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Guanylyl cyclases, catalyzing the production of cGMP from GTP, are classified as soluble and membrane forms (Garbers and Lowe, 1994 [PubMed 7982997]). Additionally we are shipping NPR1 Proteins (12) and NPR1 Kits (11) and many more products for this protein.
Showing 10 out of 85 products:
Human Polyclonal NPR1 Primary Antibody for IHC (p) - ABIN392702
Takahashi, Nakayama, Soma, Izumi, Kanmatsuse: Organization of the human natriuretic peptide receptor A gene. in Biochemical and biophysical research communications 1998
Show all 4 references for ABIN392702
Human Polyclonal NPR1 Primary Antibody for EIA, IF - ABIN360587
Dams, Van Acker, Gustin, Vereycken, Bunkens, Holemans, Smeulders, Clayton, Ohagen, Hertogs: A time-resolved fluorescence assay to identify small-molecule inhibitors of HIV-1 fusion. in Journal of biomolecular screening 2007
Show all 2 references for ABIN360587
Human Polyclonal NPR1 Primary Antibody for IF, IHC (p) - ABIN191702
Hirsch, Kruhøffer, Adermann, Heitland, Maronde, Meyer, Forssmann, Herter, Plenz, Schlatter: Cellular localization, membrane distribution, and possible function of guanylyl cyclases A and 1 in collecting ducts of rat. in Cardiovascular research 2001
Human Polyclonal NPR1 Primary Antibody for ICC, IF - ABIN441340
Kovacova, Tharp, Liu, Wei, Xie, Collins, Pratley: Adipose tissue natriuretic peptide receptor expression is related to insulin sensitivity in obesity and diabetes. in Obesity (Silver Spring, Md.) 2016
Conclude that postnatal cardiac hyperplasia in mice with global GC-A (show GUCA1A Antibodies) inactivation is provoked by systemic alterations rather than direct regulation of cardiac myocyte proliferation.
Data (including data from studies in knockout mice) suggest expression of ANP (show NPPA Antibodies)/BNP (show BNC2 Antibodies)/GC-A (show GUCA1A Antibodies) (atrial natriuretic peptide (show NPPA Antibodies), brain natriuretic peptide (show BNP Antibodies), and guanylyl cyclase-A) is important in embryonic neovascularization and organogenesis.
Suggest that the FQQI motif is essential for the internalization and subcellular trafficking of NPRA during the hormone signaling process in intact mesangial cells.
Data suggest activation of skeletal muscle (SM) Npra is important for maintenance of long-ter (show INS Antibodies)m insulin sensitivity; up-regulation of Npra signal transduction in SM (that was reduced by obesity) prevents glucose intolerance and diabetes type 2.
these findings define a novel epigenetic regulatory mechanism that governs Npr1 gene transcription.
Npr1 represses the expression of cardiac proinflammatory mediators, hypertrophic markers, and NF-kappaB/AP-1-mediated mechanisms, which seem to be associated in an Npr1 gene-dose-dependent manner
ANP (show NPPA Antibodies) is capable of attenuating agonist-induced lung edema in the absence of NPR-A.
These results demonstrate that a high-salt diet aggravates cardiac ANG II, aldosterone and pro-inflammatory cytokine levels in Npr1 gene-disrupted 1-copy mice, whereas, in Npr1 gene-duplicated (3-copy and 4-copy) mice, high salt did not render such elevation, suggesting the potential roles of Npr1 against salt loading.
ANP (show NPPA Antibodies)-NPRA system exerts an inhibitory effect on MAPKs and down-stream effector molecules, AP-1 (show JUN Antibodies), and CREB (show CREB1 Antibodies), critical for cell growth and proliferation.
Natriuretic peptide receptor guanylyl cyclase-A protects podocytes from aldosterone-induced glomerular injury.
After ligand binding, NPRA is rapidly internalized and trafficked from the cell surface into endosomes, Res and lysosomes, with concurrent generation of intracellular cyclic GMP (show NT5C2 Antibodies) in HEK (show EPHA3 Antibodies)-293 cells.
Data suggest up-regulation of NPRA in skeletal muscle (SM) correlates with whole-body insulin (show INS Antibodies) sensitivity; NPRA is down-regulated in SM in obese subjects compared to normal controls; NPRA in SM is up-regulated in response to diet-induced weight loss.
In this review we highlight the mechanisms by which NPR-A affects signaling pathways involved in inflammation and cancer, and we discuss its potential as a novel target in inflammation, cancer, and cancer-related inflammation
NPRA was detected in E11.5 cardiac progenitor cells.
Cardiac fibrosis and the endogenous natriuretic peptide system were evaluated in end-stage heart failure to assess the anti-fibrotic actions of the dual GC-A/-B activator.
High NPR1 expression is associated with esophageal squamous cell carcinomas.
Molecular dynamics analysis indicated decreases in the values of Van (show TNIP1 Antibodies) der (show GDF3 Antibodies) Waals, electrostatic energy and potential energy of NPRB (show NPR2 Antibodies)/Vasonatrin peptide compared to NPRA/Vasonatrin peptide.
ACNP stimulated both human natriuretic peptide receptors (NPRs), NPRA and NPRB (show NPR2 Antibodies), as potent as their native ligands in receptor transfected cells.
human ventricular cardiomyocytes express low levels of GC-A and GC-A in cardiomyocytes from failing human hearts is refractory to ANP (show NPPA Antibodies) stimulation.
Results demonstrate the opposite effects of NPR-A and NPR-C (show NPR3 Antibodies) in LPS (show IRF6 Antibodies)-mediated endothelial permeability and lung injury.
Guanylyl cyclases, catalyzing the production of cGMP from GTP, are classified as soluble and membrane forms (Garbers and Lowe, 1994
aatriuretic peptide receptor A
, atrial natriuretic peptide receptor 1
, guanylyl cyclase beta 1, soluable
, natriuretic peptide receptor A/guanylate cyclase A (atrionatriuretic peptide receptor A)
, natriuretic peptide receptor 1
, Nppa receptor
, atrial natriuretic peptide receptor type A
, guanylate cyclase A
, guanylyl cyclase-A
, atrionatriuretic peptide receptor A
, natriuretic peptide A type receptor
, natriuretic peptide receptor A
, atrial natriuretic peptide A-type receptor
, atrial natriuretic peptide receptor A