Carbamoyl-Phosphate Synthase (Ammonia) (Carbamoyl-Phosphate Synthetase I)

An enzyme that catalyzes the formation of carbamoyl phosphate from ATP, carbon dioxide, and ammonia. This enzyme is specific for arginine biosynthesis or the urea cycle. Absence or lack of this enzyme may cause CARBAMOYL-PHOSPHATE SYNTHASE I DEFICIENCY DISEASE. EC
Also Known As:
Carbamoyl-Phosphate Synthetase I; CP Synthase I; Carbamoyl-Phosphate Synthetase (Ammonia); Carbamoylphosphate Synthetase I; Carbamyl Phosphate Synthase (Ammonia); Carbamyl-Phosphate Synthase (Ammonia); I, Carbamoyl-Phosphate Synthetase; Synthase I, CP; Synthetase I, Carbamoyl-Phosphate; Synthetase I, Carbamoylphosphate; Carbamoyl Phosphate Synthetase I; Carbon dioxide:ammonia ligase (ADP-forming, carbamate-phosphorylating)
Networked: 27 relevant articles (0 outcomes, 0 trials/studies)

Bio-Agent Context: Research Results


1. Rubio, Vicente: 2 articles (06/2011 - 07/2010)
2. Pazos, Manuel: 1 article (12/2014)
3. Rosa Nogués, M: 1 article (12/2014)
4. Sánchez-Martos, Vanesa: 1 article (12/2014)
5. Molinar-Toribio, Eunice: 1 article (12/2014)
6. Torres, Josep L: 1 article (12/2014)
7. Medina, Isabel: 1 article (12/2014)
8. Méndez, Lucía: 1 article (12/2014)
9. Gallardo, José M: 1 article (12/2014)
10. Wong, Lee-Jun: 1 article (06/2011)

Related Diseases

1. Hepatocellular Carcinoma (Hepatoma)
2. Hyperammonemia
3. Neoplasms (Cancer)
4. Body Weight (Weight, Body)
11/01/1978 - "The increased activity of carbamyl phosphate synthetase I [carbamoyl-phosphate synthase (ammonia); ATP: carbamate phosphotransferase (diphosphorylating), EC] in tadpole liver observed during thyroxine-induced metamorphosis was markedly inhibited by intraperitoneal injection of the microbial protease inhibitor antipain (0.1 micrometermol/g of body weight, twice daily). "
12/29/1995 - "Dietary DHEA leads to: (1) decrease in body weight gain; (2) relative increases in liver weight; (3) liver color change; (4) induction of hepatic peroxisomal enzymes; (5) proliferation of hepatic peroxisomes with increased cross-sectional area; (6) decreased hepatic mitochondrial cross-sectional area; (7) elevated levels of hepatic cytosolic malic enzyme; (8) slight decreases, significant decreases, or significant increases in serum triglyceride levels, depending on mouse strain; (9) increases in total serum cholesterol levels; (10) significant decreases in the hepatic rates of fatty acid synthesis; (11) significant increases in the hepatic rates of cholesterol synthesis; (12) decreases in both protein content and specific activity of hepatic mitochondrial carbamoyl phosphate synthetase-I without concomitant changes in serum urea nitrogen; (13) induction of glutathione S-transferase activity in liver; (14) decrease in hepatic endogenous protein phosphorylation; (15) increase in hepatic AMPase and GTPase activities; (16) formation of 5-androstene-3 beta,17 beta-diol as a major metabolite of DHEA by subcellular fractions of liver, which is reflected in serum and tissue levels; and (17) reduction in serum prolactin levels."
5. Inborn Urea Cycle Disorders

Related Drugs and Biologics

1. Urea (Carbamide)
2. Adenosine Triphosphate (ATP)
3. Methionine (L-Methionine)
4. Glutathione Transferase (Glutathione S-Transferase)
5. Dexamethasone (Maxidex)
6. Catalase
7. Carbamyl Phosphate (Carbamoyl Phosphate)
8. Ammonia
9. Peroxiredoxins
10. Acyl-CoA Dehydrogenase (Medium-Chain Acyl-Coenzyme A Dehydrogenase)

Related Therapies and Procedures

1. Intraperitoneal Injections