AMPK (A2/B1/G1), Unactive(P48-14H)

AMPK (A2/B1/G1), Unactive(P48-14H)

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Description :Recombinant full-length human AMPK (combination of A2/B1/G1 subunits) was expressed by baculovirus in Sf9 insect cells using a C-terminal His tag.

Species :Human

Tag :HIS tag

Expression System:Sf9 insect cells using baculovirus

Sequence :Full Length

Genbank Number :NM_006252

Genbank Number 2 :NM_006253

Genbank Number 3 :NM_002733

Specific Activity :Sample Kinase Activity Plot. For specific information on a given lot, see related technical data sheet.

Purity :Sample Purity Data. For specific information on a given lot, see related technical data sheet.

Storage, Stability and Shipping :Store product at –70oC. For optimal storage, aliquot target into smaller quantities after centrifugation and store at recommended temperature. For most favorable performance, avoid repeated handling and multiple freeze/thaw cycles.

Applications :Kinase Assay

Molecular Weight :~69 kDa (A2), ~38kDa (B1), and ~40kDa (G1)

Gene Aliases :Subunits A2: PRKAA2, AMPK, AMPK2, PRKAA Subunit B1: PRKAB1, AMPK, HAMPKb, MGC17785 Subunit G1: PRKAG1, AMPKG, MGC8666

Scientific Background :AMPK (A2/B1/G1) plays a key role in insulin signaling pathway and is a major therapeutic target for the treatment of diabetes (1). AMPK is viewed as a fuel sensor for glucose and lipid metabolism by modulating the activity of the autonomous nervous system in vivo. Short-term overexpression of a constitutively active form of AMPK in the liver leads to mild hypoglycemia and fatty liver due to increased fatty acid utilization (2).

References :
1. Viollet, B. et al: Physiological role of AMP-activated protein kinase (AMPK): insights from knockout mouse models. Biochem. Soc. Trans. 2003; 31; 216–219.

2. Foretz, M. et al: Short-term overexpression of a constitutively active form of AMP-activated protein kinase in the liver leads to mild hypoglycemia and fatty liver. Diabetes, 2005; 54 (5);1331-1339.

Product Sheets (By Lot #) :

T1026-3.pdf

Research Areas :Apoptosis/Autophagy, Cancer, Cellular Stress, Metabolic Disorder, Ser/Thr Kinases, Apoptosis/Autophagy, Cancer, Cellular Stress, Metabolic Disorder, Ser/Thr Kinases, Cancer, Metabolic Disorder, Apoptosis/Autophagy, Cellular Stress, Ser/Thr Kinases