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ARG1 might play a pivotal role as an oncogene in the progression of hepatocellular carcinoma through promoting the EMT process.
mutations in the epigenetic regulators TET2 and DNMT3A corresponded to high ARG1 expression and activity. These findings suggest ARG1 is a biomarker of immune dysregulation in early MDS and CMML
study of the significance of heat activation and the role of metal ions in human arginase
TGF-beta1 and arginase-1 may play important roles in determining long-term graft survival.
These results showed that arginase controlled sFlt-1 elevation to some extent.
ARG1 gene polymorphisms and their association in individuals with essential hypertension in Pakistan has been presented.
A subset of well-differentiated hepatocellular carcinomas are arginase-1 negative.
The data in this study suggest that arginase I inhibition potentially represents a novel therapeutic target for the prevention and/or treatment of bronchopulmonary dysplasia-associated pulmonary hypertension.
this study shows that infiltrating macrophages expressing Arg1 are present in active allergic contact dermatitis lesions
High arginase expression is associated with glioblastoma.
Report the value of Arg-1 in distinguishing HepPar-1-positive prostatic carcinoma from hepatocellular carcinoma at metastatic sites or cases of liver metastasis from prostate carcinoma.
AEG-1 is positively activated in the tumorigenesis and deterioration of NSCLC.
Arginase-1 expression is common (62.5%) in hepatoid adenocarcinoma and hence it is not useful in distinguishing hepatocellular carcinoma from hepatoid adenocarcinoma.
Arginase 1 was highly expressed by tumor-associated Gr1+ microglia and macrophages.
The authors report here that Candida albicans blocks nitric oxide production in human-monocyte-derived macrophages by induction of host arginase activity.
Evidence for a negative association of arginase I with job strain and positive association with job control and social support in females.
Two argininemia patients were initially diagnosed by tandem mass spectrometry in newborn screening. Mutation analysis of the ARG1 gene was performed by direct sequencing.Two missense mutations, p.D100N and p.R71T, in Patient-1 were predicted to lower the stability of arginase Iota by analysis of 3D crystal structure, while two nonsense mutations, p.G12X and p.E42X, in Patient-2 were predicted to lead to truncated protein.
The results of this study suggested a novel relationship exists between ARG1, neutrophil-lymphocyte ratio , and stroke severity which may help guide future mechanistic studies of post-stroke immune suppression.
This study provides a molecular mechanism of the pathogenesis of systemic lupus erythematosus by demonstrating an Arg-1-dependent effect of myeloid-derived suppressor cells in the development of TH17 cell-associated autoimmunity.
ARG1 rs2781659 AA and rs2781667 TT genotypes were associated with lower IIEF scores (increased severity) in clinical erectile dysfunction (ED), whereas ARG1 GTCC haplotype is associated with higher IIEF scores in clinical ED, thus suggesting a genetic contribution of ARG1 variations to ED
Activity of arginase before and at the time of parturition might be a potential marker for occurrence of metritis, especially in cows that develop retained fetal membranes.
Arginase has a role in preventing angiogenesis in endothelial cells exposed to hypoxia
Ang II increases endothelial arginase activity/expression through a p38 MAPK/ATF-2 pathway leading to reduced endothelial NO production
results indicate that arginase induction depends in part on epidermal growth factor (EGF) receptor activity, and that EGFR inhibitors may attenuate vascular remodeling without affecting nitric oxide release
high glucose (HG)-treated bovine coronary endothelial cells (BCECs) showed increased arginase activity and diminished NO production
this study shows that Arginase-1 is neither constitutively expressed in nor required for myeloid-derived suppressor cell-mediated inhibition of T-cell proliferation
Arg II was identified as a factor promoting EAE likely via an Arg I-independent mechanism; Arg II may promote EAE by enhancing dendritic cells production of Th17-differentiating cytokines; specific inhibition of Arg II could be a potential therapy for multiple sclerosis
Our studies provide proof-of-concept for gene-editing at the Arg1 locus and highlight the challenges that lie ahead to restore sufficient liver-based urea cycle function in patients with urea cycle disorders.
This study shows for the first time that diabetes-induced increases in arginase 1 expression promotes endothelial cell senescence through the activation of p16INK4A and p53 signaling pathways.
findings identified a novel function of the VEGFR1 signaling in avoiding over-expression of Arginase 1 potentially to maintain the proper innate immune response.
Up-regulation of arginase 1 expression/activity in vascular endothelial cells has an integral role in diet-induced cardiovascular dysfunction and metabolic syndrome.
Complete ablation of Arg1 in the lung affects mRNA abundance of arginine-transporting and -metabolizing genes, and pro-inflammatory genes, but not methacholine responsiveness or accumulation of inflammatory cells.
Data suggest that Arg1 mRNA and protein expression in liver are significantly higher in obese mice (fed high-fat diet) than in control mice; hepatic Arg1 levels positively correlate with plasma Arg1 levels and negatively correlate with L-arginine bioavailability in plasma. Increased expression of hepatic Arg1 and reduced plasma L-arginine and NO(2)(-) may lead to vascular endothelial dysfunction even in early obesity.
Data suggest that chronic hypoxia enhances HIF-2alpha stability, which causes increased arginase expression and dysregulates normal vascular NO homeostasis.
high-fat/high-sucrose diet-induced visceral adipose tissue inflammation is mediated by endothelial cells-A1 expression/activity.
Deletion of Arg1 in hematopoietic cells adversely affects blood leukocyte counts and increases foam cell formation. However, no effects on atherosclerosis could be demonstrated, indicating that hematopoietic Arg1 function is not a decisive factor in atherosclerotic plaque formation.
diabetes-dependent increase in renal arginase-2 expression also requires arginase-1 expression in macrophages
this study shows that mice lacking Arg1 in macrophages develop increased allergic contact hypersensitivity
this study shows that Ron is expressed in a subpopulation of macrophages during chronic inflammation induced by obesity that exhibit a repair phenotype as determined by the expression of arginase 1
This study uncovers synergistic activation of Arg1 by retinoic acid and IL-4 in M2 macrophages.
this study shows that group 2 innate lymphoid cells selectively express arginase 1 and that this is critical for their bioenergetics, proliferation and function
this study shows that c-Jun regulates the activation state of macrophages and promotes arthritis via differentially regulating cyclooxygenase-2 and arginase-1 levels
deletion or TNF-mediated restriction of Arg1 unleashes the production of nitric oxide by NOS2, which is critical for pathogen control.
Data indicate that transfected mouse arginase-1 (Arg-I) promotes endothelial senescence and inflammatory responses through eNOS-uncoupling in human umbilical vein endothelial cells (HUVEC cells).
The immunosuppressive effect of a purified substance (ISF) in the culture medium of neonatal pig liver fragments was due to arginase activity that decreased arginine concentration in culture medium, not to another function of ISF.
Results show that ischemia markedly potentiated the expression of arginase-1, and also induced the SOD2 in the wound tissue.
Arginase catalyzes the hydrolysis of arginine to ornithine and urea. At least two isoforms of mammalian arginase exist (types I and II) which differ in their tissue distribution, subcellular localization, immunologic crossreactivity and physiologic function. The type I isoform encoded by this gene, is a cytosolic enzyme and expressed predominantly in the liver as a component of the urea cycle. Inherited deficiency of this enzyme results in argininemia, an autosomal recessive disorder characterized by hyperammonemia. Two transcript variants encoding different isoforms have been found for this gene.
, liver-type arginase
, type I arginase
, arginase 1
, arginase I
, arginase 1, liver
, AI type I arginase
, arginase, hepatic