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ACE
SNP Table
| variant | genotype | frequency | risk allele |
|---|---|---|---|
| rs4330 | |||
| rs4343 | |||
| rs12720743 | |||
| rs754265941 | |||
| rs1230587529 | |||
| rs4459610 | |||
| rs4362 | |||
| rs4363 | |||
| rs4316 | |||
| rs4331 | |||
| rs4364 | |||
| rs117134739 | |||
| rs117647476 | |||
| rs12709426 | |||
| rs12709442 | |||
| rs12720742 | |||
| rs12720745 | |||
| rs12720754 | |||
| rs1277816308 | |||
| rs1281544974 |
Summary
Protein names
Found in These Blog Articles
GHR Function
The ACE gene provides instructions for making the angiotensin-converting enzyme. This enzyme is able to cut (cleave) proteins. It is part of the renin-angiotensin system, which regulates blood pressure and the balance of fluids and salts in the body. By cutting a protein called angiotensin I at a particular location, the angiotensin-converting enzyme converts this protein to angiotensin II. Angiotensin II causes blood vessels to narrow (constrict), which results in increased blood pressure. This protein also stimulates production of the hormone aldosterone, which triggers the absorption of salt and water by the kidneys. The increased amount of fluid in the body also increases blood pressure. Proper blood pressure during fetal growth, which delivers oxygen to the developing tissues, is required for normal development of the kidneys, particularly of structures called the proximal tubules, and other tissues. In addition, angiotensin II may play a more direct role in kidney development, perhaps by affecting growth factors involved in the development of kidney structures.
The angiotensin-converting enzyme can cleave other proteins, including bradykinin. Bradykinin causes blood vessels to widen (dilate), which decreases blood pressure. Cleavage by the angiotensin-converting enzyme inactivates bradykinin, helping to increase blood pressure.
More Information
Having genes that increase ACE or angiotensin converting enzyme increase the stress response, causing the release of adrenaline and noradrenaline (Ref, Ref2)
The Renin-Angiotensin System (and ACE) increases the fight or flight nervous system, HPA axis (Ref), vasoconstriction, blood pressure, aldosterone, cortisol, vasopressin (Ref).
Higher levels of ACE are associated with depression (Ref)
Secretion of CRH, ACTH, and cortisol is increased by stimulation of angiotensin AT(1) receptors.(Ref)
Elevated levels of ACE are also found in leprosy, hyperthyroidism, acute hepatitis, primary biliary cirrhosis, diabetes mellitus, multiple myelomas, osteoarthritis, amyloidosis, Gaucher disease, pneumoconiosis, histoplasmosis, miliary tuberculosis.
Levels are decreased in renal disease, obstructive pulmonary disease, and hypothyroidism.
ACE gene polymorphisms correlate with different ACE levels in blood [R].
Increased cardiac levels of angiotensin II could be a result of the homozygous deletion ACE genotype, leading to increased risk of heart disease [R]. Africans had a higher frequency of Deletion alleles, Asians had a lower frequency, compared to Caucasians [R].
Deletion=higher ACE
Ace Genes are associated with:
- Greater risk of heart attack (deletion) [R, R] and heart disease (deletion) [R, R], sudden cardiac disease (deletion) [R, R]. DD genotype is only slightly associated with greater heart disease risk [R].
- Ventricular hypertrophy (thickening of the left ventricular wall) (deletion) [R,R, R].
- Greater progression and severity of IgA nephropathy (deletion) [R].
- Resistance to normal therapies for renal disease (deletion) [R].
- Acute Respiratory distress syndrome mortality, based on the RAS-pathway (deletion) [R].
- Higher blood pressure in males (deletion) [R, R].
- Lacunar stroke (deletion) [R].
- Response to beta-blockers (deletion) [R].
- Hypertension and hypertension treatment response (deletion) [R]. African-Americans have a greater risk for hypertension with the DD polymorphism. [R].
- Higher risk for diabetic nephropathy (deletion) [R].
- Kidney deterioration in diabetic patients; patients with the deletion genotype needed dialysis within 10 years of diabetes diagnosis [R].
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