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mTOR Gene Editing    

mTOR (mammalian rapamycin target protein) is a member of the phosphatidylinositol 3-kinase-associated kinase family and is a key component of two different protein complexes, mTORC1 and mTORC2, which phosphorylate different substrate groups to regulate different cellular processes. mTOR1 can sense and integrate a variety of nutritional and environmental factors, including growth factors, energy levels, cellular stress, and amino acids. These signals are linked by phosphorylation that enhances anabolic processes (such as mRNA translation and lipid synthesis) or substrates that limit catabolic processes (such as autophagy) to promote cell growth. mTORC2 promotes actin cytoskeletal rearrangement, cell survival, and cell cycle progression, and affects cell metabolism and survival by phosphorylating AKT/PKB (Figure 1).

 signals sensed by mTORC1 and mTORC2 and the processes they regulateFigure 1: signals sensed by mTORC1 and mTORC2 and the processes they regulate

Over activation of mTOR signaling significantly promotes tumorigenesis and progression, and mTOR activity is found to be dysregulated in many types of cancer, including breast cancer, prostate cancer, lung cancer, melanoma, bladder cancer, brain cancer, and kidney cancer, which due to the role of mTOR in promoting protein synthesis, affecting cell cycle progression and increasing cell proliferation, and inhibition of autophagy indirectly supporting tumor growth. Rapalogs and mTOR inhibitors have made some advances in immunosuppression and a small number of cancer treatments, but there are limitations that make their utility significantly limited. Physiological studies in mice have shown that mTOR signaling is also essential for proper metabolic regulation at the body level, including glucose homeostasis, muscle mass and function regulation, lipogenesis, and liposome homeostasis, immune function and brain function regulation.

The mTOR pathway plays an important role in sensing environmental conditions and regulating metabolism in almost all aspects of cell and organism levels. In the past few years, many new insights into the function and regulation of mTOR have been elucidated, and extensive genetic and pharmacological studies in mice have enhanced our understanding of how mTOR dysfunction leads to disease. However, a comprehensive understanding of the relative importance of these signals and their important background remains unclear, and whether these molecular insights can improve the therapeutic targeting of clinical mTOR also requires further resolution.

mTOR Gene Editing Service

CRISPR/Cas9 PlatformCB is one of the leading gene editing biotechnology companies and specializing in offering efficient systems and procedures to meet the needs and timelines of clients working in the CRISPR/Cas9 gene editing. Our scientists have deep gene editing knowledge and extensive experience in experimental operation and data processing. Tell us your needs, we will help you generate CRISPR/Cas9 knockout/knockin/point mutation cell lines or animal models within shorter turnaround time and lower price.

  • mTOR Gene Editing Cell Line Generation

CRISPR/Cas9 PlatformCB is very familiar with the culture conditions and genetic backgrounds of >200 distinct cell lines, and have successfully implemented mTOR CRISPR/Cas9 gene edit in both easy-to-transfect cell lines and hard-to-transfect cells. Based on our platform, we will offer you professional custom mTOR gene editing services from strategy design to final stable cells. Our mTOR 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 mTOR 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.

  • mTOR 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 provide a one-stop-shop mTOR CRISPR/Cas9 gene editing animal services and guarantee at least 2 founders or 3 F1 animals. Our mTOR gene editing animal model generation services include:

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

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

CRISPR/Cas9 PlatformCB has national-class labs and professional gene editing scientists from world-class universities, and provide you a one-stop-shop CRISPR/Cas9 gene editing service. 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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References:

  1. Mitra A. et al. Dual mTOR Inhibition Is Required to Prevent TGF-β-Mediated Fibrosis: Implications for Scleroderma. The Journal of Investigative Dermatology. 2015; 135(11):2873–6.
  2. Lipton JO, Sahin M. The neurology of mTOR. Neuron. 2014: 84(2):275–291.
  3. Zoncu R. et al. mTOR: from growth signal integration to cancer, diabetes and ageing. Molecular Cell Biology. 2011; 12 (1):21–35.
  4. Robert A. Saxton and David M. Sabatini. mTOR Signaling in Growth, Metabolism, and Disease. Cell. 2017 Mar 9; 168(6):960–976.
  5. Katarzyna Switon. Molecular neurobiology of mTOR. Neuroscience. 2017 Jan 26; 342:112-153.
  6. David A. Guertin. David M. Sabatini. Defining the Role of mTOR in Cancer. Cancer Cell. 2007 July 10; 12(1):9-22.
  7. Thoreen, C.C. et al. A unifying model for mTORC1-mediated regulation of mRNA translation. Nature.2012; 485: 109-113.
  8. Charles Betz, Michael N. Hall. Where is mTOR and what is it doing there? JCB. 2013; 203 (4): 563.
For research use only. Not intended for any clinical use.
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