Panoply™ Human AKT1 Over-expressing Stable Cell Line

Name: Panoply™ Human AKT1 Over-expressing Stable Cell Line
SKU: CSC-SC000464
Availability: InStock

For research use only. Not intended for any clinical use.

Cat. No. : CSC-SC000464

Host Cell : HEK293 (CHO and other cell types are also available) Size : >1x10⁶ frozen cells/vial

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Cell Line Information

Cell Culture Information

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Gene Information

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.
Target Gene	AKT1
Gene Species	Homo sapiens (Human)
Host Cell	HEK293 (CHO and other cell types are also available)
Host Cell Species	Species varies
Applications	1. Gene expression studies 2. Signaling pathway research 3. Drug screening and toxicology 4. Disease research
Size	2 × 10^6 cells / vial
Stability	Validated for at least 10 passages
Quality Control	Negative for bacteria, yeast, fungi and mycoplasma.
Storage	Liquid nitrogen
Shipping	Dry Ice

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.

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

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
Uni Prot ID	B0LPE5
m RNA 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

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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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