Phosphorylation-dependent regulation of the guanylyl cyclase-linked natriuretic peptide receptor B: dephosphorylation is a mechanism of desensitization.
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Identification of a potent serum factor that causes desensitization of the receptor for C-Type natriuretic peptideCatalytically Active Guanylyl Cyclase B Requires Endoplasmic Reticulum-mediated Glycosylation, and Mutations That Inhibit This Process Cause DwarfismInteraction of guanylyl cyclase C with SH3 domain of Src tyrosine kinase. Yet another mechanism for desensitizationCalcium-dependent dephosphorylation mediates the hyperosmotic and lysophosphatidic acid-dependent inhibition of natriuretic peptide receptor-B/guanylyl cyclase-BRegulation of the guanylyl cyclase-B receptor by alternative splicingNatriuretic peptide receptor-B in adult rat ventricle is predominantly confined to the nonmyocyte populationGuanylyl cyclase-linked natriuretic peptide receptors: structure and regulation.Guanylyl cyclase (GC)-A and GC-B activities in ventricles and cardiomyocytes from failed and non-failed human hearts: GC-A is inactive in the failed cardiomyocyte.Phosphorylation of the kinase homology domain is essential for activation of the A-type natriuretic peptide receptorCellular refractoriness to the heat-stable enterotoxin peptide is associated with alterations in levels of the differentially glycosylated forms of guanylyl cyclase C.A functional screen provides evidence for a conserved, regulatory, juxtamembrane phosphorylation site in guanylyl cyclase a and B.Dephosphorylation and inactivation of NPR2 guanylyl cyclase in granulosa cells contributes to the LH-induced decrease in cGMP that causes resumption of meiosis in rat oocytes.Natriuretic peptides: their structures, receptors, physiologic functions and therapeutic applicationsThe indolocarbazole, Gö6976, inhibits guanylyl cyclase-A and -B.Guanylyl cyclases A and B are asymmetric dimers that are allosterically activated by ATP binding to the catalytic domain.A human skeletal overgrowth mutation increases maximal velocity and blocks desensitization of guanylyl cyclase-B.Photoreceptor guanylate cyclase variants: cGMP production under control.C-type natriuretic peptide and endothelium-dependent hyperpolarization in the guinea-pig carotid artery.Guanylyl cyclase structure, function and regulation.Regulation and therapeutic targeting of peptide-activated receptor guanylyl cyclases.A constitutively "phosphorylated" guanylyl cyclase-linked atrial natriuretic peptide receptor mutant is resistant to desensitizationDephosphorylation of juxtamembrane serines and threonines of the NPR2 guanylyl cyclase is required for rapid resumption of oocyte meiosis in response to luteinizing hormone.The natriuretic peptide uroguanylin elicits physiologic actions through 2 distinct topoisomersHomologous and heterologous desensitization of guanylyl cyclase-B signaling in GH3 somatolactotropesAdenine nucleotides decrease the apparent Km of endogenous natriuretic peptide receptors for GTP.Four peptide hormones' specific decrease (up to 97%) of human prostate carcinoma cells.Soluble guanylate cyclase is allosterically inhibited by direct interaction with 2-substituted adenine nucleotides.Activation of protein kinase C stimulates the dephosphorylation of natriuretic peptide receptor-B at a single serine residue: a possible mechanism of heterologous desensitization.Homologous desensitization of the human guanylate cyclase C receptor. Cell-specific regulation of catalytic activity.Identification and characterization of the major phosphorylation sites of the B-type natriuretic peptide receptor.Mass spectrometric identification of phosphorylation sites in guanylyl cyclase A and B.Vascular natriuretic peptide receptor-linked particulate guanylate cyclases are modulated by nitric oxide-cyclic GMP signalling.Molecular and biochemical characterization of a CNP-sensitive guanylyl cyclase in bovine tracheal smooth muscle.Reciprocal antagonism coordinates C-type natriuretic peptide and mitogen-signaling pathways in fibroblasts.Coordinated control of endothelial nitric-oxide synthase phosphorylation by protein kinase C and the cAMP-dependent protein kinase.Vasopressin-dependent inhibition of the C-type natriuretic peptide receptor, NPR-B/GC-B, requires elevated intracellular calcium concentrations.Catalytically active guanylyl cyclase-B requires glycosylation and mutations that inhibit this process cause dwarfism.Dephosphorylation of the NPR2 guanylyl cyclase contributes to inhibition of bone growth by fibroblast growth factor.Skeletal overgrowth-causing mutations mimic an allosterically activated conformation of guanylyl cyclase-B that is inhibited by 2,4,6,-trinitrophenyl ATP.A Glutamate-Substituted Mutant Mimics the Phosphorylated and Active Form of Guanylyl Cyclase-A.
P2860
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P2860
Phosphorylation-dependent regulation of the guanylyl cyclase-linked natriuretic peptide receptor B: dephosphorylation is a mechanism of desensitization.
description
1998 nî lūn-bûn
@nan
1998年の論文
@ja
1998年論文
@yue
1998年論文
@zh-hant
1998年論文
@zh-hk
1998年論文
@zh-mo
1998年論文
@zh-tw
1998年论文
@wuu
1998年论文
@zh
1998年论文
@zh-cn
name
Phosphorylation-dependent regu ...... mechanism of desensitization.
@en
Phosphorylation-dependent regu ...... mechanism of desensitization.
@nl
type
label
Phosphorylation-dependent regu ...... mechanism of desensitization.
@en
Phosphorylation-dependent regu ...... mechanism of desensitization.
@nl
prefLabel
Phosphorylation-dependent regu ...... mechanism of desensitization.
@en
Phosphorylation-dependent regu ...... mechanism of desensitization.
@nl
P356
P1433
P1476
Phosphorylation-dependent regu ...... mechanism of desensitization.
@en
P2093
L R Potter
P304
P356
10.1021/BI972303K
P407
P577
1998-02-01T00:00:00Z