Argininosuccinate Synthase: An enzyme of the urea cycle that catalyzes the formation of argininosuccinic acid from citrulline and aspartic acid in the presence of ATP. Absence or deficiency of this enzyme causes the metabolic disease CITRULLINEMIA in humans. EC 6.3.4.5.Argininosuccinate Lyase: An enzyme of the urea cycle which splits argininosuccinate to fumarate plus arginine. Its absence leads to the metabolic disease ARGININOSUCCINIC ACIDURIA in man. EC 4.3.2.1.CitrullineArginine: An essential amino acid that is physiologically active in the L-form.Argininosuccinic Acid: This amino acid is formed during the urea cycle from citrulline, aspartate and ATP. This reaction is catalyzed by argininosuccinic acid synthetase.Argininosuccinic Aciduria: Rare autosomal recessive disorder of the urea cycle which leads to the accumulation of argininosuccinic acid in body fluids and severe HYPERAMMONEMIA. Clinical features of the neonatal onset of the disorder include poor feeding, vomiting, lethargy, seizures, tachypnea, coma, and death. Later onset results in milder set of clinical features including vomiting, failure to thrive, irritability, behavioral problems, or psychomotor retardation. Mutations in the ARGININOSUCCINATE LYASE gene cause the disorder.Citrullinemia: A group of diseases related to a deficiency of the enzyme ARGININOSUCCINATE SYNTHASE which causes an elevation of serum levels of CITRULLINE. In neonates, clinical manifestations include lethargy, hypotonia, and SEIZURES. Milder forms also occur. Childhood and adult forms may present with recurrent episodes of intermittent weakness, lethargy, ATAXIA, behavioral changes, and DYSARTHRIA. (From Menkes, Textbook of Child Neurology, 5th ed, p49)Lyases: A class of enzymes that catalyze the cleavage of C-C, C-O, and C-N, and other bonds by other means than by hydrolysis or oxidation. (Enzyme Nomenclature, 1992) EC 4.Methylobacillus: A genus of short, aerobic, gram-negative rods which are obligate methylotrophs, growing on one-carbon compounds other than methane. (From Bergey's Manual of Determinative Bacteriology, 9th ed)Pseudomonas putida: A species of gram-negative, aerobic bacteria isolated from soil and water as well as clinical specimens. Occasionally it is an opportunistic pathogen.Homoserine Dehydrogenase: An enzyme that catalyzes the reduction of aspartic beta-semialdehyde to homoserine, which is the branch point in biosynthesis of methionine, lysine, threonine and leucine from aspartic acid. EC 1.1.1.3.Research Report: Detailed account or statement or formal record of data resulting from empirical inquiry.Mortuary Practice: Activities associated with the disposition of the dead. It excludes cultural practices such as funeral rites.Internet: A loose confederation of computer communication networks around the world. The networks that make up the Internet are connected through several backbone networks. The Internet grew out of the US Government ARPAnet project and was designed to facilitate information exchange.User-Computer Interface: The portion of an interactive computer program that issues messages to and receives commands from a user.Databases, Protein: Databases containing information about PROTEINS such as AMINO ACID SEQUENCE; PROTEIN CONFORMATION; and other properties.Software: Sequential operating programs and data which instruct the functioning of a digital computer.Molecular Sequence Annotation: The addition of descriptive information about the function or structure of a molecular sequence to its MOLECULAR SEQUENCE DATA record.Urea Cycle Disorders, Inborn: Rare congenital metabolism disorders of the urea cycle. The disorders are due to mutations that result in complete (neonatal onset) or partial (childhood or adult onset) inactivity of an enzyme, involved in the urea cycle. Neonatal onset results in clinical features that include irritability, vomiting, lethargy, seizures, NEONATAL HYPOTONIA; RESPIRATORY ALKALOSIS; HYPERAMMONEMIA; coma, and death. Survivors of the neonatal onset and childhood/adult onset disorders share common risks for ENCEPHALOPATHIES, METABOLIC, INBORN; and RESPIRATORY ALKALOSIS due to HYPERAMMONEMIA.Hyperammonemia: Elevated level of AMMONIA in the blood. It is a sign of defective CATABOLISM of AMINO ACIDS or ammonia to UREA.Ornithine Carbamoyltransferase Deficiency Disease: An inherited urea cycle disorder associated with deficiency of the enzyme ORNITHINE CARBAMOYLTRANSFERASE, transmitted as an X-linked trait and featuring elevations of amino acids and ammonia in the serum. Clinical features, which are more prominent in males, include seizures, behavioral alterations, episodic vomiting, lethargy, and coma. (Menkes, Textbook of Child Neurology, 5th ed, pp49-50)Metabolism, Inborn Errors: Errors in metabolic processes resulting from inborn genetic mutations that are inherited or acquired in utero.Hyperargininemia: A rare autosomal recessive disorder of the urea cycle. It is caused by a deficiency of the hepatic enzyme ARGINASE. Arginine is elevated in the blood and cerebrospinal fluid, and periodic HYPERAMMONEMIA may occur. Disease onset is usually in infancy or early childhood. Clinical manifestations include seizures, microcephaly, progressive mental impairment, hypotonia, ataxia, spastic diplegia, and quadriparesis. (From Hum Genet 1993 Mar;91(1):1-5; Menkes, Textbook of Child Neurology, 5th ed, p51)Sodium Benzoate: The sodium salt of BENZOIC ACID. It is used as an antifungal preservative in pharmaceutical preparations and foods. It may also be used as a test for liver function.Nitrogen: An element with the atomic symbol N, atomic number 7, and atomic weight [14.00643; 14.00728]. Nitrogen exists as a diatomic gas and makes up about 78% of the earth's atmosphere by volume. It is a constituent of proteins and nucleic acids and found in all living cells.Dinoflagellida: Flagellate EUKARYOTES, found mainly in the oceans. They are characterized by the presence of transverse and longitudinal flagella which propel the organisms in a rotating manner through the water. Dinoflagellida were formerly members of the class Phytomastigophorea under the old five kingdom paradigm.Harmful Algal Bloom: An algal bloom where the algae produce powerful toxins that can kill fish, birds, and mammals, and ultimately cause illness in humans. The harmful bloom can also cause oxygen depletion in the water due to the death and decomposition of non-toxic algae species.Marine Toxins: Toxic or poisonous substances elaborated by marine flora or fauna. They include also specific, characterized poisons or toxins for which there is no more specific heading, like those from poisonous FISHES.Oxocins: Compounds based on an 8-membered heterocyclic ring including an oxygen. They can be considered medium ring ethers.Nitrogen Compounds: Inorganic compounds that contain nitrogen as an integral part of the molecule.Dianisidine: Highly toxic compound which can cause skin irritation and sensitization. It is used in manufacture of azo dyes.2-Naphthylamine: A naphthalene derivative with carcinogenic action.Hydrobromic Acid: Hydrobromic acid (HBr). A solution of hydrogen bromide gas in water.Nitrites: Salts of nitrous acid or compounds containing the group NO2-. The inorganic nitrites of the type MNO2 (where M=metal) are all insoluble, except the alkali nitrites. The organic nitrites may be isomeric, but not identical with the corresponding nitro compounds. (Grant & Hackh's Chemical Dictionary, 5th ed)Agave: A genus known for fibers obtained from their leaves: sisal from A. sisalana, henequen from A. fourcroyoides and A. cantala, or Manila-Maguey fiber from A. cantala. Some species provide a sap that is fermented to an intoxicating drink, called pulque in Mexico. Some contain agavesides.Hydrochloric Acid: A strong corrosive acid that is commonly used as a laboratory reagent. It is formed by dissolving hydrogen chloride in water. GASTRIC ACID is the hydrochloric acid component of GASTRIC JUICE.PolyaminesCulture Media: Any liquid or solid preparation made specifically for the growth, storage, or transport of microorganisms or other types of cells. The variety of media that exist allow for the culturing of specific microorganisms and cell types, such as differential media, selective media, test media, and defined media. Solid media consist of liquid media that have been solidified with an agent such as AGAR or GELATIN.Amino Acids, Peptides, and Proteins: Amino acids and chains of amino acids connected by peptide linkages.Lipid Metabolism, Inborn Errors: Errors in the metabolism of LIPIDS resulting from inborn genetic MUTATIONS that are heritable.Peroxisomal Disorders: A heterogeneous group of inherited metabolic disorders marked by absent or dysfunctional PEROXISOMES. Peroxisomal enzymatic abnormalities may be single or multiple. Biosynthetic peroxisomal pathways are compromised, including the ability to synthesize ether lipids and to oxidize long-chain fatty acid precursors. Diseases in this category include ZELLWEGER SYNDROME; INFANTILE REFSUM DISEASE; rhizomelic chondrodysplasia (CHONDRODYSPLASIA PUNCTATA, RHIZOMELIC); hyperpipecolic acidemia; neonatal adrenoleukodystrophy; and ADRENOLEUKODYSTROPHY (X-linked). Neurologic dysfunction is a prominent feature of most peroxisomal disorders.Acyl-CoA Dehydrogenase, Long-Chain: A flavoprotein oxidoreductase that has specificity for long-chain fatty acids. It forms a complex with ELECTRON-TRANSFERRING FLAVOPROTEINS and conveys reducing equivalents to UBIQUINONE.Acyl-CoA Dehydrogenase: A flavoprotein oxidoreductase that has specificity for medium-chain fatty acids. It forms a complex with ELECTRON TRANSFERRING FLAVOPROTEINS and conveys reducing equivalents to UBIQUINONE.Gene Rearrangement: The ordered rearrangement of gene regions by DNA recombination such as that which occurs normally during development.Dual-Specificity Phosphatases: A sub-class of protein tyrosine phosphatases that contain an additional phosphatase activity which cleaves phosphate ester bonds on SERINE or THREONINE residues that are located on the same protein.MicroRNAs: Small double-stranded, non-protein coding RNAs, 21-25 nucleotides in length generated from single-stranded microRNA gene transcripts by the same RIBONUCLEASE III, Dicer, that produces small interfering RNAs (RNA, SMALL INTERFERING). They become part of the RNA-INDUCED SILENCING COMPLEX and repress the translation (TRANSLATION, GENETIC) of target RNA by binding to homologous 3'UTR region as an imperfect match. The small temporal RNAs (stRNAs), let-7 and lin-4, from C. elegans, are the first 2 miRNAs discovered, and are from a class of miRNAs involved in developmental timing.Streptomyces griseus: An actinomycete from which the antibiotics STREPTOMYCIN, grisein, and CANDICIDIN are obtained.3' Untranslated Regions: The sequence at the 3' end of messenger RNA that does not code for product. This region contains transcription and translation regulating sequences.Protein Tyrosine Phosphatases: An enzyme group that specifically dephosphorylates phosphotyrosyl residues in selected proteins. Together with PROTEIN-TYROSINE KINASE, it regulates tyrosine phosphorylation and dephosphorylation in cellular signal transduction and may play a role in cell growth control and carcinogenesis.Insectivora: An order of insect eating MAMMALS including MOLES; SHREWS; HEDGEHOGS and tenrecs.Cyclin-Dependent Kinases: Protein kinases that control cell cycle progression in all eukaryotes and require physical association with CYCLINS to achieve full enzymatic activity. Cyclin-dependent kinases are regulated by phosphorylation and dephosphorylation events.

Hepatocyte gene therapy in a large animal: a neonatal bovine model of citrullinemia. (1/173)

The development of gene-replacement therapy for inborn errors of metabolism has been hindered by the limited number of suitable large-animal models of these diseases and by inadequate methods of assessing the efficacy of treatment. Such methods should provide sensitive detection of expression in vivo and should be unaffected by concurrent pharmacologic and dietary regimens. We present the results of studies in a neonatal bovine model of citrullinemia, an inborn error of urea-cycle metabolism characterized by deficiency of argininosuccinate synthetase and consequent life-threatening hyperammonemia. Measurements of the flux of nitrogen from orally administered 15NH4 to [15N]urea were used to determine urea-cycle activity in vivo. In control animals, these isotopic measurements proved to be unaffected by pharmacologic treatments. Systemic administration of a first-generation E1-deleted adenoviral vector expressing human argininosuccinate synthetase resulted in transduction of hepatocytes and partial correction of the enzyme defect. The isotopic method showed significant restoration of urea synthesis. Moreover, the calves showed clinical improvement and normalization of plasma glutamine levels after treatment. The results show the clinical efficacy of treating a large-animal model of an inborn error of hepatocyte metabolism in conjunction with a method for sensitively measuring correction in vivo. These studies will be applicable to human trials of the treatment of this disorder and other related urea-cycle disorders.  (+info)

Metabolic capacity for L-citrulline synthesis from ammonia in rat isolated colonocytes. (2/173)

Ammonia is present at high concentration in the colon lumen and is considered a colon cancer suspect. Furthermore, ammonia usually eliminated by the liver in the ornithine cycle is considered highly toxic to cerebral function when present in excess in the blood plasma. Therefore, the metabolic pathways involved in ammonia metabolism in colonocytes were studied in the present study. Rat colonocytes were found equipped with low carbamoylphosphate synthase I activity, high ornithine carbamoyltransferase and arginase activities and low argininosuccinate synthase activity. High (10 and 50 mmol/l) NH4Cl concentrations but not low concentrations (1 and 5 mmol/l) were found able to increase respectively 3- and 10-fold the conversion of radioactive L-arginine to L-citrulline. In contrast, very low capacity for L-citrulline conversion to L-arginine is found in colonocytes. It is concluded that an incomplete ornithine cycle is operative in colonocytes which results in ammonia stimulated L-citrulline production. The contribution of this metabolic pathway in relation to ammonia detoxication by colonocytes is discussed.  (+info)

An adult-onset case of argininosuccinate synthetase deficiency presenting with atypical citrullinemia. (3/173)

A 52-year-old heavy drinker presented with repeated episodes of disturbance of consciousness and an increase in serum ammonia level, triggered by excessive alcohol intake. He was diagnosed as having adult-onset citrullinemia with deficiency of hepatic argininosuccinate synthetase (ASS) activity. Cranial magnetic resonance imaging (MRI) showed high-intensity lesions in the central pons and the bilateral middle cerebellar peduncles on T2-weighted images. Although almost all cases of adult-onset citrullinemia have been reported to be enzymologically classified as type II, the serum amino acid pattern and serum level of human pancreatic secretory trypsin inhibitor (hPSTI) were atypical for type II in the present case.  (+info)

Induction of argininosuccinate synthetase in rat brain glial cells after striatal microinjection of immunostimulants. (4/173)

The enzyme argininosuccinate synthetase (ASS) initiates the metabolic pathway leading from L-citrulline to L-arginine, the only physiological substrate of all isoforms of nitric oxide synthases. The presence of ASS in glial cells in vivo was investigated by immunohistochemical methods in a model of rat brain inflammation. Phosphate-buffered saline or a mixture of bacterial lipopolysaccharide and interferon-gamma was injected into the left striatum, and animals were killed 24 hours later. Ipsilateral and contralateral sides of brain sections were incubated with an antiserum against ASS or antibodies against cell-specific markers. In the three areas examined, striatum, corpus callosum, and cortex, a strong induction of ASS immunoreactivity was observed in glial cells after injection of immunostimulants. A detailed quantitative analysis of double-stained sections revealed that ASS was almost exclusively expressed in reactive, ED1-positive microglial cells/brain macrophages in immunostimulant- or sham-injected ipsilateral sides of the sections. Furthermore, ASS/ED1 costaining was observed in perivascular cells. Colocalization of ASS with astroglial marker glial fibrillary acidic protein was given only occasionally after immunostimulation. ASS-positive neurons were detected in control and experimental animals; staining intensity was comparable in both cases. The results suggest that neurons express ASS constitutively, whereas the enzyme is induced in glial cells in response to proinflammatory stimuli. This finding is the first demonstration of an induction of a pathway auxiliary to generation of nitric oxide in brain in response to immunostimulants and provides new insight into neural arginine metabolism.  (+info)

Using genomic information to investigate the function of ThiI, an enzyme shared between thiamin and 4-thiouridine biosynthesis. (5/173)

The gene thiI encodes a protein (ThiI) that plays a role in the transfer of sulfur from cysteine to both thiamin and 4-thiouridine, but the reaction catalyzed by ThiI remains undetermined. Based upon sequence alignments, ThiI shares a unique "P-loop" motif with the PPi synthetase family, four enzymes that catalyze adenylation and subsequent substitution of carbonyl oxygens. To test whether or not this motif is critical for ThiI function, the Asp in the motif was converted to Ala (D189A), and a screen for in vivo 4-thiouridine production revealed the altered enzyme to be inactive. Further scrutiny of sequence data and the crystal structures of two members of the PPi synthetase family implicated Lys321 in the proposed adenylation function of ThiI, and the critical nature of Lys321 has been demonstrated by site-directed mutagenesis and genetic screening. Our results, then, indicate that ThiI catalyzes the adenylation of a substrate at the expense of ATP, a narrowing of possible reactions that provides a strong new basis for deducing the early steps in the transfer of sulfur from cysteine to both thiamin and 4-thiouridine.  (+info)

Augmentation of urea-synthetic capacity by inhibition of nitric oxide synthesis in butyrate-induced differentiated human hepatocytes. (6/173)

We have recently developed an in vitro differentiation model of immortalized non-transformed human hepatocytes using butyrate, and observed the induction of inducible NO synthase (iNOS). In this study, we analyzed the effect of NO on the urea-synthetic capacity of these cells. The inhibition of iNOS during butyrate treatment significantly increased the urea-synthetic capacity as compared to that of butyrate treatment alone, possibly through the further induction of ornithine transcarbamylase expression. Therefore, the inhibition of NO production might be useful for obtaining more differentiated hepatocytes in the process of in vitro induction of hepatocyte-specific differentiation.  (+info)

Regulation of diaphragmatic nitric oxide synthase expression during hypobaric hypoxia. (7/173)

Nitric oxide (NO) is normally synthesized inside skeletal muscle fibers by both endothelial (eNOS) and neuronal (nNOS) nitric oxide synthases. In this study, we evaluated the influence of hypobaric hypoxia on the expression of NOS isoforms, argininosuccinate synthetase (AS), argininosuccinate lyase (AL), and manganese superoxide dismutase (Mn SOD) in the ventilatory muscles. Rats were exposed to hypobaric hypoxia ( approximately 95 mmHg) from birth for 60 days or 9-11 mo. Age-matched control groups of rats also were examined. Sixty days of hypoxia elicited approximately two- and ninefold increases in diaphragmatic eNOS and nNOS protein expression (evaluated by immunoblotting), respectively, and about a 50% rise in diaphragmatic NOS activity. In contrast, NOS activity and the expression of these proteins declined significantly in response to 9 mo of hypoxia. Hypoxia elicited no significant alterations in AS, AL and Mn SOD protein expression. Moreover, the inducible NOS (iNOS) was not detected in normoxic and hypoxic diaphragmatic samples. We conclude that diaphragmatic NOS expression and activity undergo significant adaptations to hypobaric hypoxia and that iNOS does not participate in this response.  (+info)

Mutation analysis of Korean patients with citrullinemia. (8/173)

Citrullinemia is an autosomal recessive disease due to the mutations in the argininosuccinate synthetase (ASS) gene. Mutation analysis was performed on three Korean patients with citrullinemia. All of the three patients had the splicing mutation previously reported as IVS6-2A>G mutation. Two had Gly324Ser mutation and the other patient had a 67-bp insertion mutation in exon 15. The IVS6-2A>G mutation was reported to be found frequently in Japanese patients with citrullinemia, but Caucasian patients showed the extreme mutational heterogeneity. Although a limited number of Korean patients were studied, the IVS6-2A>G mutation appears to be one of the most frequent mutant alleles in Korean patients with citrullinemia. The Gly324Ser mutation identified in two patients also suggests the possible high frequency of this mutation in Korean patients as well.  (+info)

Citrullinemia type I is an autosomal recessive disorder that is caused by a deficiency of the urea cycle enzyme argininosuccinate synthetase (ASS1). Deficiency of ASS1 shows various clinical manifestations encompassing severely affected patients with fatal neonatal hyperammonemia as well as asymptomatic individuals with only a biochemical phenotype. This is a comprehensive report of all 87 mutations found to date in the ASS1 gene on chromosome 9q34.1. A large proportion of the mutations (n=27) are described here for the first time. Mutations are distributed throughout exons 3 to 15, most of them being identified in exons 5, 12, 13, and 14. The mutation G390R in exon 15 is the single most common mutation in patients with the classical phenotype. Certain mutations clearly link to specific clinical courses but the clinical phenotype cannot be anticipated in all patients. This update presents a survey of the correlation between mutations in the ASS1 gene and the respective clinical courses as ...
TY - JOUR. T1 - Targeting argininosuccinate synthetase negative melanomas using combination of arginine degrading enzyme and cisplatin. AU - Savaraj, Niramol. AU - Wu, Chunjing. AU - Li, Ying Ying. AU - Wangpaichitr, Medhi. AU - You, Min. AU - Bomalaski, John. AU - He, Wei. AU - Kuo, Macus Tien. AU - Feun, Lynn G. PY - 2015. Y1 - 2015. N2 - Loss of argininosuccinate synthetase (ASS) expression in melanoma makes these tumor cells vulnerable to arginine deprivation. Pegylated arginine deiminase (ADIPEG20) which degrades arginine to citrulline and ammonia has been used clinically and partial responses and stable disease have been noted with minimal toxicity. In order to improve the therapeutic efficacy of ADI-PEG20, we have combined ADI-PEG20 with a DNA damaging agent, cisplatin. We have shown that the combination of the two drugs together significantly improved the therapeutic efficacy when compared to ADI-PEG20 alone or cisplatin alone in 4 melanoma cell lines, regardless of their BRAF mutation. ...
Although accumulating evidence highlights the importance of p53-mediated metabolism in tumor suppression (2, 47), the mechanisms by which p53 drives dynamic nutrient status in harmony with canonical p53 functions remain poorly understood. Here, we show that p53 activates the penultimate step of de novo arginine synthesis pathway through the direct induction of the rate-limiting enzyme ASS1. Furthermore, we demonstrate that ASS1 deficiency induced anomalous Akt phosphorylation, resulting in rendering cells more susceptible to genotoxic stress.. Although we have demonstrated that p53 drives the de novo arginine synthesis pathway via ASS1 induction under genotoxic conditions, argininosuccinate lyase (ASL), which directly produces arginine from argininosuccinate, was not induced by p53 in HCT116 cells. These results suggest that ASS1 is the sole node connecting p53 to the de novo arginine synthesis pathway. Because ASS1 is a rate-limiting enzyme of the de novo arginine synthesis pathway, ASS1 ...
L-citrulline plays an important role in human health and nutrition and is an intermediate of the L-arginine biosynthetic pathway. L-citrulline is a by-product of L-arginine production by Corynebacterium glutamicum. In this study, C. glutamicum was engineered for overproduction of L-citrulline as major product without L-arginine being produced as by-product. To this end, L-arginine biosynthesis was derepressed by deletion of the arginine repressor gene argR and conversion of L-citrulline towards L-arginine was avoided by deletion of the argininosuccinate synthetase gene argG. Moreover, to facilitate L-citrulline production the gene encoding a feedback resistant N-acetyl L-glutamate kinase argBfbr as well as the gene encoding L-ornithine carbamoylphosphate transferase argF were overexpressed. The resulting strain accumulated 44.1 ± 0.5 mM L-citrulline from glucose minimal medium with a yield of 0.38 ± 0.01 g⋅g−1 and a volumetric productivity of 0.32 ± 0.01 g⋅l−1⋅h−1. In addition, production
Many melanomas do not express argininosuccinate synthetase (ASS) which is a key enzyme in the process of arginine biosynthesis. As a result, these melanoma cells need exogenous arginine supply for survival and proliferation while normal cell do not. A new drug targeting this metabolic defect of melanoma has been developed by Polaris, Inc. (recombinant arginine deiminase conjugated with polyethylene glycol-20 or ADI-PEG20). This complex can effectively degrade blood arginine to citrulline. Phase I/II clinical trials with ADI-PEG20 have shown promising activity in patients with advanced melanoma. However, our laboratory studies have demonstrated that after treatment with ADI-PEG20, some melanoma cells are able to induce the production of ASS, while others have the ability to undergo prolonged autophagy as well as low requirement for arginine to survive. Thus, arginine deprivation results in growth inhibition without cell death. On the other hand, TRAIL has been used to induce apoptosis in certain ...
Pancreatic cancer is a leading cause of cancer-related deaths in the world with a 5-year survival rate of less than 6%. Currently, there is no successful therapeutic strategy for advanced pancreatic cancer, and new effective strategies are urgently needed. Recently, an arginine deprivation agent, arginine deiminase, was found to inhibit the growth of some tumor cells (i.e., hepatocellular carcinoma, melanoma, and lung cancer) deficient in argininosuccinate synthetase (ASS), an enzyme used to synthesize arginine. The purpose of this study was to evaluate the therapeutic efficacy of arginine deiminase in combination with gemcitabine, the first line chemotherapeutic drug for patients with pancreatic cancer, and to identify the mechanisms associated with its anticancer effects. In this study, we first analyzed the expression levels of ASS in pancreatic cancer cell lines and tumor tissues using immunohistochemistry and RT-PCR. We further tested the effects of the combination regimen of arginine deiminase
1KH2: Crystal structure of argininosuccinate synthetase from Thermus thermophilus HB8. Structural basis for the catalytic action.
Proc Natl Acad Sci U S A. 2013 Dec 17;110(51):E5006-15. doi: 10.1073/pnas.1321305110. Epub 2013 Dec 2. Research Support, N.I.H., Extramural
TY - JOUR. T1 - Arginine deprivation and tumour cell death: arginase and its inhibition. AU - Wheatley, Denis. AU - Philip, R.. AU - Campbell, E.. PY - 2003. Y1 - 2003. N2 - Arginase treatment of cell cultures reduced arginine in the medium to similar to micromolar levels within 5-30 min, and proved as effective as arginine-free medium (AFM) prepared by formulation. The enzyme was heat stable and as active at pH 7.2 as at pH 9.9. It persisted in culture for at least 3 days with only a small diminution in its speed of action, and still actively destroyed arginine after 6 days, since arginine supplementation failed to rescue viable cells.Addition of L-norvaline, an inhibitor of arginase, rescued cells from arginase-induced deprivation. Its efficacy at low concentrations was short-lived (probably , 1 day), while at higher concentrations it did not appear to inhibit completely the enzyme. However, L-norvaline at these same levels also slowed the growth of positive non-enzyme treated controls ...
Complete information for ASS1P12 gene (Pseudogene), Argininosuccinate Synthetase 1 Pseudogene 12, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Complete information for ASS1P14 gene (Pseudogene), Argininosuccinate Synthetase 1 Pseudogene 14, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
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For example, the fact that methylation-dependent silencing of argininosuccinate synthetase (ASS1) [40], a rate-limiting enzyme involved in the biosynthesis of arginine, has been implicated in therapeutic resistance in several cancer types including renal cell carcinoma, hepatocellular carcinoma, malignant melanoma, glioblastoma multiforme, and platinum-resistant epithelial. ovarian cancer suggests a role for demethylating agents in these ASS1 drug-resistant find more cancers [41]. Nevertheless, despite their current nonspecific promiscuity, epigenetic agents may act on most or all tumor types, since aberrant methylation and deacetylation patterns are a hallmark of cancer cells. In particular, several of the anticancer agents described in this review activate and upregulate p53, which itself affects multiple targets [19]. Following genotoxic stress. in response to traditional therapeutic strategies such as cisplatin, doxorubicin, 5-fluorouracil, fludarabine, mitoxantrone, etoposide, or X-ray ...
SWISS-MODEL Template Library (SMTL) entry for 1kh3.1. Crystal Structure of Thermus thermophilus HB8 Argininosuccinate Synthetase in complex with inhibitor
Principal Investigator:MORI Masataka, Project Period (FY):1998 - 2000, Research Category:Grant-in-Aid for Scientific Research (B)., Section:展開研究, Research Field:Pathological medical chemistry
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There are many analytical techniques covered in this review, which describes their specific uses and even set up details for some analytical techniques. The references at the end of the report describe many specific instances of the analysis of thermoset materials published over the last 10 years. The review is accompanied by around 400 abstracts from papers and books in the Rapra Polymer Library database, to facilitate further reading on this subject. A subject index and a company index are included.
We report three cases of adult-onset type II citrullinemia (CTLN2) treated with different therapies including one case successfully treated with p.o. administration of sodium pyruvate and low-carbohydrate diet. Although recent advances in liver transplantation have enabled successful treatment of patients with CTLN2, several issues concerning liver transplantation remain. Further, there is still an urgent need for therapies that do not rely on liver transplantation. The first case was a 41-year-old man who developed impaired consciousness in 1992. The patient was treated with conventional therapy for hepatic encephalopathy and died of severe brain edema. The second case was a 31-year-old man who suddenly presented a syncope-like attack with hyperammonemia. He was treated with carbohydrate-restricted diet but the encephalopathy could not be controlled, and he received emergency living donor liver transplantation. The third patient was a 67-year-old man who developed abnormal behavior with hyperammonemia.
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class="publication">Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href="http://www.nrbook.com/b/bookcpdf.php">Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
TY - JOUR. T1 - Requirement of argininosuccinate lyase for systemic nitric oxide production. AU - Erez, Ayelet. AU - Nagamani, Sandesh C.S.. AU - Shchelochkov, Oleg A.. AU - Premkumar, Muralidhar H.. AU - Campeau, Philippe M.. AU - Chen, Yuqing. AU - Garg, Harsha K.. AU - Li, Li. AU - Mian, Asad. AU - Bertin, Terry K.. AU - Black, Jennifer O.. AU - Zeng, Heng. AU - Tang, Yaoping. AU - Reddy, Anilkumar K.. AU - Summar, Marshall. AU - OBrien, William E.. AU - Harrison, David G.. AU - Mitch, William E.. AU - Marini, Juan C.. AU - Aschner, Judy L.. AU - Bryan, Nathan S.. AU - Lee, Brendan. PY - 2011/12/1. Y1 - 2011/12/1. N2 - Nitric oxide (NO) is crucial in diverse physiological and pathological processes. We show that a hypomorphic mouse model of argininosuccinate lyase (encoded by Asl) deficiency has a distinct phenotype of multiorgan dysfunction and NO deficiency. Loss of Asl in both humans and mice leads to reduced NO synthesis, owing to both decreased endogenous arginine synthesis and an ...
TY - JOUR. T1 - Argininosuccinate lyase interacts with cyclin A2 in cytoplasm and modulates growth of liver tumor cells. AU - Hung, Yu Hsuan. AU - Huang, Hau Lun. AU - Chen, Wei Ching. AU - Yen, Meng Chi. AU - Cho, Chien Yu. AU - Weng, Tzu Yang. AU - Wang, Chih Yang. AU - Chen, Yi Ling. AU - Chen, Li Tzong. AU - Lai, Ming Derg. PY - 2017/2. Y1 - 2017/2. N2 - Arginine is a critical amino acid in specific cancer types including hepatocellular carcinoma (HCC) and melanoma. Novel molecular mechanisms and therapeutic targets in arginine metabolism-mediated cancer formation await further identification. Our laboratory has previously demonstrated that arginine metabolic enzyme argininosuccinate lyase (ASL) promoted HCC formation in part via maintenance of cyclin A2 protein expression and arginine production for channeling to nitric oxide synthase. In this study, we investigated the mechanism by which ASL regulates cyclin A2 expression. We found that ASL interacted with cyclin A2 in HCC cells and the ...
In the linear pathway (Figure 1A), GLU is converted to acetylglutamate (Ac-GLU) by N-acetylglutamate synthase (NAGS, encoded by argA) which is inhibited by ARG through negative feedback regulation [36],[39]. Sequential catalytic reactions catalyzed by the next three enzymes, N-acetylglutamate kinase (NAGK, encoded by argB), N-acetylglutamate semialdehyde dehydrogenase (encoded by argC) and N-acetylornithine transaminase (encoded by argD), which are common in the three pathways (Figure 1), yield N-acetylornithine (Ac-ORN) [34]. The next step, which distinguishes the linear pathway from the other two pathways, is deacetylation of Ac-ORN by AOase to yield ORN [40],[41]. The next and final steps are carried out by ornithine carbamoyltransferase (OTC or OTCase, encoded by argF), argininosuccinate synthase (encoded by argG) and argininosuccinate lyase (encoded by argH), which finally yield ARG [35]. This pathway has been found in a few species such as Myxococcus xanthus [41] and E. coli [36].. In many ...
... (CIT II) is a rare genetic condition. CIT II results from a mutation (error) in ones DNA. Due to this mistake, people with CIT II are unable to produce an important enzyme, citrin. The function of citrin is to move substances within a cell. Enzymes are special proteins that help break down food into pieces. Once the food is broken down it is used as energy to make other proteins the body needs. People without citrin may not break down citrulline, which is a building block found in many proteins we eat. These substances are important for breaking down sugars, making proteins, and for the normal function of the liver. Those affected by CIT II typically develop symptoms in infancy, adolescence, or adulthood. Symptoms include yellowish skin and eyes (jaundice), low birth weight, confusion, restlessness, memory loss, low blood sugar, and abnormal behaviors.. CIT II is inherited in an autosomal recessive pattern. Meaning, the child must inherit two copies of the non-working gene ...
Citrullinemia definition at Dictionary.com, a free online dictionary with pronunciation, synonyms and translation. Look it up now!
Background Arginine depletion has shown promising anticancer effects among arginine auxotrophic cancers that are deficient in argininosuccinate synthetase (ASS) and/or ornithine transcarbamylase (OTC). Pegylated arginase (PEG-BCT-100 (rhArg1peg5000)) works as an arginine depletor by converting arginine to ornithine. However, accumulated ornithine can be channeled via ornithine decarboxylase (ODC) to produce polyamines that are known to promote tumor growth. We postulate that ODC inhibition enhances anticancer effects of BCT-100 in lung adenocarcinoma. Methods The activity of BCT-100 was tested in a panel of lung adenocarcinoma cell lines (H23, H358, HCC827, H1650, H1975, HCC2935 and HCC4006). Cell viability was measured using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Protein expression was evaluated by Western Blot. Nude mice subcutaneous xenograft models (XMs) derived from these cell lines were used for in vivo study. An ODC inhibitor ...
FAP48 was identified and cloned thanks to its interaction with FK506-binding proteins (FKBPs) such as FKBP52 and FKBP12, which belong to the large family of immunophilins that bind the macrolide immunosuppressant drugs FK506 and rapamycin. We have previously shown that FAP48-FKBP complexes are dissociated by FK506 and rapamycin, suggesting that FAP48 is an endogenous ligand of FKBP. The present work describes the biochemical consequences of FAP48 overexpression, induced by the tetracycline analogue doxycycline, in an established cell line derived from Jurkat T cells. We report that overexpression of FAP48 results in the inhibition of cellular proliferation as does the exposure of Jurkat T cells to FK506. We also show that the expression levels of argininosuccinate synthetase and the Myc antagonist Mxi1 are modified by overexpression of FAP48, suggesting that these proteins could be good candidates to mediate the antiproliferative effect of FAP48. FAP48 affects neither the calcineurin-dependent ...
Currie, G A.; Gyure, L; and Cifuentes, L, "Microenvironmental arginine depletion by macrophages in vivo." (1979). Subject Strain Bibliography 1979. 3434 ...
Information, Tools, and Resources to aid Primary Care Physicians in caring for Children with Special Health Care Needs (CSHCN) and providing a Medical Home for all of their patients.
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Death threats and threats of violent beatings were made against Stjepan Radić in parliament, without any intervention by the president of the Assembly (Parliamentary speaker). On the morning of 20 June 1928, Radić was warned of the danger of an assassination attempt against him and was begged to stay away from the Assembly for that day. He replied that he was like a soldier in war, in the trenches and as such it was his duty to go but he nevertheless promised not to utter a single word.[citation needed]. In the Assembly, Puniša Račić, a member of Peoples Radical Party from Montenegro, got up and made a provocative speech which produced a stormy reaction from the opposition but Radić himself stayed completely silent. Finally, Ivan Pernar shouted in response, "thou plundered beys" (referring to accusations of corruption related to him). In an earlier speech Radić accused Račić of stealing from civilian population and later refused to apologize when Račić asked him to.[14] Puniša ...
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Waelbroeck, C. , Paul, A. , Kucera, M. , Rosell-Melé, A. , Weinelt, M. , Schneider, R. , Mix, A. C. , Abelmann, A. , Armand, L. , Barker, S. , Barrows, T. T. , Benway, H. , Cacho, I. , Chen, M. T. , Cortijo, E. , Crosta, X. , de Vernal, A. , Dokken, T. , Duprat, J. , Elderfield, H. , Eynaud, F. , Gersonde, R. , Hayes, A. , Henry, M. , Hillaire-Marcel, C. , Huang, C. C. , Jansen, E. , Juggins, S. , Kallel, N. , Kiefer, T. , Kienast, M. , Labeyrie, L. , Leclaire, H. , Londeix, L. , Mangin, S. , Matthießen, J. , Marret, F. , Meland, M. , Morey, A. E. , Mulitza, S. , Pflaumann, U. , Pisias, N. G. , Radi, T. , Rochon, A. , Rohling, E. J. , Sbaffi, L. , Schäfer-Neth, C. , Solignac, S. , Spero, H. , Tachikawa, K. and Turon, J. L. (2009 ...
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... or synthetase (ASS; EC 6.3.4.5) is an enzyme that catalyzes the synthesis of argininosuccinate from ... Haines RJ, Pendleton LC, Eichler DC (2011). "Argininosuccinate synthase: at the center of arginine metabolism". Int J Biochem ... The enzyme endothelial nitric oxide synthase produces nitric oxide from arginine in endothelial cells. Argininosuccinate ... a novel argininosuccinate synthase site at serine 328 during calcium-dependent stimulation of endothelial nitric-oxide synthase ...
... argininosuccinate synthase MeSH D08.811.464.259.350 --- carbamoyl-phosphate synthase (ammonia) MeSH D08.811.464.259.400 --- ... riboflavin synthase MeSH D08.811.913.225.825 --- spermidine synthase MeSH D08.811.913.225.912 --- spermine synthase MeSH ... nitric oxide synthase type i MeSH D08.811.682.664.500.772.500 --- nitric oxide synthase type ii MeSH D08.811.682.664.500.772. ... glycogen synthase kinases MeSH D08.811.913.696.620.682.700.429.500 --- glycogen synthase kinase 3 MeSH D08.811.913.696.620.682. ...
Argininosuccinate synthetase (EC 6.3.4.5) CTP synthase (EC 6.3.4.2) Pyruvate carboxylase (EC 6.4.1.1) Acetyl-CoA carboxylase ( ... Tryptophan synthase (EC 4.2.1.20) Category:EC 4.3.1 Phenylalanine ammonia-lyase (EC 4.3.1.24) Category:EC 4.4.1 Cystathionine ... ATP synthase (EC 3.6.3.14) Kynureninase EC 3.7.1.3 EC 3.8.1.3 Haloacetate dehalogenase Category:EC 4.1.1 Ornithine ... EC 1.14.13 Nitric oxide synthase EC 1.14.13.39 Category:EC 1.14.14 Aromatase EC 1.14.14.1 CYP2D6 EC 1.14.14.1 CYP2E1 EC 1.14. ...
Argininosuccinate synthase. *Holocarboxylase synthetase. *GMP synthase. *Asparagine synthetase. *Carbamoyl phosphate synthetase ...
Argininosuccinate synthase. *Holocarboxylase synthetase. *GMP synthase. *Asparagine synthetase. *Carbamoyl phosphate synthetase ... This entry also includes folylpolyglutamate synthase that transfers glutamate to folylpolyglutamate and cyanophycin synthetase ...
Argininosuccinate synthase. *Holocarboxylase synthetase. *GMP synthase. *Asparagine synthetase. *Carbamoyl phosphate synthetase ... Carbamoyl phosphate synthase (CPSase) is a heterodimeric enzyme composed of a small and a large subunit (with the exception of ... Carbamoyl phosphate synthase has three main steps in its mechanism and is, in essence, irreversible.[4] ... "Inhibition of carbamoyl-phosphate synthase (ammonia) by Tris and Hepes. Effect on Ka for N-acetylglutamate" (PDF). Biochem. J ...
Argininosuccinate synthase. *Holocarboxylase synthetase. *GMP synthase. *Asparagine synthetase. *Carbamoyl phosphate synthetase ... In enzymology, a phosphoribosylformylglycinamidine synthase (EC 6.3.5.3) is an enzyme that catalyzes the chemical reaction ... Retrieved from "https://en.wikipedia.org/w/index.php?title=Phosphoribosylformylglycinamidine_synthase&oldid=808965560" ...
Argininosuccinate synthase. *Holocarboxylase synthetase. *GMP synthase. *Asparagine synthetase. *Carbamoyl phosphate synthetase ...
Argininosuccinate synthase. *Holocarboxylase synthetase. *GMP synthase. *Asparagine synthetase. *Carbamoyl phosphate synthetase ... Asparagine synthase (glutamine-hydrolysing) (EC 6.3.5.4, asparagine synthetase (glutamine-hydrolysing), glutamine-dependent ... Retrieved from "https://en.wikipedia.org/w/index.php?title=Asparagine_synthase_(glutamine-hydrolysing)&oldid=917335771" ...
Argininosuccinate synthase. *Argonaute. *Argos (EGFR Inhibitor). *Aromatic L-amino acid decarboxylase. *Arrestin ...
Argininosuccinate synthase. *Holocarboxylase synthetase. *GMP synthase. *Asparagine synthetase. *Carbamoyl phosphate synthetase ... "Synthases and ligases". chem.qmul.ac.uk. Archived from the original on October 15, 2012. Retrieved July 28, 2013.. .mw-parser- ... Under one definition, synthases do not use energy from nucleoside triphosphates (such as ATP, GTP, CTP, TTP, and UTP), whereas ... It is also said that a synthase is a lyase (a lyase is an enzyme that catalyzes the breaking of various chemical bonds by means ...
The enzyme CTP synthase catalyzes the next reaction step: the conversion of UTP to CTP by transferring an amino group from ... Then, the enzymes citrulline and argininosuccinate convert ornithine to arginine. There are two distinct lysine biosynthetic ... 4-hydroxy-tetrahydrodipicolinate synthase adds a pyruvate group to the β-aspartyl-4-semialdehyde, and a water molecule is ... The next reaction is catalyzed by the enzyme pyrroline-5-carboxylate synthase (P5CS), which catalyzes the reduction of the ϒ- ...
... and argininosuccinate lyase (ASL). This is an energetically costly process, because for each molecule of argininosuccinate that ... Citrulline can be derived from multiple sources: from arginine itself via nitric oxide synthase (NOS), as a byproduct of the ... Andrew PJ, Mayer B (Aug 1999). "Enzymatic function of nitric oxide synthases". (review). Cardiovascular Research. 43 (3): 521- ... from citrulline in arginine and proline metabolism by the sequential action of the cytosolic enzymes argininosuccinate ...
... adenylosuccinate synthase EC 6.3.4.5: argininosuccinate synthase EC 6.3.4.6: urea carboxylase EC 6.3.4.7: ribose-5-phosphate- ... arginine b-lactam-synthase EC 6.3.4.1: GMP synthase. Now included in EC 6.3.5.2, GMP synthase (glutamine-hydrolysing). EC 6.3. ... imidazole ribonucleotide synthase EC 6.3.4.19: tRNAIle-lysidine synthase EC 6.3.4.20: 7-cyano-7-deazaguanine synthase EC 6.3. ... glutathionylspermidine synthase EC 6.3.1.9: trypanothione synthase EC 6.3.1.10: adenosylcobinamide-phosphate synthase EC 6.3. ...
Argininosuccinate synthetase (EC 6.3.4.5). *CTP synthase (EC 6.3.4.2). Category:EC 6.4 (form carbon-carbon bonds)Edit. * ... EC 2.9.1.2: O-phospho-L-seryl-tRNA(Sec):L-selenocysteinyl-tRNA synthase ... 2-Succinyl-5-enolpyruvyl-6-hydroxy-3-cyclohexene-1-carboxylic-acid synthase EC 2.2.1.9 ... EC 6.2.1.38: (2,2,3-trimethyl-5-oxocyclopent-3-enyl)acetyl-CoA synthase ...
"Gene sharing by delta-crystallin and argininosuccinate lyase". Proceedings of the National Academy of Sciences of the United ... "Crystal structure of albaflavenone monooxygenase containing a moonlighting terpene synthase active site". The Journal of ...
N-acetylneuraminate synthase NINJ1: ninjurin-1 NOL6: nucleolar protein 6 NUDT2: nudix hydrolase 2 OLFM1: olfactomedin 1 PHF2: ... argininosuccinate synthetase BNC2: zinc finger protein basonuclin-2 C9orf64: chromosome 9 open reading frame 64 C9orf78: ...
11-diene synthase EC 4.2.3.25: S-linalool synthase EC 4.2.3.26: R-linalool synthase EC 4.2.3.27: isoprene synthase EC 4.2.3.28 ... argininosuccinate lyase EC 4.3.2.2: adenylosuccinate lyase EC 4.3.2.3: ureidoglycolate lyase EC 4.3.2.4: purine imidazole-ring ... d-cadinene synthase EC 4.2.3.14: pinene synthase EC 4.2.3.15: myrcene synthase EC 4.2.3.16: (4S)-limonene synthase EC 4.2.3.17 ... chorismate synthase EC 4.2.3.6: trichodiene synthase EC 4.2.3.7: pentalenene synthase EC 4.2.3.8: casbene synthase EC 4.2.3.9: ...
This reaction is ATP dependent and is catalyzed by argininosuccinate synthetase. 3) Argininosuccinate undergoes cleavage by ... Synthesis of NAcGlu by N-acetylglutamate synthase (NAGS) is stimulated by both Arg, allosteric stimulator of NAGS, and Glu, a ... The reactions of the urea cycle 1 L-ornithine 2 carbamoyl phosphate 3 L-citrulline 4 argininosuccinate 5 fumarate 6 L-arginine ... N-Acetylglutamate synthase deficiency Carbamoyl phosphate synthetase deficiency Ornithine transcarbamoylase deficiency ...
... and N-Acetylglutamate synthase deficiency. Other diseases that may appear similar to CTLN1 include the organic acidemias and ... is a rare disease caused by a deficiency in argininosuccinate synthetase, an enzyme involved in excreting excess nitrogen from ...
Nagamani SC, Erez A, Lee B (May 2012). "Argininosuccinate lyase deficiency". Genetics in Medicine. 14 (5): 501-7. doi:10.1038/ ... encoding enzyme Alpha-aminoadipic semialdehyde synthase, mitochondrial ARHGEF35: encoding protein Rho guanine nucleotide ...
Argininosuccinate synthaseUniRule annotation. ,p>Manual validated information which has been generated by the UniProtKB ... Belongs to the argininosuccinate synthase family. Type 1 subfamily.UniRule annotation. ,p>Manual validated information which ... sp,Q1H0L1,ASSY_METFK Argininosuccinate synthase OS=Methylobacillus flagellatus (strain KT / ATCC 51484 / DSM 6875) GN=argG PE=3 ... Argininosuccinate lyase (argH). This subpathway is part of the pathway L-arginine biosynthesis, which is itself part of Amino- ...
Argininosuccinate synthase 1 is an intrinsic Akt repressor transactivated by p53. By Takafumi Miyamoto, Paulisally Hau Yi Lo, ... Argininosuccinate synthase 1 is an intrinsic Akt repressor transactivated by p53. By Takafumi Miyamoto, Paulisally Hau Yi Lo, ... Argininosuccinate synthase 1 is an intrinsic Akt repressor transactivated by p53 Message Subject. (Your Name) has forwarded a ... We show that argininosuccinate synthase 1 (ASS1), a citrulline-aspartate ligase in de novo arginine synthesis pathway, was ...
ASS1 deficiency -- Argininosuccinate synthase 1. *Citrin deficiency -- Citrin. *CPSI deficiency -- Carbamoyl phosphate ...
Savaraj, N, Wu, C, Li, YY, Wangpaichitr, M, You, M, Bomalaski, J, He, W, Kuo, MT & Feun, LG 2015, Targeting argininosuccinate ... Targeting argininosuccinate synthetase negative melanomas using combination of arginine degrading enzyme and cisplatin. In: ... Loss of argininosuccinate synthetase (ASS) expression in melanoma makes these tumor cells vulnerable to arginine deprivation. ... Targeting argininosuccinate synthetase negative melanomas using combination of arginine degrading enzyme and cisplatin. / ...
... and a nitric oxide synthase (NOS)-independent NO donor restored NO-dependent vascular reactivity in humans with ASL deficiency ... Requirement of argininosuccinate lyase for systemic nitric oxide production. In: Nature Medicine. 2011 ; Vol. 17, No. 12. pp. ... Requirement of argininosuccinate lyase for systemic nitric oxide production. Nature Medicine. 2011 Dec 1;17(12):1619-1626. ... Requirement of argininosuccinate lyase for systemic nitric oxide production. Ayelet Erez, Sandesh C.S. Nagamani, Oleg A. ...
... in part via maintenance of cyclin A2 protein expression and arginine production for channeling to nitric oxide synthase. In ... Hung, Y. H., Huang, H. L., Chen, W. C., Yen, M. C., Cho, C. Y., Weng, T. Y., ... Lai, M. D. (2017). Argininosuccinate lyase ... Argininosuccinate lyase interacts with cyclin A2 in cytoplasm and modulates growth of liver tumor cells. In: Oncology Reports. ... Hung, YH, Huang, HL, Chen, WC, Yen, MC, Cho, CY, Weng, TY, Wang, CY, Chen, YL, Chen, LT & Lai, MD 2017, Argininosuccinate ...
  • Administration of nitrite, which can be converted into NO in vivo, rescued the manifestations of NO deficiency in hypomorphic Asl mice, and a nitric oxide synthase (NOS)-independent NO donor restored NO-dependent vascular reactivity in humans with ASL deficiency. (elsevier.com)
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