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Arginase catalyzes the hydrolysis of arginine to ornithine and urea. Additionally we are shipping Arginase, Type II Proteins (22) and Arginase, Type II Kits (11) and many more products for this protein.
Showing 10 out of 103 products:
Cow (Bovine) Polyclonal ARG2 Primary Antibody for WB - ABIN610964
Gomeza, Joly, Kuhn, Knöpfel, Bockaert, Pin: The second intracellular loop of metabotropic glutamate receptor 1 cooperates with the other intracellular domains to control coupling to G-proteins. in The Journal of biological chemistry 1996
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Human Polyclonal ARG2 Primary Antibody for IHC, IHC (p) - ABIN4281383
Grönros, Jung, Lundberg, Cerrato, Ostenson, Pernow: Arginase inhibition restores in vivo coronary microvascular function in type 2 diabetic rats. in American journal of physiology. Heart and circulatory physiology 2011
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Cow (Bovine) Polyclonal ARG2 Primary Antibody for WB - ABIN2785775
Mumenthaler, Yu, Tze, Cederbaum, Pegg, Seligson, Grody: Expression of arginase II in prostate cancer. in International journal of oncology 2008
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Human Polyclonal ARG2 Primary Antibody for ELISA, WB - ABIN1451040
Vockley, Jenkinson, Shukla, Kern, Grody, Cederbaum: Cloning and characterization of the human type II arginase gene. in Genomics 1997
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Data show that transfection with Arginase II-small interfering RNA prevented hypoxia-induced cell proliferation.
circulating Arginase 2 concentrations increase in clinical erectile dysfunction (ED) and are associated with increased risk for ED
arginase 2 impairs endothelial autophagy independently of the L-arginine ureahydrolase activity through activation of RPS6KB1 (show RPS6KB1 Antibodies) and inhibition of PRKAA (show PRKAA2 Antibodies), which is implicated in atherogenesis
High arginase II expression correlates with poor survival for patients with neuroblastoma (show ARHGEF16 Antibodies). Neuroblastoma (show ARHGEF16 Antibodies) suppresses T-cell proliferation via arginase II expression and activity.
high fat diet enhanced arginase-II expression/activity and p38mapk (show MAPK14 Antibodies) activity, which was associated with eNOS (show NOS3 Antibodies)-uncoupling as revealed by decreased nitric oxide
Arg1 (show ARG1 Antibodies) expression is decreased, and Arg2 expression is increased in the newborn congenital obstructive nephropathy and in the mouse model.
Arg-II, p38 (show CRK Antibodies), and S6K1 (show RPS6KB1 Antibodies) form a positive circuit which regulates endothelial senescence and cardiovascular aging.
OxLDL triggers retrograde translocation of arginase2 in aortic endothelial cells via ROCK and mitochondrial processing peptidase.
These results demonstrate that S6K1 (show RPS6KB1 Antibodies) and arginase-II form a positive circuit mediating the detrimental effects of chronic L-arginine (show GATM Antibodies) supplementation on endothelial cells.
We speculate that cytomegalovirus may contribute to endothelial dysfunction via ARG II induction and reduced eNOS (show NOS3 Antibodies) production.
Arginase 2 deletion prevents hyperoxia-induced retinal vascular injury by preventing NOS (show NOS Antibodies) uncoupling resulting in decreased reactive oxygen species formation and increased nitric oxide bioavailability.
ERK2 (show MAPK1 Antibodies) and p38 (show CRK Antibodies) regulate arginase II induction in LPS (show TLR4 Antibodies)-stimulated macrophages, but iNOS (show NOS2 Antibodies) induction by LPS (show TLR4 Antibodies) is dependent on p38 (show CRK Antibodies) activation
Suggest that retinal arginase is involved in the hyperoxia-induced neuronal degeneration in the OIR model, through the regulation of polyamine metabolism.
miR155-induced repression of Arg2 expression is critical for the ability of dendritic cells to drive T cell activation by controlling arginine availability in the extracellular environment.
HDAC2 (show HDAC2 Antibodies) is a critical regulator of Arg2 expression and thereby endothelial nitric oxide and endothelial function.
results indicate that arginase induction depends in part on epidermal growth factor (EGF (show EGF Antibodies)) receptor (show EGFR Antibodies) activity, and that EGFR (show EGFR Antibodies) inhibitors may attenuate vascular remodeling without affecting nitric oxide release
In heart failure, increased iNOS (show NOS2 Antibodies) and arginase II expression results in unchanged NO species and protein S-nitrosylation; with substrate limitation, uncoupled iNOS (show NOS2 Antibodies) produces superoxide anions and contributes to contractile dysfunction.
Arginase catalyzes the hydrolysis of arginine to ornithine and urea. At least two isoforms of mammalian arginase exists (types I and II) which differ in their tissue distribution, subcellular localization, immunologic crossreactivity and physiologic function. The type II isoform encoded by this gene, is located in the mitochondria and expressed in extra-hepatic tissues, especially kidney. The physiologic role of this isoform is poorly understood\; it is thought to play a role in nitric oxide and polyamine metabolism. Transcript variants of the type II gene resulting from the use of alternative polyadenylation sites have been described.
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, arginase-2, mitochondrial-like
, L-arginine amidinohydrolase
, L-arginine ureahydrolase
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, arginase II
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, mitochondrial arginase 2
, mitochondrial arginase type II