Anti-Guanylyl Cyclase alpha 1/GUCY1A3 antibody [EPR12270] - BSA and Azide free

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

Guanylyl Cyclase alpha 1 also known as GUCY1A3 is a subunit of the soluble guanylyl cyclase enzyme often referred to simply as guanylyl cyclase. This enzyme plays an important mechanical role by synthesizing cyclic guanosine monophosphate (cGMP) from guanosine triphosphate (GTP). The GUCY1A3 subunit exists primarily as part of a heterodimer typically pairing with the beta subunit GUCY1B3 to form the active enzyme complex. The protein has an approximate mass of 70 kDa and is widely expressed in various tissues with abundant expression in vascular smooth muscle cells platelets and neurons.

Biological function summary

The guanylyl cyclase enzyme containing GUCY1A3 acts as a signal transducer in nitric oxide (NO) signaling pathways. The enzyme activity governed by GUCY1A3 produces cGMP in response to NO which then functions as a secondary messenger. This secondary messenger plays an important role in vasodilation inhibiting platelet aggregation and neurotransmission. The guanylyl cyclase-GUCY1A3 complex significantly influences vascular tone and hence blood pressure regulation.

Pathways

GUCY1A3 integrates firmly into critical biological routes like the nitric oxide-cGMP pathway and the cGMP-PKG signaling pathway. In the nitric oxide-cGMP pathway GUCY1A3-related enzymatic activity leads to smooth muscle relaxation a pivotal process in cardiovascular physiology. Through its involvement in the cGMP-PKG pathway GUCY1A3 influences signal transductions that affect myocardial contractility and neuronal signaling. Interactions with other proteins such as PKG (protein kinase G) serve as downstream signaling processes initiated by cGMP.

Associated diseases and disorders

Alterations in GUCY1A3 function associate with cardiovascular diseases like hypertension and pulmonary arterial hypertension. Disruption in GUCY1A3 activity affects normal NO-cGMP signaling leading to inappropriate blood pressure control and vascular anomalies. Moreover genetic mutations or dysregulation of GUCY1A3 have links to thrombosis primarily due to its role in modulating platelet activity through the NO-cGMP pathway. The protein connexin to disorders typically involves its interactions with soluble guanylyl cyclase subunit beta (GUCY1B3) as imbalances in their complex formation often result in impaired vascular homeostasis.