Anti-Angiotensin Converting Enzyme 1 antibody [EPR2757] - BSA and Azide free

Supplementary info

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

Activity summary

Angiotensin Converting Enzyme 1 also known as ACE1 or ACE is an important enzyme in the renin-angiotensin system. This enzyme exhibits a significant role in blood pressure regulation. ACE1 is a zinc-metallopeptidase with a molecular weight of approximately 130 kDa. It converts angiotensin I into the potent vasoconstrictor angiotensin II a critical function in cardiovascular physiology. ACE1 is widely expressed in endothelial cells particularly in the lungs kidneys and the small intestine.

Biological function summary

The enzyme generates angiotensin II by cleaving angiotensin I. Angiotensin II an important effector peptide impacts cardiovascular and renal systems influencing vasoconstriction and fluid balance. While not directly forming a complex ACE1's activity increases the potency of angiotensin II which binds to angiotensin II receptors to exert its effects therefore indirectly forming a functional signaling complex.

Pathways

ACE1 plays a central role in the renin-angiotensin system and the kallikrein-kinin system. The enzyme's activity boosts angiotensin II production which connects it to the regulation of blood pressure via the renin-angiotensin pathway. ACE1 also indirectly interacts with proteins like bradykinin by degrading them modulating kinin-related functions and influencing inflammation and tension in vascular smooth muscle.

Associated diseases and disorders

Understanding ACE1 is important for addressing hypertension and congestive heart failure. ACE1's conversion of angiotensin I to angiotensin II means overactivity can cause elevated blood pressure leading to hypertension. This makes ACE inhibitors such as lisinopril and ramipril therapeutic for these conditions. Furthermore its connection with aldosterone production places ACE1 in relevance to heart failure as excessive aldosterone can cause detrimental remodeling of cardiac tissue.