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Natriuretic peptide receptor A/guanylate cyclase A

Guanylate Cyclase
Guanylyl cyclases, catalyzing the production of cGMP from GTP, are classified as soluble and membrane forms (Garbers and Lowe, 1994 [PubMed 7982997]). The membrane guanylyl cyclases, often termed guanylyl cyclases A through F, form a family of cell-surface receptors with a similar topographic structure: an extracellular ligand-binding domain, a single membrane-spanning domain, and an intracellular region that contains a protein kinase-like domain and a cyclase catalytic domain. GC-A and GC-B function as receptors for natriuretic peptides; they are also referred to as atrial natriuretic peptide receptor A (NPR1) and type B (NPR2; MIM 108961). Also see NPR3 (MIM 108962), which encodes a protein with only the ligand-binding transmembrane and 37-amino acid cytoplasmic domains. NPR1 is a membrane-bound guanylate cyclase that serves as the receptor for both atrial and brain natriuretic peptides (ANP (MIM 108780) and BNP (MIM 600295), respectively).[supplied by OMIM, May 2009] (from NCBI)
Top mentioned proteins: V1a, CAN, iNOS, HAD, ACID
Papers using Guanylate Cyclase antibodies
Prolonged exposure toYC-1 induces apoptosis in adrenomedullary endothelial and chromaffin cells through a cGMP-independent mechanism.
Torres Magdalena et al., In BMC Biochemistry, 2000
... DETA/NO, DEA/NO, rabbit anti-GC (soluble) and guanylate cyclase (soluble) blocking peptide were provided by Cayman Chemical (Ann Arbor, MI, ...
Papers on Guanylate Cyclase
Disrupted Nitric Oxide Signaling due to GUCY1A3 Mutations Increases Risk for Moyamoya Disease, Achalasia and Hypertension.
Milewicz et al., London, United Kingdom. In Clin Genet, Feb 2016
Biochemical studies of one of these alleles, GUCY1A3 Cys517Tyr, showed that the mutant protein (a subunit of soluble guanylate cyclase) has a significantly blunted signaling response with exposure to nitric oxide.
Enhanced Nitric Oxide Synthase Activation via Protease-Activated Receptor 2 Is Involved in the Preserved Vasodilation in Aortas from Metabolic Syndrome Rats.
Shinozuka et al., Nishinomiya, Japan. In J Vasc Res, Feb 2016
Treatments of aortas with inhibitors of NO synthase and soluble guanylate cyclase abolished the sustained 2fly- and residual acetylcholine-induced vasodilation in SHRSP.ZF at 18 weeks of age.
Novel investigational drugs for constipation-predominant irritable bowel syndrome: a review.
Fichna et al., Łódź, Poland. In Expert Opin Investig Drugs, Feb 2016
The authors put a special interest on glucagon-like peptide 1 analogue, bile acid modulators, serotonergic agents, guanylate cyclase C and cannabinoid antagonists.
Stimulation of calcium-sensing receptors induces endothelium-dependent vasorelaxations via nitric oxide production and activation of IKCa channels.
Albert et al., London, United Kingdom. In Vascul Pharmacol, Feb 2016
[Ca(2+)]o-induced relaxations were reduced by inhibitors of endothelial NO synthase, guanylate cyclase, and protein kinase G. CaSR activation also induced NO production in freshly isolated endothelial cells (ECs) in experiments using the fluorescent NO indicator DAF-FM.
Effect of Vericiguat, a Soluble Guanylate Cyclase Stimulator, on Natriuretic Peptide Levels in Patients With Worsening Chronic Heart Failure and Reduced Ejection Fraction: The SOCRATES-REDUCED Randomized Trial.
SOCRATES-REDUCED Investigators and Coordinators et al., Athens, Greece. In Jama, Jan 2016
OBJECTIVE: To determine the optimal dose and tolerability of vericiguat, a soluble guanylate cyclase stimulator, in patients with worsening chronic HF and reduced left ventricular ejection fraction (LVEF).
Riociguat for the treatment of pulmonary hypertension.
Granton et al., Hamilton, Canada. In Expert Rev Respir Med, Dec 2015
NO activates soluble guanylate cyclase (sGC) resulting in the synthesis of cyclic guanosine monophosphate (cGMP) - a key mediator of pulmonary artery vasodilatation that may also inhibit smooth muscle proliferation and platelet aggregation.
CO-CBS-H2 S axis: From vascular mediator to cancer regulator.
Kabe et al., Tokyo, Japan. In Microcirculation, Dec 2015
Such CO-directed target macromolecules include soluble guanylate cyclase and cystathionine β-synthase (CBS).
[Octarphin--Nonopioid Peptide of the Opioid Origin].
Navolotskaya, In Bioorg Khim, Sep 2015
Taking into account that NO acts as a primary activator of soluble guanylate cyclase (sGC), it can be assumed that the activating effect of octarphin on macrophages is realized in the following way: increase in th iNOS expression --> increase in the NO production --> increase in the sGC activity --> increase in intracellular levels of cGMP.
Heme-nitrosyls: electronic structure implications for function in biology.
Lehnert et al., Ann Arbor, United States. In Acc Chem Res, Aug 2015
These results are then discussed in the context of the biological functions of heme-nitrosyls, in particular in soluble guanylate cyclase (sGC; NO signaling), nitrophorins (NO transport), and NO-producing enzymes.
Current developments in pharmacological therapeutics for chronic constipation.
Sun et al., Nanjing, China. In Acta Pharm Sin B, Jul 2015
The 5-HT4 receptor modulators velusetrag and naronapride, the guanylate cyclase C agonist plecanatide and the ileal bile acid transporter inhibitor elobixibat are recognized as the most promising drugs under investigation.
Protein and Signaling Networks in Vertebrate Photoreceptor Cells.
Dell'Orco et al., Oldenburg, Germany. In Front Mol Neurosci, 2014
It is catalyzed by membrane bound sensory guanylate cyclases (GCs) and is regulated by specific neuronal Ca(2+)-sensor proteins called guanylate cyclase-activating proteins (GCAPs).
Riociguat for the treatment of pulmonary arterial hypertension.
PATENT-1 Study Group et al., Gießen, Germany. In N Engl J Med, 2013
BACKGROUND: Riociguat, a soluble guanylate cyclase stimulator, has been shown in a phase 2 trial to be beneficial in the treatment of pulmonary arterial hypertension.
Riociguat for the treatment of chronic thromboembolic pulmonary hypertension.
CHEST-1 Study Group et al., Gießen, Germany. In N Engl J Med, 2013
BACKGROUND: Riociguat, a member of a new class of compounds (soluble guanylate cyclase stimulators), has been shown in previous clinical studies to be beneficial in the treatment of chronic thromboembolic pulmonary hypertension.
Familial diarrhea syndrome caused by an activating GUCY2C mutation.
Knappskog et al., Bergen, Norway. In N Engl J Med, 2012
METHODS: We used linkage analysis, based on arrays with single-nucleotide polymorphisms, to identify a candidate region on chromosome 12 and then sequenced GUCY2C, encoding guanylate cyclase C (GC-C), an intestinal receptor for bacterial heat-stable enterotoxins.
Opposite effects of ANP receptors in attenuation of LPS-induced endothelial permeability and lung injury.
Birukova et al., Chicago, United States. In Microvasc Res, 2012
Results demonstrate the opposite effects of NPR-A and NPR-C in LPS-mediated endothelial permeability and lung injury.
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.
Potter et al., Minneapolis, United States. In J Mol Cell Cardiol, 2012
human ventricular cardiomyocytes express low levels of GC-A and GC-A in cardiomyocytes from failing human hearts is refractory to ANP stimulation.
ATP potentiates competitive inhibition of guanylyl cyclase A and B by the staurosporine analog, Gö6976: reciprocal regulation of ATP and GTP binding.
Potter et al., Minneapolis, United States. In J Biol Chem, 2011
Go6976 reduces GTP binding to the catalytic site of GC-A and GC-B and that ATP increases the magnitude of the inhibition.
The functional genomics of guanylyl cyclase/natriuretic peptide receptor-A: perspectives and paradigms.
Pandey, New Orleans, United States. In Febs J, 2011
review attempts to provide insights and to delineate the current concepts in the field of functional genomics and signaling of GC-A/NPRA in hypertension and cardiovascular disease states at the molecular level
Natriuretic peptide receptor a as a novel target for prostate cancer.
Mohapatra et al., Tampa, United States. In Mol Cancer, 2010
NPRA promotes prostate cancer development in part by regulating macrophage migration inhibitory factor
Administration of BAY 41-2272 prevents bladder dysfunction in nitric-oxide deficient rats.
Antunes et al., Campinas, Brazil. In Einstein (sao Paulo), 2010
OBJECTIVE: to evaluate the protective effects of BAY 41-2272, a soluble guanylate cyclase activator, on changes in cystometric parameters in rats deficient in nitric oxide (NO).
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