Anti-liver Arginase/ARG1 Antibody Picoband® Fluoro647 Conjugated

ARG1 (arginase, live) is a cytosolic enzyme and expressed predominantly in the liver as a component of the urea cycle. The isoform encoded by ARG1, referred to as the liver, or A-I, isoform, contributes 98% of the arginase activity in liver but is also present in red cells. Using a rat liver ARG1 cDNA clone to probe a human liver cDNA library, Haraguchi et al. (1987) isolated and characterized a cDNA corresponding to the ARG1 gene. The ARG1 gene is mapped on 6q23.2 and the arginase gene contains 8 exons. By immunologic studies, 90% of the arginase in red blood cell and liver was precipitated by the antibody, whereas only 50% of the arginase in kidney, brain, and the gastrointestinal tract reacted with it. 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.

Within the immune system initially reported to be selectively expressed in granulocytes (polymorphonuclear leukocytes [PMNs]) . Also detected in macrophages mycobacterial granulomas. Expressed in group2 innate lymphoid cells (ILC2s) during lung disease.

Apoptosis, Cancer, Cell Biology, Cell Cycle, Cell Cycle Inhibitors, Cell Death, Epigenetics and Nuclear Signaling, Invasion/Microenvironment, Nucleus, Transcription

Key element of the urea cycle converting L-arginine to urea and L-ornithine, which is further metabolized into metabolites proline and polyamides that drive collagen synthesis and bioenergetic pathways critical for cell proliferation, respectively; the urea cycle takes place primarily in the liver and, to a lesser extent, in the kidneys. Functions in L-arginine homeostasis in nonhepatic tissues characterized by the competition between nitric oxide synthase (NOS) and arginase for the available intracellular substrate arginine. Arginine metabolism is a critical regulator of innate and adaptive immune responses. Involved in an antimicrobial effector pathway in polymorphonuclear granulocytes (PMN) . Upon PMN cell death is liberated from the phagolysosome and depletes arginine in the microenvironment leading to suppressed T cell and natural killer (NK) cell proliferation and cytokine secretion. In group 2 innate lymphoid cells (ILC2s) promotes acute type 2 inflammation in the lung and is involved in optimal ILC2 proliferation but not survival. In humans, the immunological role in the monocytic/macrophage/dendritic cell (DC) lineage is unsure.

1. Cardoso, M. L., Martins, E., Vasconcelos, R., Vilarinho, L., Rocha, J. Identification of a novel R21X mutation in the liver-type arginase gene (ARG1) in four Portuguese patients with argininemia. Hum. Mutat. 14: 355-356, 1999. 2. Grody, W. W., Dodson, A., Klein, D., Kern, R. M., Bassand, P., Cederbaum, S. D. Molecular genetic study of human arginase deficiency. (Abstract) Am. J. Hum. Genet. 45 (suppl.) : A191 only, 1989. 3. Haraguchi, Y., Takiguchi, M., Amaya, Y., Kawamoto, S., Matsuda, I., Mori, M. Molecular cloning and nucleotide sequence of cDNA for human liver arginase. Proc. Nat. Acad. Sci. 84: 412-415, 1987.