Prkag1 (NM_016781) Mouse Recombinant Protein

Specifications

Product Data
Species	Mouse
Expression Host	HEK293T
Expression cDNA Clone or AA Sequence	Protein Sequence (showhide) >MR204858 representing NM_016781 Red=Cloning site Green=Tags(s) MESVAAESSPALENEHFQETPESNNSVYTSFMKSHRCYDLIPTSSKLVVFDTSLQVKKAFFALVTNGVRA APLWDSKKQSFVGMLTITDFINILHRYYKSALVQIYELEEHKIETWREVYLQDSFKPLVCISPNASLFDA VSSLIRNKIHRLPVIDPESGNTLYILTHKRILKFLKLFITEFPKPEFMSKSLQELQIGTYANIAMVRTTT PVYVALGIFVQHRVSALPVVDEKGRVVDIYSKFDVINLAAEKTYNNLDVSVTKALQHRSHYFEGVLKCYL HETLETIINRLVEAEVHRLVVVDEHDVVKGIVSLSDILQALVLTGGEKKP TRTRPLEQKLISEEDLAANDILDYKDDDDKV
Tag	C-MYC/DDK
Predicted MW	38 kDa
Concentration	>0.05 µg/µL as determined by microplate BCA method
Purity	> 80% as determined by SDS-PAGE and Coomassie blue staining
Buffer	25 mM Tris-HCl, 100 mM glycine, pH 7.3, 10% glycerol
Note	For testing in cell culture applications, please filter before use. Note that you may experience some loss of protein during the filtration process.
Storage	Store at -80°C after receiving vials.
Stability	Stable for 12 months from the date of receipt of the product under proper storage and handling conditions. Avoid repeated freeze-thaw cycles.
Reference Data
RefSeq	NP_058061
Locus ID	19082
UniProt ID	O54950
Refseq Size	1680
Cytogenetics	15 54.73 cM
Refseq ORF	990
Synonyms	AA571379; BB036179; Prkaac
Summary	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 (By similarity).[UniProtKB/Swiss-Prot Function]

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