DDR1 Gene Editing

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DDR1 Gene Editing    

DDR1 (Discoidin Domain Receptor Tyrosine Kinase 1), also named CD167a, belongs to the tyrosine kinase receptor DDRs subfamily and is activated by collagen. The DDR1 gene is located at human chromosome at 6p21.33 and comprises 17 exons, expressing five different isoforms. The binding of collagen activates DDR1, and activated DDR1 regulates many cellular activities via triggering a series of intracellular cascades signaling, including attachment of cells to extracellular matrices, remodeling of extracellular matrices, cell migration, differentiation, survival, and cell proliferation.

DDR1 abnormalities are closely related to human diseases such as pulmonary fibrosis, idiopathic and breast cancer. The researchers believe that this may be caused by the DDR1 signaling pathway that promotes cell movement. Studies have shown that DDR1 actively participates in the development of tumors and promotes the proliferation of tumor cells. DDR1 prolongs tumor cell survival by interacting with Notch1. In addition, DDR1 also plays a role in tumor cell invasion, and DDR1 participates in the collective migration of cancer cells by coordinating the cell polarity regulators Par3 and Par6. Based on the cellular function of DDR1, the development of new drugs for DDR1 drug targets is expected to become a new cancer treatment strategy.

DDR1 Gene Editing Service

As a leading genomic editing company, CRISPR/Cas9 PlatformCB is specialized in providing a set of services for CRISPR-Cas9 genome editing. We can provide you custom CRISPR/Cas9 gene-editing services from strategy design to genetic edited cell lines or animal models to meet your specific project needs and provide experienced scientific support at every step.

  • DDR1 Gene Editing Cell Line Generation

CRISPR/Cas9 PlatformCB has successfully implemented gene editing of DDR1 in a variety of cell lines, including easy-to-transfect cell lines and hard-to-transfect cells. Our DDR1 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 DDR1 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.

  • DDR1 Gene Editing Animal Model Generation

CRISPR/Cas9 PlatformCB also has extensive experience in incorporating CRISPR-Cas9 technology into animal models. We have obtained >300 mouse models with very high efficiency and success rate by using CRISPR/Cas9-mediated genome editing technology. Based on our platform, we can provide you with CRISPR/Cas DDR1 gene-editing animal models at a reasonable cost and in a shorter time. Our DDR1 gene editing animal model generation services include:

➢ DDR1 gene conventional knockout animals
➢ DDR1 gene conditional knockout animals
➢ DDR1 point mutation animals
➢ DDR1 knockin animals

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

If you don't see the gene editing service related to DDR1 you need above, don't hesitate to contact us. CRISPR/Cas9 PlatformCB is professional in providing custom CRISPR/Cas genome engineering projects. Tell us your needs, we will provide you with a custom one-stop-shop CRISPR/Cas gene editing service. We guarantee our clients the most reliable and efficient research services to best match your research goals, and faster turnaround times, lower prices.

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References:

  1. Hidalgo-Carcedo C. et al. Collective cell migration requires suppression of actomyosin at cell-cell contacts mediated by DDR1 and the cell polarity regulators Par3 and Par6. Nat Cell Biol. 2011 Jan;13(1):49-58.
  2. Kim HG. et al. DDR1 receptor tyrosine kinase promotes prosurvival pathway through Notch1 activation. J Biol Chem. 2011 May 20;286(20):17672-81.
For research use only. Not intended for any clinical use.

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