Purified anti-AMPKα, anti-AMPKalpaha, 5C9-5B10-6D3,BioLegend,600551

This clone was also tested for ICC using 4% PFA fixed HeLa cells, Triton X-100 or MeOH permeabilization, and produced mainly nuclear staining.

Host

Mouse

Reactivity

Human, Mouse

Application

WB - Quality testedIHC-P, ICC - Verified

Platform ID

BAB441445000

BioLegend

Headquarters

8999 BioLegend Way San Diego, CA 92121 United States

Contact

Tel: 1-858-455-9588
Fax: +49 (4131) 7023913

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Product Specifications
Scientific Background

Specifications

NamePurified anti-AMPKα, anti-AMPKalpaha, 5C9-5B10-6D3
Cat. No.600551
HostMouse
RRIDAB_2910471 (BioLegend Cat. No. 600551)AB_2910471 (BioLegend Cat. No. 600552)
IsotypeMouse IgG1, κ
ReactivityHuman, Mouse
ApplicationWB - Quality testedIHC-P, ICC - Verified
ClonalityMonoclonal
Clone Number5C9-5B10-6D3
Concentration0.5 mg/mL
TargetAMPKalpha
PurityThe antibody was purified by affinity chromatography.
FormulationPhosphate-buffered solution, pH 7.2, containing 0.09% sodium azide
StorageThe antibody solution should be stored undiluted between 2°C and 8°C.
Regulatory StatusResearch Use Only

Scientific Background

AMP-activated protein kinase alpha (AMPKα) is a subunit of the αβγ heterotrimeric AMPK protein complex. It is a key regulator of metabolism and energy homeostasis in eukaryotes through induction of catabolic pathways and deactivation of anabolic pathways. As an inhibitor of mammalian target of rapamycin complex 1 (mTORC1) pathway, AMPKα is involved in the regulation of cellular growth, cell cycle progression, autophagy, and may play a dual role as both tumor suppressor and promotor. AMPKα is activated via phosphorylation of Threonine residue 172 (Thr172) within the activation loop of the α subunit and is promoted by the allosteric binding of AMP and/or ADP to AMPK’s γ subunit. This phosphorylation is mediated by the serine/threonine kinase liver kinase B1 (LKB1) in conjunction with accessory subunits STRAD and MO25, and also by calcium/calmodulin-dependent protein kinase 2 (CAMKK2 aka CAMKKβ). Activation is induced by increases in the cellular AMP:ATP and ADP:ATP ratios  following a decline in ATP levels as well as by cellular stress, DNA damage, glucose starvation, and fluxes in calcium and nutrient levels. Localization of AMPKα (Thr172) at the spindle poles suggests a novel role for AMPK in mitotic spindle orientation. AMPKα is a key therapeutic target in the treatment of metabolic disorders and an emerging potential treatment target for cancer.

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