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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 107 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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our data provide compelling evidence that human cytomegalovirus reduced the level of microRNA-613 which functions as an anti-onco-miRNA in glioblastoma, primarily by downregulating the expression of arginase-2
overexpression of AMPK (show PRKAA1 Antibodies) induced arginase II protein expression and viable cells numbers in human Pulmonary artery smooth muscle cell .
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.
diabetes-dependent increase in renal arginase-2 expression also requires arginase-1 (show ARG1 Antibodies) expression in macrophages
Arginase II expression is reduced in aortic endothelial cells and macrophages following PARP-1 (show PARP1 Antibodies) knockout.
This study shows for the first time that neurovascular injury after retinal ischemia/reperfusion is mediated through increased expression of Arginase 2.
Arg2 KO female (not male) mice are protected from age-associated glucose intolerance and reveal greater glucose induced-insulin (show INS Antibodies) release, larger islet size and beta-cell mass, and more proliferative and less apoptotic beta-cells compared with the age-matched WT controls. Arg2 is mainly expressed in acinar cells and is upregulated with aging, which enhances p38 MAPK (show MAPK14 Antibodies) activation and release of TNF-alpha (show TNF Antibodies).
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
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
Kidneys from circulation-restricted fetuses showed arginase-2 protein induction.
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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