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 ...

Argininosuccinate synthetase (ASS), an integral enzyme to synthesize arginine is usually down regulated in many tumors including hepatocellular carcinoma (HCC). only occurs in SNU398 and SNU387, and not in HepG2 and Huh-1 (ASS(+)) cells, purchase EPZ-5676 and it is partly because of reduced anti-apoptotic protein X-linked inhibitor of apoptosis proteins (XIAP), myeloid leukemia cell differentiation proteins (Mcl-1) and B-cell lymphoma-2 (Bcl-2). Significantly, insufficient ASS also affects important enzymes in pyrimidine synthesis (carbamoyl-phosphate synthetase2, aspartate transcarbamylase and dihydrooratase (CAD) and thymidylate synthase (TS)) and malate dehydrogenase-1 (MDH-1) in TCA routine. ADI-PEG20 treatment reduced these enzymes and produced them more purchase EPZ-5676 susceptible to 5-FU. Transfection of ASS restored these enzymes and abolished the awareness to mixture and ADI-PEG20 treatment. General, our data claim that ASS affects multiple enzymes involved with 5-FU sensitivity. ...

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

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TY - JOUR. T1 - Arginine starvation kills tumor cells through aspartate exhaustion and mitochondrial dysfunction. AU - Cheng, Chun Ting. AU - Qi, Yue. AU - Wang, Yi Chang. AU - Chi, Kevin K.. AU - Chung, Yiyin. AU - Ouyang, Ching. AU - Chen, Yun Ru. AU - Oh, Myung Eun. AU - Sheng, Xiangpeng. AU - Tang, Yulong. AU - Liu, Yun Ru. AU - Lin, H. Helen. AU - Kuo, Ching Ying. AU - Schones, Dustin. AU - Vidal, Christina M.. AU - Chu, Jenny C.Y.. AU - Wang, Hung Jung. AU - Chen, Yu Han. AU - Miller, Kyle M.. AU - Chu, Peiguo. AU - Yen, Yun. AU - Jiang, Lei. AU - Kung, Hsing-Jien. AU - Ann, David K.. PY - 2018/12/1. Y1 - 2018/12/1. N2 - Defective arginine synthesis, due to the silencing of argininosuccinate synthase 1 (ASS1), is a common metabolic vulnerability in cancer, known as arginine auxotrophy. Understanding how arginine depletion kills arginine-auxotrophic cancer cells will facilitate the development of anti-cancer therapeutic strategies. Here we show that depletion of extracellular arginine in ...

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 ASS1P14 gene (Pseudogene), Argininosuccinate Synthetase 1 Pseudogene 14, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium

Complete information for ASS1P12 gene (Pseudogene), Argininosuccinate Synthetase 1 Pseudogene 12, 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

Immune cells in the brain may be abnormally consuming the nutrient arginine, and this may be a cause of Alzheimers disease: new study.

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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Homework: The Punnet squares show the enzymatic [colour] and growth [+ or -] phenotypes of two crosses between two dihybrid auxotrophic mutants Assume dominance of the wild-type allele at each locus (x+). What general principles can be drawn from the patterns, as related to tri-hybrid crosses, and other forms of gene interactions in metabolic pathways ...

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