|Datasheet||Specific References||Reviews||Related Products||Protocols|
|Vector Type||Mammalian Expression Vector|
|Expression Method||Constiutive, Stable / Transient|
|Selection In Mammalian Cells||Hygromycin|
A polyhistidine-tag is an amino acid motif in proteins that consists of at least five histidine (His) residues, often at the N- or C-terminus of the protein.
Polyhistidine-tags are often used for affinity purification of polyhistidine-tagged recombinant proteins expressed in Escherichia coli and other prokaryotic expression systems.
|Mouse AKT1 ORF mammalian expression plasmid, C-GFPSpark tag||MG50254-ACG|
|Mouse AKT1 ORF mammalian expression plasmid, C-OFPSpark / RFP tag||MG50254-ACR|
|Mouse AKT1 ORF mammalian expression plasmid, C-Flag tag||MG50254-CF|
|Mouse AKT1 ORF mammalian expression plasmid, C-His tag||MG50254-CH|
|Mouse AKT1 ORF mammalian expression plasmid, C-Myc tag||MG50254-CM|
|Mouse AKT1 ORF mammalian expression plasmid, C-HA tag||MG50254-CY|
|Mouse AKT1 Gene cDNA clone plasmid||MG50254-M|
|Mouse AKT1 ORF mammalian expression plasmid, Flag tag||MG50254-M-F|
|Mouse AKT1 ORF mammalian expression plasmid, N-Flag tag||MG50254-NF|
|Mouse AKT1 ORF mammalian expression plasmid, N-His tag||MG50254-NH|
|Mouse AKT1 ORF mammalian expression plasmid, N-Myc tag||MG50254-NM|
|Mouse AKT1 ORF mammalian expression plasmid, N-HA tag||MG50254-NY|
|Mouse AKT1 natural ORF mammalian expression plasmid||MG50254-UT|
|Learn more about expression Vectors|
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.