An antibody raised against guanylate cyclase soluble subunit alpha-1 (GUCY1A1). GUCY1A1 is involved in NO-sGC-cGMP signalling and cardiovascular pathways.
Catalogue number crb2005739 Antibody Anti-GUCY1A1 antibody Antigen Peptide KLH conjugated synthetic peptide crb1200948 Protein ID UniProtKB - Q02108 (Human) Aliases GCS-alpha-1, Guanylate cyclase soluble subunit alpha-3, GUC1A3, GUCSA3, GUCY1A3, Soluble guanylate cyclase large subunit Cross-Reactivity Human Host Species Rabbit Antibody Type Polyclonal Concentration 1.0 mg/ml Glycine (G), 0.5 mg/ml TEA (T) Target GUCY1A1 Family Adenylyl cyclase class-4/guanylyl cyclase family Storage This material is supplied in PBS containing 0.01% sodium azide and 1% trehalose. The product should be stored at +4°C for short term storage and -20°C for long term storage. Avoid repeated freeze/thaw cycles. References
Buys et al., (2018). Discovery and development of next generation sGC stimulators with diverse multidimensional pharmacology and broad therapeutic potential. Nitric Oxide, 78: 72.
Wang et al., (2020). Pathogenesis of premature coronary artery disease: Focus on risk factors and genetic variants. Genes Dis., doi: 10.1016/j.gendis.2020.11.003.
Soluble guanylate cyclases (sGCs) are heterodimeric enzymes that convert GTP to 3′,5′-cyclic GMP and pyrophosphate. Most complexes consist of an alpha subunit, such as alpha-1 (GUCY1A1), and a beta subunit, typically beta-1 (GUCY1B3). In the presence of magnesium or manganese ions, enzyme activity is stimulated by nitric oxide (NO). sGCs are the principal receptors for nitric oxide (NO), NO-releasing drugs, and NO-sGC-cGMP signalling. Impaired NO availability within the cell is linked to cardiovascular and metabolic disorders due to the role of sGCs in cGMP signalling pathways.
sGC plays a role in several cardiovascular pathways. Reduced sGC function contributes to several conditions, including cardiovascular diseases. GUCY1A1 loss of function mutations are associated with atherosclerosis development, increased risk of hypertension and coronary artery disease. An inactivating mutation in GUCY1A1 is linked to premature coronary artery disease. Individuals with homozygous mutations in GUCY1A1develop autosomal-recessive moyamoya and early-onset achalasia.