Disease relevance of Cps1

• Mice deficient in the urea-cycle enzyme, carbamoyl phosphate synthetase I, die during the early neonatal period from hyperammonemia [1].
• These findings suggest that the pronounced reduction of CPS and OTC activities reported in Reye's syndrome in man are not a general manifestation of the severity of influenza infection [2].
• The production of a capsular polysaccharide (CPS; K antigen) is characteristic of Klebsiella pneumoniae, but CPS structure varies among strains, and many different serotypes are now known [3].
• We have studied the regulation of expression of the carbamoyl-phosphate synthetase II-aspartate transcarbamylase-dihydroorotase gene in F9 teratocarcinoma cells during their differentiation into parietal endoderm cells by induction with a combination of retinoic acid and dibutyryl cyclic AMP [4].
• One of the factors determining the toxicity of chlorpyrifos (CPS), an organophosphorus (OP) insecticide, is its biotransformation [5].

High impact information on Cps1

• We have examined the virulence of T. gondii mutants that lack carbamoyl phosphate synthetase II (uracil auxotrophs) to determine whether de novo pyrimidine biosynthesis is required in vivo [6].
• The in vivo relevance of the transcription factors interacting with the enhancer in the regulation of CPS expression in the liver was assessed by the analysis of knockout mice [7].
• Carbamoyl phosphate synthetase I (CPSase I; EC 6.3.4.16) is located within the inner mitochondrial matrix and catalyzes the initial rate-limiting step of the urea cycle [1].
• The upstream regulatory region of the carbamoyl-phosphate synthetase I gene controls its tissue-specific, developmental, and hormonal regulation in vivo [8].
• In the second group spatial, temporal, and hormonal regulation of expression of the reporter gene and the endogenous carbamoyl-phosphate synthetase gene were identical [8].

Chemical compound and disease context of Cps1

• 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 [9].
• Acivicin, an antimetabolite elaborated by Streptomyces sviceus, inhibits a spectrum of L-glutamine utilizing enzymes including carbamoyl phosphate synthetase II, the inaugurating enzyme of de novo pyrimidine biosynthesis [10].
• A simple, specific, sensitive and reproducible ELISA has been developed to quantify the level of CPS (capsular polysaccharide) production in supernatants of Streptococcus pneumoniae cell cultures [11].
• Administration of paraoxonase 30 min before CPS increased plasma enzyme activity toward CPO by 35-fold, and protected against its toxicity; protection was still present at 24 h, when enzyme activity was still 20-fold over basal [12].
• In the present study we have investigated whether exogenous paraoxonase administered to mice would offer protection toward the acute toxicity of a phosphorothioate, chlorpyrifos (CPS) [12].

Biological context of Cps1

• The changes in gene expression of CPS, ASS and PEPCK caused by the fatty acids in the cultured hepatocytes were very similar to those observed in the liver of JVS mice [13].
• A single far-upstream enhancer is sufficient to confer hepatocyte-specific, glucocorticoid- and cyclic AMP-inducible periportal expression to the carbamoylphosphate synthetase I (CPS) gene [7].
• Caspase-dependent cleavage of carbamoyl phosphate synthetase II during apoptosis [14].
• Auxotrophic his alleles introduced into recipient strains provided selectable markers to coinherit the adjacent cps gene clusters from donors expressing a heterologous CPS [3].
• Group B Streptococcus (GBS) type III capsular polysaccharide (CPS III) was conjugated to recombinant cholera toxin B subunit (rCTB) using three different methods which employed (i) cystamine and N-succinimidyl-3-(2-pyridyldithio)propionate (SPDP), (ii) carbodiimide with adipic acid dihydrazide (ADH) as a spacer, or (iii) reductive amination (RA) [15].

Anatomical context of Cps1

• CPS III was present exclusively in the liver mitochondria of both lungfishes, but the majority of the arginase activities were present in the cytosolic fractions of their livers [16].
• However, during the perinatal period, the pericentral hepatocytes temporarily accumulated CPS protein [17].
• We also observed heterochrony between species in the appearance of CPS protein in the small intestine [17].
• In fibroblast-like CHO cells, on the other hand, the GRE in the CPS enhancer does not cooperate with the C/EBP and HNF3 elements in transactivation of the CPS promoter [7].
• The carbamoyl-phosphate synthetase I gene is expressed in the periportal region of the liver, where it is activated by glucocorticosteroids and glucagon (via cyclic AMP), and in the crypts of the intestinal mucosa [8].

Associations of Cps1 with chemical compounds

• Furthermore, there was an increase in the hepatic ornithine-urea cycle (OUC) capacity, with significant increases in the activities of CPS III (3.8-fold), argininosuccinate synthetase + lyase (1.8-fold) and, more importantly, glutamine synthetase (2.2-fold) [18].
• Like the marine ray Taeniura lymma, the African lungfish Protopterus dolloi possesses carbamoyl phosphate III (CPS III) in the liver and not carbamoyl phosphate I (CPS I), as in the mouse Mus musculus or as in other African lungfish reported elsewhere [18].
• Carnitine administration relieved the suppression of the developmental induction of two urea cycle enzymes examined, carbamoyl-phosphate synthetase and argininosuccinate synthase, and kept the activities of enzymes normal [19].
• Addition of a synthetic glucocorticoid hormone, dexamethasone, caused increases in CPS and ASS mRNAs [13].
• Further addition of oleic acid suppressed the induction of CPS and ASS mRNAs by dexamethasone [13].

Other interactions of Cps1

• Urea synthesis in the African lungfish Protopterus dolloi--hepatic carbamoyl phosphate synthetase III and glutamine synthetase are upregulated by 6 days of aerial exposure [18].
• Citrin, ASS, CPS and Ornt1 showed similar patterns of developmental changes in the liver and small intestine, where they play a role in urea and arginine synthesis [20].
• These results, together with the developmental changes of these transcription factor mRNA levels, suggest that HNF-4 and C/EBP-alpha are involved in the suppression of CPS expression [21].
• These distribution profiles are different from the restricted of Ornt1, ASS and CPS [20].
• In addition, expression of hepatocyte-specific genes (alphaFP, transthyretin, carbamoyl-phosphate synthetase, and coagulation factor-2) was detected by reverse transcription polymerase chain reaction [22].

Analytical, diagnostic and therapeutic context of Cps1

• The levels and also the authenticity of translation of rat liver albumin and mouse liver carbamoyl phosphate synthetase I were tested by immunoprecipitation with monospecific antibodies [23].
• Specific antibody was used to stabilize the CPS on the surface of K. pneumoniae, and the structural organization of the homologous and heterologous capsules was examined by electron microscopy [3].
• This ELISA allowed selection of an appropriate vaccine strain, for a natural polysaccharide vaccine, among several 23F pneumococcal clinical isolates and constituted a valuable analytical tool for Strep. pneumoniae fermentation and CPS purification follow-up [11].
• N-Acetyl-L-glutamate (NAG), the activator of mitochondrial carbamoyl phosphate synthetase (CPS), is demonstrated by several methods, including a new HPLC assay, in the brain of mammals and of chicken [24].

References