• CRISPR/Cas9 Genome Editing

CRISPR/Cas9 Genome Editing

Leverage our extensive expertise in CRISPR/Cas9 genome editing technologies to generate genetically modified mouse, rat, cancer cell lines, and stem cell models with a variety of modifications in a targeted gene of interest. As one of the earliest licensees of CRISPR/Cas9 technology, we have genetically engineered > 1000 unique models for biomedical research applications such as disease modeling, functional genomics, target identification, antibody validation, target identification and validation for drug discovery and screening, and more.

CRISPR/Cas9 Genome Editing Categories

Cell Line Models

Custom stable cell line model generation using CRISPR/Cas9 for disease modeling, antibody validation, and drug screening.

Cell Line Models

Mouse Models

Custom CRISPR/Cas9 engineered mouse models with a variety of genetic modifications; generated in our AAALAC-accredited animal facility in the USA.

Mouse Models

Rat Models

Custom CRISPR/Cas9 rat models for disease modeling and drug screening; generated in our AAALAC-accredited animal facility in the USA.

Rat Models

Products and Services
Catalog ID#Product Name Price
$7,000.00
$10,000.00

26 Items

per page
FAQs
What genome editing method do you use in your Cell Line service?
Is there a size limit on DNA to be inserted into the genome (CRISPR Knock-in)?
Have you encountered difficulties in genome editing in cell lines?
How many guide RNAs do you typically design for a CRISPR Genome Editing Service?
Can you provide off-target analysis report?
Are you currently providing gene editing service to biotech/pharmaceutical companies as well?
Can we have a confidentiality disclosure agreement (CDA) before disclosing my project details?
What is the efficiency of CRISPR-Cas9 technology as compared to TARGATT™ and random transgenesis for mouse model generation?
Which technology is suitable for inserting a gene of interest with GFP or Cre-ERT in a mouse model?
What is the basis of your design algorithm for the sgRNAs?
Publications

CRISPR Cell Line Models:  Knock-Out, Knock-in, Point Mutation

Applied StemCell publications and citations:

  • Selvan, N., George, S., Serajee, F. J., Shaw, M., Hobson, L., Kalscheuer, V. M., ... & Schwartz, C. E. (2018). O-GlcNAc transferase missense mutations linked to X-linked intellectual disability deregulate genes involved in cell fate determination and signaling. Journal of Biological Chemistry, jbc-RA118.

  • Smalley, E. (2018). FDA warns public of dangers of DIY gene therapy. https://doi.org/10.1038/nbt0218-119

  • Chai, S., Wan, X., Ramirez-Navarro, A., Tesar, P. J., Kaufman, E. S., Ficker, E., ... & Deschênes, I. (2018). Physiological genomics identifies genetic modifiers of long QT syndrome type 2 severity. The Journal of clinical investigation, 128(3).

  • Boi, S., Ferrell, M. E., Zhao, M., Hasenkrug, K. J., & Evans, L. H. (2018). Mouse APOBEC3 expression in NIH 3T3 cells mediates hypermutation of AKV murine leukemia virus. Virology, 518, 377-384. https://doi.org/10.1016/j.virol.2018.03.014.

  • Molinski, S. V., et al. (2017). Orkambi® and amplifier co‐therapy improves function from a rare CFTR mutation in gene‐edited cells and patient tissue. EMBO Molecular Medicine, e201607137.

  • Petrovic, P. B. (2017). Myosin Phosphatase Rho-interacting Protein Regulates DDR1-mediated Collagen Tractional Remodeling (Doctoral dissertation, University of Toronto (Canada)).

  • Peng, L., Zhang, H., Hao, Y., Xu, F., Yang, J., Zhang, R., ... & Chen, C. (2016). Reprogramming macrophage orientation by microRNA 146b targeting transcription factor IRF5. EBioMedicine, 14, 83-96.

  • Hu, J. K., Crampton, J. C., Locci, M., & Crotty, S. (2016). CRISPR-mediated Slamf1Δ/Δ Slamf5Δ/Δ Slamf6Δ/Δ triple gene disruption reveals NKT cell defects but not T follicular helper cell defects. PloS one, 11(5), e0156074.

  • Smalley, E. (2016). CRISPR mouse model boom, rat model renaissance. Nature Biotechnology. 34, 893–894.

  • Baker, M. (2014). Gene editing at CRISPR speed. Nature biotechnology, 32(4), 309-313.

CRISPR Technology:

CRISPR Mouse/ Rat Models:  Knock-in, Knockout, and Conditional Knockout (*cited/published articles)

CRISPR Technology

CRISPR Knock-in H11 Locus in Pigs

  • Ruan, J., Li, H., Xu, K., Wu, T., Wei, J., Zhou, R., ... & Chen-Tsai, R. Y. (2015). Highly efficient CRISPR/Cas9-mediated transgene knockin at the H11 locus in pigs. Scientific reports, 5, 14253.

Knock-in, Knockout, Conditional Knock-out

  • *Peng, L., Zhang, H., Hao, Y., Xu, F., Yang, J., Zhang, R., ... & Chen, C. (2016). Reprogramming macrophage orientation by microRNA 146b targeting transcription factor IRF5. EBioMedicine, 14, 83-96.

  • *Hu, J. K., Crampton, J. C., Locci, M., & Crotty, S. (2016). CRISPR-mediated Slamf1Δ/Δ Slamf5Δ/Δ Slamf6Δ/Δ triple gene disruption reveals NKT cell defects but not T follicular helper cell defects. PloS one, 11(5), e0156074.

  • *Besschetnova, T. Y., Ichimura, T., Katebi, N., Croix, B. S., Bonventre, J. V., & Olsen, B. R. (2015). Regulatory mechanisms of anthrax toxin receptor 1-dependent vascular and connective tissue homeostasis. Matrix Biology, 42, 56-73.

  • *McKenzie, C. W., Craige, B., Kroeger, T. V., Finn, R., Wyatt, T. A., Sisson, J. H., ... & Lee, L. (2015). CFAP54 is required for proper ciliary motility and assembly of the central pair apparatus in mice. Molecular biology of the cell, 26(18), 3140-3149.

  • *Bishop, K. A., Harrington, A., Kouranova, E., Weinstein, E. J., Rosen, C. J., Cui, X., & Liaw, L. (2016). CRISPR/Cas9-mediated insertion of loxP sites in the mouse Dock7 gene provides an effective alternative to use of targeted embryonic stem cells. G3: Genes, Genomes, Genetics, 6(7), 2051-2061.

Mouse/ Rat Models: Homologous Recombination Conditional Knockout Mouse (*cited/published articles)

  • Li, C., Zheng, Z., Ha, P., Chen, X., Jiang, W., Sun, S., ... & Chen, E. C. (2018). Neurexin Superfamily Cell Membrane Receptor Contactin‐Associated Protein Like‐4 (Cntnap4) is Involved in Neural EGFL Like 1 (Nell‐1)‐responsive Osteogenesis. Journal of Bone and Mineral Research https://doi.org/10.1002/jbmr.3524.

  • Geraets, R. D., Langin, L. M., Cain, J. T., Parker, C. M., Beraldi, R., Kovacs, A. D., ... & Pearce, D. A. (2017). A tailored mouse model of CLN2 disease: A nonsense mutant for testing personalized therapies. PloS one, 12(5), e0176526.

  • Miller, J. N., Kovács, A. D., & Pearce, D. A. (2015). The novel Cln1R151Xmouse model of infantile neuronal ceroid lipofuscinosis (INCL) for testing nonsense suppression therapy. Human Molecular Genetics, 24(1), 185–196. http://doi.org/10.1093/hmg/ddu428.

Technical Details

Genetic modifications available through our CRISPR/Cas9 gene editing platform:
Gene knockout, point mutation knock-in, gene insertion in any locus, including safe harbor locus (large fragment insertion, reporter gene knock-in, gene replacement), conditional knockout/ knock-in models, conditional/ inducible gene expression models.

CRISPR applications:
Functional genomics, disease modeling, target identification and validation for drug discovery and screening, and many more.

Choosing the right genome editing technology:
Applied StemCell uses two complementary genome editing technologiesto generate advanced cell line and animal models very efficiently and effectively: the CRISPR/Cas9 technology and our propriety site-specific gene integration technology, TARGATT™ for large fragment (up to 20 kb) knock-in into a safe harbor locus.

Project Purpose

CRISPR/Cas9

TARGATT™

Knock-Out (KO)

Yes

 

Point Mutation

Yes

 

Conditional KO

Yes

 

Knock-In

(<200 Nucleotide ssODN Donor)

Yes

 

Knock-In Transgenes in

Safe Harbor Loci (>2kb)

Challenging

(but limitations on size)

Yes

 (up to 20kb)

Knock-In

 (Plasmid DNA)

Challenging

(but limitations on size)

Yes

 (2 steps: KI docking site; KI transgene) 

Have Questions?

An Applied StemCell technical expert is happy to help, contact us today!