Cat.No. : CSC-SC000464 Host Cell: HEK293 (CHO and other cell types are also available)
| Cat. No. | CSC-SC000464 |
| Description | Using Creative Biogene's proprietary lentiviral vectors, we subclone the target gene into lentivector, generate the lentivirus particles, sequentially infect the cell line HEK293 (other cell types are also available according to your requirements), and select the clones constantly expressing target gene at high level. |
| Gene | AKT1 |
| Gene Species | Homo sapiens (Human) |
| Host Cell | HEK293 (CHO and other cell types are also available) |
| Stability | Validated for at least 10 passages |
| Application | 1. Gene expression studies 2. Signaling pathway research 3. Drug screening and toxicology 4. Disease research |
| Quality Control | Negative for bacteria, yeast, fungi and mycoplasma. |
| Size Form | 2 × 10^6 cells / vial |
| Shipping | Dry Ice |
| Storage | Liquid nitrogen |
| Revival | Rapidly thaw cells in a 37°C water bath. Transfer contents into a tube containing pre-warmed media. Centrifuge cells and seed into a 25 cm2 flask containing pre-warmed media. |
| Gene Name | AKT1 v-akt murine thymoma viral oncogene homolog 1 [ Homo sapiens ] |
| Gene Symbol | AKT1 |
| Synonyms | AKT; PKB; RAC; PRKBA; PKB-ALPHA; RAC-ALPHA |
| Gene Description | v-akt murine thymoma viral oncogene homolog 1 |
| Gene ID | 207 |
| UniProt ID | B0LPE5 |
| mRNA Refseq | NM_001014431.1 |
| Protein Refseq | NP_001014431.1 |
| Chromosome Location | 14q32.32 |
| Function | ATP binding; ATP binding; enzyme binding; identical protein binding; kinase activity; nitric-oxide synthase regulator activity; phosphatidylinositol-3,4,5-trisphosphate binding; phosphatidylinositol-3,4-bisphosphate binding; protein binding; protein kinase C binding; protein kinase activity; protein serine/threonine kinase activity; protein serine/threonine kinase activity; |
| Pathway | AKT phosphorylates targets in the cytosol, organism-specific biosystem; AKT phosphorylates targets in the nucleus, organism-specific biosystem; AKT-mediated inactivation of FOXO1A, organism-specific biosystem; AMPK signaling, organism-specific biosystem; Activation of BAD and translocation to mitochondria, organism-specific biosystem; Activation of BH3-only proteins, organism-specific biosystem; Acute myeloid leukemia, organism-specific biosystem; |
| MIM | 164730 |
| Mycoplasma | Negative |
| Format | One frozen vial containing millions of cells |
| Storage | Liquid nitrogen |
| Safety Considerations |
The following safety precautions should be observed. 1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum. 2. No eating, drinking or smoking while handling the stable line. 3. Wash hands after handling the stable line and before leaving the lab. 4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells. 5. All waste should be considered hazardous. 6. Dispose of all liquid waste after each experiment and treat with bleach. |
| Ship | Dry ice |
Arginine vasopressin (AVP) levels are elevated in patients with heart failure, and increased plasma AVP concentrations are positively correlated with disease severity and mortality. Metoprolol (Met) is a β-blocker widely used clinically to treat pathological cardiac hypertrophy and improve cardiac function. However, the specific mechanisms by which Met alleviates AVP-induced pathological cardiac hypertrophy remain unclear. Here, researchers found that AKT1, but not AKT2, mediated the pathological process of AVP-induced cardiomyocyte hypertrophy. Sustained AVP stimulation led to hypertrophy in H9C2 rat cardiomyocytes, characterized by downregulated AKT1 and SERCA2 expression, upregulated PLN expression, and increased cytoplasmic calcium concentration. Furthermore, AKT1 overexpression increased SERCA2 expression and decreased PLN expression in H9C2 cells. The researchers also found that Met could attenuate the AVP-induced changes in AKT1, SERCA2, and PLN expression and reduce the cytoplasmic calcium concentration in H9C2 cells. These findings suggest that the AKT1-SERCA2 signaling pathway plays an important regulatory role in AVP-induced pathological cardiac hypertrophy.
To further understand the mechanisms of cardiomyocyte hypertrophy during AKT1 overexpression, researchers conducted a series of studies. Compared to untreated cardiomyocytes, long-term treatment with AVP significantly reduced the expression of SERCA2 protein and increased the expression of PLN in cardiomyocytes. Furthermore, in AKT1-overexpressing cells, SERCA2 expression was upregulated, while PLN expression was downregulated. In AKT1 overexpressing H9C2 cells, the effects of AVP on SERCA2 and PLN expression were significantly attenuated (Figure 1a, b). In addition, researchers measured intracellular calcium storage and found that AVP treatment significantly increased intracellular Ca2+ concentration, while this effect on intracellular Ca2+ concentration was almost completely abolished in AVP-treated H9C2 cells overexpressing AKT1 (Figure 1c, d).
Figure 1. AKT1 overexpression upregulated the protein expression of SERCA2 and downregulated the protein expression of PLN. (Zhao J, et al., 2020)
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