AKT2 Protein, Human, Recombinant (His & GST)

AKT (AK mouse plus Transforming or Thymoma) is a frequent oncogene expressed in most tissues which includes three isoforms AKT1, AKT2, and AKT3. Hyperactivation of AKT signaling is a central key in many human cancer progressions, through modulating angiogenesis, tumor growth, and cell migration, invasion, metastasis, and chemoresistance. Among all three isoforms, AKT2 is most related to cancer cell invasion, metastasis, and survival. Amplification and overexpression of AKT2 have been shown in many cancers. Accumulating evidence shows the potential role of different miRNA involvements in cancer progression by activating or suppressing AKT2 expression. The AKT2/NAB1/SPK1 pathway is a novel regulating factor of macrophage migration and cardiac remodeling after myocardial infarction. The novel mechanism of the AKT2-PKM2-STAT3/NF-kappaB axis in the regulation of ovarian cancer progression, that both AKT2 and PKM2 may be potential targets for the treatment of ovarian cancer. AKT1 and AKT2, the AKT isoforms that are highly expressed in skeletal muscle, have distinct and overlapping functions, with AKT2 more important for insulin-stimulated glucose metabolism. In adipocytes, AKT2 versus AKT1 has greater susceptibility for insulin-mediated redistribution from cytosolic to membrane localization, and insulin also causes subcellular redistribution of AKT Substrate of 160 kDa (AS160), an AKT2 substrate and crucial mediator of insulin-stimulated glucose transport.

Pack Size	Availability	Price/USD	Quantity
50 μg	5 days	$ 498.00

Description

Species	Human
Expression System	Baculovirus-Insect Cells
Tag	His,GST
Accession Number	P31751-1
Synonyms	RAC-β, RAC-BETA, HIHGHH, PKBBETA, PKBβ, PRKBB, PKBB, v-akt murine thymoma viral oncogene homolog 2
Construction	A DNA sequence encoding the human AKT2 (NP_001617.1) (Met1-Glu481) was expressed with a C-terminal polyhistidine-tagged GST tag at the N-terminus (his-GST).
Protein Purity	> 90 % as determined by SDS-PAGE.
Molecular Weight	Approxiamtely 83.6 kDa

Endotoxin	< 1.0 EU per μg protein as determined by the LAL method.
Formulation	Supplied as sterile 20 mM Tris, 500 mM NaCl, 10 % glycerol,pH 7.4. Please contact us for any concerns or special requirements. Please refer to the specific buffer information in the hard copy of CoA.
Reconstitution	A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.
Stability & Storage	Samples are stable for up to twelve months from date of receipt at -20℃ to -80℃. Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
Shipping	Kinases are highly recommended to be shipped at frozen temperature with blue ice or dry ice. Shipment made at ambient temperature may seriously affect the activity of the ordered products.
Research Background	AKT (AK mouse plus Transforming or Thymoma) is a frequent oncogene expressed in most tissues which includes three isoforms AKT1, AKT2, and AKT3. Hyperactivation of AKT signaling is a central key in many human cancer progressions, through modulating angiogenesis, tumor growth, and cell migration, invasion, metastasis, and chemoresistance. Among all three isoforms, AKT2 is most related to cancer cell invasion, metastasis, and survival. Amplification and overexpression of AKT2 have been shown in many cancers. Accumulating evidence shows the potential role of different miRNA involvements in cancer progression by activating or suppressing AKT2 expression. The AKT2/NAB1/SPK1 pathway is a novel regulating factor of macrophage migration and cardiac remodeling after myocardial infarction. The novel mechanism of the AKT2-PKM2-STAT3/NF-kappaB axis in the regulation of ovarian cancer progression, that both AKT2 and PKM2 may be potential targets for the treatment of ovarian cancer. AKT1 and AKT2, the AKT isoforms that are highly expressed in skeletal muscle, have distinct and overlapping functions, with AKT2 more important for insulin-stimulated glucose metabolism. In adipocytes, AKT2 versus AKT1 has greater susceptibility for insulin-mediated redistribution from cytosolic to membrane localization, and insulin also causes subcellular redistribution of AKT Substrate of 160 kDa (AS160), an AKT2 substrate and crucial mediator of insulin-stimulated glucose transport.

Calculator

Reconstitution Calculator

Recombinant Proteins Dilute Calculator

Specific Activity Calculator

Volume (to add to vial)

Mass (in vial)

Desired Reconstitution Concentration

bottom

AKT2 Protein, Human, Recombinant (His & GST)

Calculator

Tech Support

Keywords