anti-Arginase, Type II (ARG2) Antibodies

Human Arginase, Type II (ARG2) interaction partners

1. Findings demonstrate that hypoxia-induced arginase II expression and cellular proliferation depend on autocrine epidermal growth factor production leading to epidermal growth factor receptor activation in human pulmonary microvascular endothelial cells.

2. KLF15 is a critical regulator of pulmonary endothelial homeostasis via repression of endothelial Arg2 expression. KLF15 abundance and nuclear compartmentalization are regulated by SUMOylation/deSUMOylation-a hypoxia-sensitive process that is controlled by SENP1.

3. xpression profiles revealed miR-1299 downregulation concomitant with arginase-2 (ARG2) upregulation in hyperpigmented skin of melasma patients.

4. ARG2 promotes tumorigenesis, and HCMV may contribute to GBM pathogenesis by upregulating ARG2.

5. fetal dendritic cells promote prenatal T-cell immune suppression through arginase-2; results reveal a previously unappreciated role of dendritic cells within the developing fetus and indicate that they mediate homeostatic immune-suppressive responses during gestation

6. Schizophrenia patients had increased arginase II protein expression in the frontal cortex compared to controls.

7. 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

8. overexpression of AMPK induced arginase II protein expression and viable cells numbers in human Pulmonary artery smooth muscle cell .

9. Data show that transfection with Arginase II-small interfering RNA prevented hypoxia-induced cell proliferation.

10. circulating Arginase 2 concentrations increase in clinical erectile dysfunction (ED) and are associated with increased risk for ED

11. arginase 2 impairs endothelial autophagy independently of the L-arginine ureahydrolase activity through activation of RPS6KB1 and inhibition of PRKAA, which is implicated in atherogenesis

12. High arginase II expression correlates with poor survival for patients with neuroblastoma. Neuroblastoma suppresses T-cell proliferation via arginase II expression and activity.

13. high fat diet enhanced arginase-II expression/activity and p38mapk activity, which was associated with eNOS-uncoupling as revealed by decreased nitric oxide

14. Arg1 expression is decreased, and Arg2 expression is increased in the newborn congenital obstructive nephropathy and in the mouse model.

15. Arg-II, p38, and S6K1 form a positive circuit which regulates endothelial senescence and cardiovascular aging.

16. OxLDL triggers retrograde translocation of arginase2 in aortic endothelial cells via ROCK and mitochondrial processing peptidase.

17. These results demonstrate that S6K1 and arginase-II form a positive circuit mediating the detrimental effects of chronic L-arginine supplementation on endothelial cells.

18. We speculate that cytomegalovirus may contribute to endothelial dysfunction via ARG II induction and reduced eNOS production.

19. study identified arginase II as a new target of miR-17-5p in human pulmonary artery smooth muscle cells (hPASMC), with miR-17-5p involved in the hypoxic induction of arginase II in hPASMC; also found evidence supporting a feedback loop between arginase II and miR-17-5p, such that arginase II regulates miR-17-5p expression in hPASMC

20. Data indicate that arginase II (Arg II) expressions were higher in breast tumor tissues compared to the matched normal.

Mouse (Murine) Arginase, Type II (ARG2) interaction partners

1. Arg2 is a critical effector of the hepatic glucose fasting response.

2. in vivo and in vitro experiments demonstrate that Arg-II negatively regulates AQP2 and the urine-concentrating capability in kidneys via a mechanism that is not associated with the modulation of the cAMP pathway.

3. 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

4. The possibility that the Gas6-Mer-PI3K/Akt-STAT1-LXR-Arg2 pathway plays an essential role for resolving inflammatory response in acute lung injury.

5. ARG2 which hydrolyzes arginine into ornithine and urea, is induced upon obesity, and silencing or loss of ARG2 markedly suppresses pancreatic ductal adenocarcinoma.

6. the finding of this study is that ARG2 contributes to the immune evasion of H. pylori by restricting M1 macrophage activation and polyamine metabolism.

7. diabetes-dependent increase in renal arginase-2 expression also requires arginase-1 expression in macrophages

8. Arginase II expression is reduced in aortic endothelial cells and macrophages following PARP-1 knockout.

9. This study shows for the first time that neurovascular injury after retinal ischemia/reperfusion is mediated through increased expression of Arginase 2.

10. Arg2 KO female (not male) mice are protected from age-associated glucose intolerance and reveal greater glucose induced-insulin 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 activation and release of TNF-alpha.

11. arginase 2 impairs endothelial autophagy independently of the L-arginine ureahydrolase activity through activation of RPS6KB1 and inhibition of PRKAA, which is implicated in atherogenesis

12. high fat diet enhanced arginase-II expression/activity and p38mapk activity, which was associated with eNOS-uncoupling as revealed by decreased nitric oxide

13. Arg1 expression is decreased, and Arg2 expression is increased in the newborn congenital obstructive nephropathy and in the mouse model.

14. Arg-II, p38, and S6K1 form a positive circuit which regulates endothelial senescence and cardiovascular aging.

15. Arginase 2 deletion prevents hyperoxia-induced retinal vascular injury by preventing NOS uncoupling resulting in decreased reactive oxygen species formation and increased nitric oxide bioavailability.

16. ERK2 and p38 regulate arginase II induction in LPS-stimulated macrophages, but iNOS induction by LPS is dependent on p38 activation

17. OxLDL triggers retrograde translocation of arginase2 in aortic endothelial cells via ROCK and mitochondrial processing peptidase.

18. Suggest that retinal arginase is involved in the hyperoxia-induced neuronal degeneration in the OIR model, through the regulation of polyamine metabolism.

19. 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.

20. HDAC2 is a critical regulator of Arg2 expression and thereby endothelial nitric oxide and endothelial function.

Cow (Bovine) Arginase, Type II (ARG2) interaction partners

1. 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.

2. 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

Rabbit Arginase, Type II (ARG2) interaction partners

1. Kidneys from circulation-restricted fetuses showed arginase-2 protein induction.

2. In heart failure, increased iNOS and arginase II expression results in unchanged NO species and protein S-nitrosylation; with substrate limitation, uncoupled iNOS produces superoxide anions and contributes to contractile dysfunction.