GeneInactivation of G-protein-coupled receptor 48 (Gpr48/Lgr4) impairs definitive erythropoiesis at midgestation through down-regulation of the ATF4 signaling pathway.Structural and kinetic modeling of an activating helix switch in the rhodopsin-transducin interfaceProbing heterotrimeric G protein activation: applications to biased ligands.Mutagenesis of the conserved residue Glu259 of Gsalpha demonstrates the importance of interactions between switches 2 and 3 for activation.The untapped potential of tyrosine-based G protein signaling.
P2860
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P2860
G-protein diseases furnish a model for the turn-on switch.
description
1998 nî lūn-bûn
@nan
1998年の論文
@ja
1998年学术文章
@wuu
1998年学术文章
@zh
1998年学术文章
@zh-cn
1998年学术文章
@zh-hans
1998年学术文章
@zh-my
1998年学术文章
@zh-sg
1998年學術文章
@yue
1998年學術文章
@zh-hant
name
G-protein diseases furnish a model for the turn-on switch.
@en
G-protein diseases furnish a model for the turn-on switch.
@nl
type
label
G-protein diseases furnish a model for the turn-on switch.
@en
G-protein diseases furnish a model for the turn-on switch.
@nl
prefLabel
G-protein diseases furnish a model for the turn-on switch.
@en
G-protein diseases furnish a model for the turn-on switch.
@nl
P2093
P356
P1433
P1476
G-protein diseases furnish a model for the turn-on switch.
@en
P2093
P2888
P356
10.1038/27831
P407
P577
1998-07-01T00:00:00Z
P6179
1043980398