CDK8 Gene Editing

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CDK8 Gene Editing    

CDK8 is a nuclear serine-threonine kinase that belongs to the cyclin-dependent kinase family and is involved in transcriptional regulation from yeast to mammals. CDK8 is a major SER2 kinase, and several CDK8 phosphorylation targets currently validated include RNA polymerase II (RNAPII) C-terminal domain (CTD), histone H3, subunits of general transcription factors (base transferases) and certain transactivators, However, how these phosphorylation events contribute to the overall biological activity of CDK8 remains unclear.

CDK8 as a transcription regulator

  • CDK8 kinase forms the "CDK8 submodule" of the mediator complex with cyclin C, MED12 and MED13. Mediator complexes are transcription factors, chromatin modifiers, promoters and enhancers that bridge the RNA Pol II and play a central role in the transcription process.
  • CDK8 can suppress and activate mammalian gene transcription.
  • In addition to initiating transcription, CDK8 also regulates transcriptional elongation.
  • CDK8 promotes transcription factor activity and degradation.

CDK8 function and its relationship with physiological (purple) and pathological (red) conditions (outer circle). Figure 1: CDK8 function and its relationship with physiological (purple) and pathological (red) conditions (outer circle). (Ingeborg Menzl. 2019)

CDK8 and cancers

Since most of the CDK8-dependent pathways described are altered in cancer. CDK8 has been described as an oncogene for colorectal cancer (CRC) and several other cancer types, including melanoma and breast cancer. However, the exact mechanism by which CDK8 activity promotes cancer development remains to be elucidated. CDK8 has been shown to be a positive regulator of the transcriptional program that drives cancer cell proliferation and survival, including Wnt/β-catenin, ERK/MAP kinase signaling, and HIF1A. Therefore, by simultaneously reducing the activity of multiple carcinogenic pathways, the pharmacological inhibitory effect of CDK8 may have therapeutic value.

Targeting the therapeutic benefits of CDK8 in cancer

  • By reducing the aggressiveness and growth of solid cancers
  • Reduces the amount of energy available to cancer cells by reducing glucose uptake
  • Forces cancer cells to differentiate due to loss of self-renewal capacity
  • Activate tumor monitoring by enhancing the cytotoxicity of NK cell

Potential therapeutic benefits of targeting CDK8 in cancer. Figure 2: Potential therapeutic benefits of targeting CDK8 in cancer. (Ingeborg Menzl. 2019)

The dynamic association of CDK8 or CDK19 modules with mediators and the highly flexible composition of mediators may enhance or limit the potential of CDK8 as a drug target.

CDK8 Gene Editing Service

CRISPR/Cas9 PlatformCB has excellent quality management and quality assurance capabilities, providing the best gene-editing services and products for academic research, biotechnology research, and drug discovery. From early strategic design to the final model, we can adapt the solution to your detailed requirements. We guarantee to provide our customers with excellent service.

  • Details of our CDK8 gene editing service

Our customized CDK8 gene editing services include

  • Constitutive knockout
  • Induced expression
  • Point mutation
  • Conditional knockout
  • Rosa26 knock-in
  • Fluorescent proteins or immune-tags insertion
Project WorkflowService
gRNA design and synthesis, donor DNA design and synthesis (if needed)CDK8 Gene Editing Cell Line Generation Service
CRISPR/Cas9 vector construction
Transfection into the cell lines you're interested
Select the high expression cells and sort monoclonal cell
Validate the right edited monoclonal cells by PCR and sequencing
Delivery the stable cells and a final report
  
gRNA design and synthesis, donor DNA design and synthesis (if needed)CDK8 Gene Editing Animal Model Generation Service
CRISPR/Cas9 vector construction
Microinjection
Breed the founder mice, and validation
Delivery the F0 or F1 mice

What kind of models we deal with?

Model Types 
Blood Lineage CellsRAW264.7, HMC1.2, K562, U937, etc.
Cancer Cell LinesHEK293, HEK293T, Hela, MCF7, Neuro2a, HepG2, U87, etc.
Stem CellsiPSC
Other Cell LinesNIH3T3, MCF10, HEME, SW10, etc.
Animal modelsMouse, rat, rabbit, zebrafish, C. elegans, etc.

If you have any questions, please feel free to contact us.

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References

  1. Ingeborg Menzl. et al. CDK8-Novel Therapeutic Opportunities. Pharmaceuticals (Basel). 2019; 12(2): 92.
  2. Josipa Nemet. et al. The two faces of Cdk8, a positive/negative regulator of transcription. Biochimie. 2014; 97:22-27.
  3. Kim S. et al. Mediator is a transducer of Wnt/beta-catenin signaling. J Biol Chem. 2006; 281:14066–14075.
  4. Matthew D Galbraith. et al. CDK8: A positive regulator of transcription. Transcription. 2010; 1(1):4–12.
  5. Matthew D. Galbraith. et al. CDK8 kinase activity promotes glycolysis. Cell Rep. 2017; 21(6):1495–1506.
  6. Marius Volker Dannappel. et al. Molecular and in vivo Functions of the CDK8 and CDK19 Kinase Modules. Front. Cell Dev. Biol. 2019; 8:171.
  7. Xi, M. et al. CDK8 as a therapeutic target for cancers and recent developments in discovery of CDK8 inhibitors. European Journal of Medicinal Chemistry. 2019; 164:77–91.
  8. Xu, W. & Ji. J.-Y. Dysregulation of CDK8 and Cyclin C in tumorigenesis. Journal of Genetics and Genomics. 2011; 38(10):439–452.
For research use only. Not intended for any clinical use.

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