|Other Accession||NP_059127.2, 53632|
|Calculated MW||54258 Da|
|Other Names||5'-AMP-activated protein kinase subunit gamma-3, AMPK gamma3, AMPK subunit gamma-3, PRKAG3, AMPKG3|
|Format||0.5 mg/ml in Tris saline, 0.02% sodium azide, pH7.3 with 0.5% bovine serum albumin|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||PRKAG3 Antibody (internal region) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||AMP/ATP-binding subunit of AMP-activated protein kinase (AMPK), an energy sensor protein kinase that plays a key role in regulating cellular energy metabolism. In response to reduction of intracellular ATP levels, AMPK activates energy-producing pathways and inhibits energy-consuming processes: inhibits protein, carbohydrate and lipid biosynthesis, as well as cell growth and proliferation. AMPK acts via direct phosphorylation of metabolic enzymes, and by longer-term effects via phosphorylation of transcription regulators. Also acts as a regulator of cellular polarity by remodeling the actin cytoskeleton; probably by indirectly activating myosin. Gamma non-catalytic subunit mediates binding to AMP, ADP and ATP, leading to activate or inhibit AMPK: AMP-binding results in allosteric activation of alpha catalytic subunit (PRKAA1 or PRKAA2) both by inducing phosphorylation and preventing dephosphorylation of catalytic subunits. ADP also stimulates phosphorylation, without stimulating already phosphorylated catalytic subunit. ATP promotes dephosphorylation of catalytic subunit, rendering the AMPK enzyme inactive.|
|Tissue Location||Skeletal muscle, with weak expression in heart and pancreas|
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Provided below are standard protocols that you may find useful for product applications.
Gain-of-function R225W mutation in human AMPKgamma3 causing increased glycogen and decreased triglyceride in skeletal muscle. Costford SR, Kavaslar N, Ahituv N, Chaudhry SN, Schackwitz WS, Dent R, Pennacchio LA, McPherson R, Harper ME. PLoS ONE. 2007 Sep 19;2(9):e903. PMID: 17878938
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