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Cow (Bovine) Polyclonal ASS1 Primary Antibody for IHC (p), IHC - ABIN314255
Hao, Xie, Gross: Argininosuccinate synthetase is reversibly inactivated by S-nitrosylation in vitro and in vivo. in The Journal of biological chemistry 2004
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Cow (Bovine) Polyclonal ASS1 Primary Antibody for ELISA, IF - ABIN190834
Corbin, Pendleton, Solomonson, Eichler: Phosphorylation of argininosuccinate synthase by protein kinase A. in Biochemical and biophysical research communications 2008
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Cow (Bovine) Polyclonal ASS1 Primary Antibody for IHC, WB - ABIN2776769
Hu, Lausted, Yoo, Yan, Brightman, Chen, Wang, Bu, Hood: Quantitative liver-specific protein fingerprint in blood: a signature for hepatotoxicity. in Theranostics 2014
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Human Polyclonal ASS1 Primary Antibody for ICC, IF - ABIN4281472
Slebos, Jehmlich, Brown, Yin, Chung, Yarbrough, Liebler: Proteomic analysis of oropharyngeal carcinomas reveals novel HPV-associated biological pathways. in International journal of cancer 2012
Human Monoclonal ASS1 Primary Antibody for ICC, FACS - ABIN969502
Laróvere, Angaroni, Antonozzi, Bezard, Shimohama, de Kremer: Citrullinemia type I, classical variant. Identification of ASS-p~G390R (c.1168G>A) mutation in families of a limited geographic area of Argentina: a possible population cluster. in Clinical biochemistry 2009
Overexpression of ASS1 inhibits hepatocellular carcinoma progression by inactivating the pSTAT3Ser727 pathway, which subsequently decreases the expression of ID1.
Arginine starvation induces p300 dissociation, allowing histone HDAC2 and cofactor Sin3A to deacetylate these histones at the ASS1 promoter, thereby facilitating HIF-1alpha-proteasomal complex, driven by PHD2, to degrade HIF-1alpha in situ.
associated with sonic hedgehog activation as part of a periportal program expressed in hepatocellular adenomas
results propose that ASS1 might contribute to gastric cancer (GC) metastasis and support its utility as a prognostic predictor of GC.
In ASS1-knockout cells, DEPTOR, an inhibitor of mTORC1 signal, was downregulated and mTORC1 signaling was more activated in response to arginine.
findings uncover a new function of p53 in the regulation of Akt signaling and reveal how p53, ASS1, and Akt are interrelated to each other.
The remaining five patients were diagnosed with neonatal intrahepatic cholestasis due to citrin deficiency, and have respectively carried mutations of the SLC25A13 gene including [c.851-854delGTAT+c.851-854delGTAT], [c.851-854delGTAT+IVS6+5G>A], [c.851-854delGTAT+IVS16ins3kb], [c.851-854delGTAT+IVS6-11A>G] and [c.851-854delGTAT+c.1638-1660dup23]
Results indicate that the reduced ASS1 expression in Dox-resistant sarcomas may contribute to drug resistance in association with the expression of P-glycoprotein.
Cisplatin-induced synthetic lethality to arginine-starvation therapy by transcriptional suppression of ASS1 is regulated by DEC1, HIF-1alpha, and c-Myc transcription network and is independent of ASS1 promoter DNA methylation.
Low expression of ASS1 is associated with glioblastoma.
defined a new hepatocellular adenoma subgroup at a high risk of bleeding
ASS1 acetylation by CLOCK exhibits circadian oscillation in human cells and mouse liver, possibly caused by rhythmic interaction between CLOCK and ASS1, leading to the circadian regulation of ASS1 and ureagenesis.
update reports 137 mutations in the ASS1 gene (64 of which are novel), consisting of 89 missense mutations, 19 nonsense mutations, 17 mutations that affect splicing, and 12 deletions; the change p.Gly390Arg is by far the most common mutation and is widely spread throughout the world
Of 21 ASS potential kinetic mutations, 13 were totally inactive while 8 exhibited decreased affinity for aspartate and citrulline.
Low ASS1 expression was associated with higher recurrence , shorter disease-free survival and shorter overall survival in patients with pancreatic ductal adenocarcinoma.
The authors showed that ASS1 mutations linked to type I citrullinemia disrupt the ASS1-PRMT7 interaction, which might explain the molecular pathogenesis of the disease.
Identification of three novel CTLN1 mutations in fourteen patients with citrullinemia type 1 has been reported.
In this trial, arginine deprivation with ADI-PEG20 improved PFS in patients with ASS1-deficient mesothelioma. Targeting arginine is safe and warrants further clinical investigation in arginine-dependent cancers.
combining hypoxia and ADI-PEG20 synergistically inhibited ASS1.
ASS1 genomic variants (rs10901080 and rs10793902) can serve as pharmacogenomic biomarkers to predict hydroxyurea treatment efficacy in sickle cell disease/beta-thalassemia compound heterozygous patients.
In diabetic mice, ablation of Ass resulted in diminished endothelium-derived nitric oxide-mediated vascular relaxation responses.
cAMP-induced Ass1 expression is important in controlling the magnitude of decidualization through regulating L-Arg level.
may contribute to liver injury by enhancing nitrosative stress
We demonstrate that the transgenic mouse system reported here has the merit of sensitivity and direct visualization advantage, and is ideal for annotating temporal and spatial expression profiles and the regulation mode of the ASS gene.
Thus, extracellular arginine fuels rapid NO production in activated macrophages, and citrulline recycling via Ass1 and Asl is a fail-safe system that sustains optimum NO production.
Partial argininosuccinate synthase ablation protects only in acute ethanol-induced liver injury by decreasing nitrosative stress but not in a more chronic scenario where oxidative stress and impaired fatty acid beta-oxidation are key events.
Loss of Ass1 is associated with citrullinemia type I and other hyperammonemic syndromes.
Argininosuccinate synthetase has a role in preventing autotoxicity from nitric oxide overproduction
Transcriptome of porcine alveolar macrophages infected by porcine reproductive and respiratory syndrome virus and activated by interferon-gamma and lipopolysaccharide showed that ASS1 and CRTAM were the most upregulated and downregulated genes, respectively.
calcium-dependent phosphorylation of argininosuccinate synthase Ser-328 is mediated by PKCalpha
dose-dependent reduction of ASS as a result of siRNA treatment corresponded to diminished capacity to produce NO, despite saturating levels of arginine in the medium; reduced expression of ASS resulted in loss of viability due to apoptosis
the function of the extended 5'-UTRs of AS mRNA was investigated
In endothelial cells TNF-alpha coordinately downregulates nitric oxide synthase (eNOS) and argininosuccinate synthase expression, resulting in a severely impaired citrulline-NO cycle.
These results represent the first demonstration that vascular endothelial nitric oxide production can be regulated by dynamic argininosuccinate synthase phosphorylation.
The protein encoded by this gene catalyzes the penultimate step of the arginine biosynthetic pathway. There are approximately 10 to 14 copies of this gene including the pseudogenes scattered across the human genome, among which the one located on chromosome 9 appears to be the only functional gene for argininosuccinate synthetase. Mutations in the chromosome 9 copy of this gene cause citrullinemia. Two transcript variants encoding the same protein have been found for this gene.
, argininosuccinate synthetase 1
, citrulline--aspartate ligase
, citrulline-aspartate ligase
, arginosuccinate synthetase 1
, arginosuccinate synthetase
, argininosuccinate synthase 1
, argininosuccinate synthase-like