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Mouse AKT1 Recombinant Protein (His Tag) (RPES6614)

SKU:
RPES6614
Product Type:
Recombinant Protein
Species:
Mouse
€189
Frequently bought together:

Description

Product Name:Mouse AKT1 Recombinant Protein (His Tag)
Product Code:RPES6614
Size:20µg
Species:Mouse
Expression Host:E.coli
Synonyms:RAC-alpha serine/threonine-protein kinase, AKT1 kinase, Protein kinase B, PKB, Protein kinase B alpha, PKB alpha, Proto-oncogene c-Akt, RAC-PK-alpha, Thymoma viral proto-oncogene, Akt, Rac
Application:Immunogen
Mol Mass:20.94 kDa
AP Mol Mass:28 kDa
Tag:N-His
Purity:> 80 % as determined by reducing SDS-PAGE.
Endotoxin Level:Please contact us for more information.
Bio Activity:Testing in progress
Sequence:Met1-Lys179
Accession:P31750-1
Storage:Generally, lyophilized proteins are stable for up to 12 months when stored at -20 to -80°C. Reconstituted protein solution can be stored at 4-8°C for 2-7 days. Aliquots of reconstituted samples are stable at < -20°C for 3 months.
Shipping:This product is provided as lyophilized powder which is shipped with ice packs.
Formulation:Lyophilized from sterile PBS, pH 7.4. Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization. Please refer to the specific buffer information in the printed manual.
Reconstitution:Please refer to the printed manual for detailed information.
Background:v-akt murine thymoma viral oncogene homolog 1 (AKT1), or protein kinase B-alpha (PKB-ALPHA) is a serine-threonine protein kinase, belonging to the Protein Kinase Superfamily. AKT1 is a major mediator of the responses to insulin, insulin-like growth factor 1 (IGF1), and glucose. AKT1 also plays a key role in the regulation of both muscle cell hypertrophy and atrophy. AKT1 activity is required for physiologic cardiac growth in response to IGF1 stimulation or exercise training. In contrast, AKT1 activity was found to antagonize pathologic cardiac growth that occurs in response to endothelin 1 stimulation or pressure overload. AKT1 selectively promotes physiological cardiac growth while AKT2 selectively promotes insulin-stimulated cardiac glucose metabolism. AKT1 deletion prevented tumor initiation as well as tumor progression, coincident with decreased Akt signaling in tumor tissues. AKT1 is the primary Akt isoform activated by mutant K-ras in lung tumors, and that AKT3 may oppose AKT1 in lung tumorigenesis and lung tumor progression. A number of separate studies have implicated AKT1 as an inhibitor of breast epithelial cell motility and invasion. AKT1 may have a dual role in tumorigenesis, acting not only pro-oncogenically by suppressing apoptosis but also anti-oncogenically by suppressing invasion and metastasis.

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