|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)|
|1.||Hepatocellular Carcinoma (Hepatoma)
01/01/2007 - "Only forkhead box A was exclusively present in hepatoma cells, and therefore appears to be an important determinant of the observed tissue specificity of carbamoylphosphate synthetase-I expression. "
01/01/2007 - "The relationship between carbamoylphosphate synthetase-I expression and in vivo occupancy of the response elements was examined by comparing a carbamoylphosphate synthetase-I-expressing hepatoma cell line with a carbamoylphosphate synthetase-I-negative fibroblast cell line. "
10/20/1995 - "The role of the proximal promoter and the far-upstream enhancer in the hepatocyte-specific and hormonal regulation of the carbamoyl-phosphate synthetase I (CPS) gene was investigated in transient transfection assays using primary rat hepatocytes, hepatoma cells, and fibroblasts. "
08/17/1987 - "Hormonal regulation of carbamoyl-phosphate synthetase I synthesis in primary cultured hepatocytes and Reuber hepatoma H-35. "
05/20/1983 - "Reuber hepatoma H-35 was found to retain the activity of carbamoyl-phosphate synthetase I. The content of this enzyme in H-35 grown in Eagle's minimal essential medium was about half that in rat liver. "
06/01/2011 - "Deficiency of carbamoyl phosphate synthetase I (CPSI) results in hyperammonemia ranging from neonatally lethal to environmentally induced adult-onset disease. "
01/01/2007 - "Carbamoylphosphate synthetase I deficiency (CPS1D) is a urea-cycle disorder characterized by episodes of life-threatening hyperammonemia. "
07/01/2010 - "Carbamoyl-phosphate synthetase I (CPS1) deficiency (CPS1D), a recessively inherited urea cycle error due to CPS1 gene mutations, causes life-threatening hyperammonemia. "
07/01/2009 - "Carbamoyl phosphate synthetase-I (CPS1) is a key enzyme in the urea cycle and patients with defects in the function or expression of CPS1 suffer from hyperammonemia. "
01/01/1999 - "Mice deficient in the urea-cycle enzyme, carbamoyl phosphate synthetase I, die during the early neonatal period from hyperammonemia."
04/21/1993 - "This stimulation with excess ammonia, which can also result from high-protein intake, is dependent on the presence of carbamoyl phosphate synthetase I, an enzyme in the liver and intestine but not in most tumors. "
03/01/1982 - "It did not cleave several of the protein and peptide substrates tested including the precursor of mitochondrial carbamoyl-phosphate synthetase I. Apparently the same protease activity is widely distributed among mitochondria of rat kidney, spleen, heart and ascites tumor cells, all of which lack ornithine carbamoyltransferase. "
|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 220.127.116.11] 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
|2.||Adenosine Triphosphate (ATP)
|4.||Glutathione Transferase (Glutathione S-Transferase)
|7.||Carbamyl Phosphate (Carbamoyl Phosphate)
|10.||Acyl-CoA Dehydrogenase (Medium-Chain Acyl-Coenzyme A Dehydrogenase)