AKT2 Gene Editing


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AKT2 Gene Editing    

Akt2 (AKT Serine/Threonine Kinase 2), is a protein encoded by an oncogene, and belongs to AKT family. AKT mediates many processes through its serine/threonine phosphorylation of its downstream substrates, including metabolism, proliferation, cell survival, growth and angiogenesis (Figure 1). AKT regulates glucose uptake by mediating insulin-induced SLC2A4 / GLUT4 glucose transporters. PTPN1 regulates its phosphatase activity, thereby preventing dephosphorylation of the insulin receptor and attenuation of insulin signaling. AKT also regulates glucose storage in glycogen form by phosphorylating GSK3B. Phosphorylation of the GSK3 isoform by AKT is also considered to be a mechanism driving cell proliferation. AKT also regulates cell survival by phosphorylation of MAP3K5. AKT mediates insulin-stimulated protein synthesis by phosphorylating TSC2, thereby activating mTORC1 signaling and leading to phosphorylation of 4E-BP1 and activation of RPS6KB1. AKT is involved in phosphorylation of FOXO factor members, resulting in binding and cytoplasmic localization of 14-3-3 proteins. AKT plays an important role in regulating NF-κB-dependent gene transcription and regulates the activity of CREB1. AKT phosphorylates citrate lyase (ACLY), which modulates ACLY activity and fatty acid synthesis. Activation of the 3B isoform of cyclic nucleotide phosphodiesterase (PDE3B) by phosphorylation results in decreased levels of cyclic AMP and inhibition of lipolysis. In addition, AKT, a key regulator of the AKT-mTOR signaling pathway, controls the rhythm of neonatal neuronal integration during adult neurogenesis, including proper neuronal localization, dendritic development, and synapse formation.

Furthermore, amplification/overexpression of AKT2 affect the malignant phenotype by overreacting tumor cells to the environmental levels of growth factors that normally do not enhance proliferation. AKT2 protein expression has been reported to be elevated in nearly 40% of hepatocellular carcinomas, and AKT2 overexpression has been found to be an independent prognostic marker, and AKT2 is a major AKT family member involved in colorectal cancer. Since many oncoproteins and tumor suppressors cross in the AKT pathway, how cell functions are finely regulated at the interface between signal transduction and classical metabolic regulation, as well as various activation and inactivation mechanisms for AKT and related proteins in human cancer therapy application is still worth studying.

Physiological targets of AKTFigure 1: Physiological targets of AKT

AKT2 Gene Editing Service

CRISPR/Cas9 PlatformCB, one of the leading gene editing biotechnology companies, is specializing in offering efficient systems and procedures to meet the needs and timelines of clients working in the CRISPR/Cas9 gene editing. With our deep gene editing knowledge and extensive experience in experimental operation and data processing, CRISPR/Cas9 PlatformCB can help you achieve CRISPR/Cas9 gene editing cell lines or animal models within shorter turnaround time and lower price. Our CRISPR/Cas9 gene editing services include DNA fragments deletion, conditional knockout/knockin, point mutation, etc.

  • AKT2 Gene Editing Cell Line Generation

CRISPR/Cas9 PlatformCB has extensive experience with >200 distinct cell lines, and are very familiar with their culture conditions and genetic backgrounds. Our scientists have successfully implemented AKT2 CRISPR/Cas9 gene edit in both easy-to-transfect cell lines and hard-to-transfect cells. Tell us the cell lines your project needs, we will offer you professional custom AKT2 gene editing services from strategy design to final stable cells with a reasonable cost and shorter time. Our AKT2 gene editing cell line generation services include:

✧ SgRNA design and synthesis
✧ Transfect the cell line you interest
✧ Select the high expression cell and sort monoclonal cell
✧ Validate the knockout/knockin/point mutation of AKT2 by PCR and sequencing
✧ Produce cryogenic preserved vials of stable cells and a final report

Typically, we develop CRISPR-mediated gene editing cell lines, including HEK239T, Hela, HepG2, U87, but we can use other cell lines according to your requirements.

Host cell line: Ba/F3, CHO, MDA-MB-453, MDA-MB-231NIH3T3, T47D, Neuro2a, MCF7, RKO, K562, RAW264.7, etc.

  • AKT2 Gene Editing Animal Model Generation

CRISPR/Cas9 PlatformCB also has extensive experience in incorporating CRISPR-Cas9 technology into animal models, which have been recognized by our clients. According to your projects’ needs, we will help you obtain AKT2 CRISPR/Cas9 gene editing animals you interest. We guarantee at least 2 founders or 3 F1 animals. Our AKT2 gene editing animal model generation services include:

➢ AKT2 gene conventional knockout animals
➢ AKT2 gene conditional knockout animals
➢ AKT2 point mutation animals
➢ AKT2 knockin animals

Alternative species: mouse, rat, rabbit, zebrafish, C. elegans, etc.

With our national-class labs and professional gene editing scientists from world-class universities, CRISPR/Cas9 PlatformCB will provide you a one-stop-shop CRISPR/Cas9 gene editing service. Tell us your needs, we guarantee our clients the most reliable and efficient research services to best match your research goals and protect your science investment. If you have any projects need CRISPR/Cas9 gene editing services, don’t hesitate to contact us.

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  1. Alfonso Bellacosa. et al. Activation of AKT Kinases in Cancer: Implications for Therapeutic Targetin. Advances in Cancer Research. 2005; 94: 29-86.
  2. Deborah A Altomare, Joseph R Tes. Perturbations of the AKT signaling pathway in human cancer. Oncogene. 2005; 24, 7455–7464.
For research use only. Not intended for any clinical use.


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