CDK2 Gene Editing

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CDK2 Gene Editing    

CDK2 (Cyclin-dependent kinase 2), also named cell division protein kinase 2, is a member of the cyclin-dependent kinase family of Ser/Thr protein kinases. Structurally, the N-terminus of CDK2 protein is a cyclin binding site, containing many β-sheets, while the C-terminus is a kinase domain rich in α-helices. CDK2 is capable of binding to many different cyclins, including cyclin A, B, E and possibly C. Studies show that CDK2 preferentially binds to cyclin A and E.

CDK2 is a known regulator of cell cycle control of G1/S and S/G2 turnover (Figure 1). In the late G1 phase, cyclin E activates CDK2 and completes phosphorylation of retinoblastoma protein (Rb), leading to a restriction point at the boundary of the G1/S phase, and to S phase initiation. Later, CDK2 played an important role in the progression of S phase by complexing with cyclin A.

 Cyclin E–CDK2: the way they wereFigure 1: Cyclin E–CDK2: the way they were (James M Roberts. 2003)

In addition to promoting cell cycle progression, CDK2 has been described to play a positive role in cell cycle arrest in DNA damage response (DDR), particularly at the G2/M checkpoint, and is involved in the activation of DNA repair proteins. Although the function of CDK2 during S phase can be fully compensated by CDK1, the DNA repair function of CDK2 in mammalian cells cannot be compensated by CDK1.

Among all CDKs, CDK2 is known to be an important kinase for tumorigenesis and proliferation in many cancer types including lung cancer, liver cancer, colon cancer, and breast cancer. There is strong evidence that CDK2 is associated with high proliferative function in a variety of cancer cells and is a potential therapeutic target for cancer therapy (Table 1).

Table 1: CDK2 inhibitors in diseases treatment

InhibitorFunction
GW8510
Seliciclib
Reduce the sensitivity of the epithelium to many cell cycle active antitumor agents
Methyl rosmarinic acidInhibit the proliferation of vascular smooth muscle cells

CDK2 Gene Editing Service

CRISPR/Cas9 PlatformCB, a global leading biotechnological company specializing in gene editing, is dedicated to offering comprehensive CRISPR/Cas9 gene editing services and products to a wide range of genomics researchers. With deep gene editing knowledge and extensive experience in experimental operation and data processing, we can help you effectively control target genes deleted, inserted or point mutated in cells or animals via CRISPR/Cas9 technology.

  • CDK2 Gene Editing Cell Line Generation

We have successfully implemented CDK2 CRISPR/Cas9 gene edited in both easy-to-transfect cell lines and hard-to-transfect cells. To support your projects, we will offer you full-length custom CDK2 gene editing service from strategy design to final stable cells. Our CDK2 gene editing cell line generation services include:

✧ gRNA design and synthesis
✧ Transfect the cell lines you're interested
✧ Select the high expression cells and sort monoclonal cell
✧ Validate the knockout/knockin/point mutation of CDK2 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.

Other host cell lines available: Ba/F3, CHO, MDA-MB-453, MDA-MB-231NIH3T3, T47D, Neuro2a, MCF7, RKO, K562, RAW264.7, etc.

  • CDK2 Gene Editing Animal Model Generation

CRISPR/Cas9 PlatformCB also has extensive experience in incorporating CRISPR/Cas9 technology into animal models, which have been fully recognized by our clients. Tell us your needs, we provide a one-stop-shop CDK2 CRISPR/Cas9 gene editing animal service and guarantee at least 2 founders or 3 F1 animals with shorter turnaround time and lower price. Our CDK2 gene editing animal model generation services include:

➢ CDK2 gene conventional knockout animals
➢ CDK2 gene conditional knockout animals
➢ CDK2 point mutation animals
➢ CDK2 knockin animals

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

CRISPR/Cas9 PlatformCB is devoted to providing the best gene editing services and products for academic research, biotech research and pharmaceutical drug discovery with excellent quality management and quality assurance capacity. To accelerate the achievement of your research goals, our gene editing expert team provides you with custom CRISPR/Cas9 services for any specific gene to help you solve problems encountered during your research. There is no doubt that CRISPR/Cas9 PlatformCB will be your best partner to support your research.

Related Products at CRISPR/Cas9 PlatformCB

References:

  1. Karin E. Bornfeldt. The Cyclin-Dependent Kinase Pathway Moves Forward. Circulation Research. 2003; 92:345–347.
  2. C Peng.et al. Cyclin-dependent kinase 2 (CDK2) is a key mediator for EGF-induced cell transformation mediated through the ELK4/c-Fos signaling pathway. Oncogene. 2016; 35: 1170–1179.
  3. Katarina Bačević. et al. Cdk2 strengthens the intra-S checkpoint and counteracts cell cycle exit induced by DNA damage. Scientific Reports. 2017; 7:13429.
  4. Ande Satyanarayana & Philipp Kaldis. A dual role of Cdk2 in DNA damage response. Cell Division. 2009; 4:9.
  5. Echalier A. et al. Recent developments in cyclin-dependent kinase biochemical and structural studies. Biochimica et Biophysica Acta. 2010; 1804 (3):511–9.
  6. Satyanarayana A. et al. Mammalian cell-cycle regulation: several Cdks, numerous cyclins and diverse compensatory mechanisms. Oncogene. 2009; 28 (33):2925–39.
  7. Wood DJ. et al. Differences in the Conformational Energy Landscape of CDK1 and CDK2 Suggest a Mechanism for Achieving Selective CDK Inhibition. Cell Chemical Biology. 2018; 26 (1):121–130.e5.
  8. James M Roberts & Charles J Sherr. Bared essentials of CDK2 and cyclin E. NATURE GENETICS. 2003; 35:1.
For research use only. Not intended for any clinical use.

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