Anti-PRKAG2 Antibody Picoband®

5'-AMP-activated protein kinase subunit gamma-2 is an enzyme that in humans is encoded by the PRKAG2 gene. AMP-activated protein kinase (AMPK) is a heterotrimeric protein composed of a catalytic alpha subunit, a noncatalytic beta subunit, and a noncatalytic regulatory gamma subunit. Various forms of each of these subunits exist, encoded by different genes. AMPK is an important energy-sensing enzyme that monitors cellular energy status and functions by inactivating key enzymes involved in regulating de novo biosynthesis of fatty acid and cholesterol. This gene is a member of the AMPK gamma subunit family. Mutations in this gene have been associated with Wolff-Parkinson-White syndrome, familial hypertrophic cardiomyopathy, and glycogen storage disease of the heart. Alternate transcriptional splice variants, encoding different isoforms, have been characterized.

Platelet basic protein; PBP; C-X-C motif chemokine 7; Leukocyte-derived growth factor; LDGF; Macrophage-derived growth factor; MDGF; Small-inducible cytokine B7; PPBP; CTAP3; CXCL7; SCYB7; TGB1; THBGB1; NAP-2

LA-PF4 stimulates DNA synthesis, mitosis, glycolysis, intracellular cAMP accumulation, prostaglandin E2 secretion, and synthesis of hyaluronic acid and sulfated glycosaminoglycan. It also stimulates the formation and secretion of plasminogen activator by human synovial cells. NAP-2 is a ligand for CXCR1 and CXCR2, and NAP-2, NAP-2 (73), NAP-2 (74), NAP-2 (1-66), and most potent NAP-2 (1-63) are chemoattractants and activators for neutrophils. TC-1 and TC-2 are antibacterial proteins, in vitro released from activated platelet alpha-granules. CTAP-III (1-81) is more potent than CTAP-III desensitize chemokine-induced neutrophil activation.

1. Akman, H. O., Sampayo, J. N., Ross, F. A., Scott, J. W., Wilson, G., Benson, L., Bruno, C., Shanske, S., Hardie, D. G., DiMauro, S. Fatal infantile cardiac glycogenosis with phosphorylase kinase deficiency and a mutation in the gamma-2-subunit of AMP-activated protein kinase. Pediat. Res. 62: 499-504, 2007. 2. Arad, M., Benson, D. W., Perez-Atayde, A. R., McKenna, W. J., Sparks, E. A., Kanter, R. J., McGarry, K., Seidman, J. G., Seidman, C. E. Constitutively active AMP kinase mutations cause glycogen storage disease mimicking hypertrophic cardiomyopathy. J. Clin. Invest. 109: 357-362, 2002. 3. Arad, M., Maron, B. J., Gorham, J. M., Johnson, W. H., Jr., Saul, J. P., Perez-Atayde, A. R., Spirito, P., Wright, G. B., Kanter, R. J., Seidman, C. E., Seidman, J. G. Glycogen storage diseases presenting as hypertrophic cardiomyopathy. New Eng. J. Med. 352: 362-372, 2005.

At -20°C for one year from date of receipt. After reconstitution, at 4°C for one month. It can also be aliquotted and stored frozen at -20°C for six months. Avoid repeated freezing and thawing.