• Crispr - Mouse Models

Mouse Models

ASC is one of the earliest service providers of CRISPR/Cas9 technology, and has successfully delivered >500 CRISPR engineered mouse models in as fast as 3 months. Our animal model portfolio includes constitutive/ conditional knockout, locus-specific/ safe harbor knock-in, controlled gene expression and gene correction, to name a few.

  • Most up-to-date CRISPR designing strategies and protocols
  • 100% target-site cutting efficiency using optimized, proprietary gRNA validation methods
  • AAALAC-accredited animal facility in the USA for engineering mouse models
  • Animal IP belongs to researchers
  • Our team of scientific experts will discuss your project needs and suitable strategic options in detail to fit your budget and research needs.
  • NEW! Downstream electrophysiology and behavioral assessments for your mouse models
Mouse Models Categories

Conditional Knockout Mouse
Models

We can generate conditional knockout mouse models to your specifications. You will have precise control over where or when your gene is knocked-out.

Conditional Knockout Mouse
Models

CRISPR Mice Generation
Service

Custom CRISPR mouse model service using advanced design strategies, optimized protocols and validation methods to generate mouse models quickly.

CRISPR Mice Generation
Service

Homologous Recombination Conditional Knockout Mouse Model and Knock-in Mouse Models

Leverage our expertise in knock-in/ knockout mouse model generation, vector designing, ES cell targeting and mouse handling to advance your research.

Homologous Recombination Conditional Knockout Mouse Model and Knock-in Mouse Models

Transgenic Mice Models

Our animal specialists can generate transgenic mouse models using bacterial artificial chromosome (BAC) or random microinjection into the pronucleus.

Transgenic Mice Models

Technical Details

CRISPR/Cas9 is a powerful new tool we use to generate mouse or rat models with point mutation(s), small reporter gene insertions, conditional or regular knockout(s). ASC is a leading CRISPR mouse model generation service company*, with more than 10 years’ experience in mouse model genetic engineering. All custom CRISPR/Cas9 mouse models are generated in the USA in our AAALAC accredited animal facility and shipped worldwide.

For knock-in large DNA fragments in mice, our proprietary site-specific knock-in technology TARGATT™ has a unique advantage and higher insertion efficiency over CRISPR.

*Smalley, E. (2016). CRISPR mouse model boom, rat model renaissance. Nat Biotech, 34(9), 893–894. Retrieved from http://dx.doi.org/10.1038/nbt0916-893

Comprehensive Technology Platform for Gene Editing

Methods

Technical Advantage

TARGATT™ phiC31 integrase

  • Site-specific integration (H11 or ROSA26)
  • Works for large DNA Knock-in (~22kb)
  • High efficiency (up to 40%)
  • Insert promoter of choice for gene overexpression/ inducible expression

CRISPR / Cas9

  • High specificity
  • High efficiency in knockout, point mutation, and conditional knockout
  • Ease of use
  • Works for large DNA knock-in (-10kb)

We also offer mouse model generation service using an expanded technology portfolio such as traditional homologous recombination via ESCs, bacterial artificial chromosome and random transgenic technologies. With our expertise in mouse model generation service and various genome editing technologies, we can assure you a custom genetically engineered mouse model perfect for your research needs.

New! Custom In Vivo (Animal Models) Assay Services for downstream evaluation of your animal models. We provide services for in vivo assessments as well as in vitro (end-of-study) evaluations using assays such as electrophysiology, immunohistochemistry, and more.

Publications

CRISPR Knock-in, CRISPR Knockout Mouse

 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

  • Deng, F., He, S., Cui, S., Shi, Y., Tan, Y., Li, Z., ... & Peng, L. (2018). A Molecular Targeted Immunotherapeutic Strategy for Ulcerative Colitis via Dual-Targeting Nanoparticles Delivering miR-146b to Intestinal Macrophages. Journal of Crohn's and Colitis.
  • Jo, S., Fonseca, T. L., Bocco, B. M. D. C., Fernandes, G. W., McAninch, E. A., Bolin, A. P., ... & Németh, D. (2018). Type 2 deiodinase polymorphism causes ER stress and hypothyroidism in the brain. The Journal of Clinical Investigation.
  • Langston, R. G., Rudenko, I. N., Kumaran, R., Hauser, D. N., Kaganovich, A., Ponce, L. B., ... & Beilina, A. (2018). Differences in Stability, Activity and Mutation Effects Between Human and Mouse Leucine-Rich Repeat Kinase 2. Neurochemical research, 1-14.
  • Amara, N., Tholen, M., & Bogyo, M. (2018). Chemical tools for selective activity profiling of endogenously expressed MMP-14 in multicellular models. ACS Chemical Biology. doi: 10.1021/acschembio.8b00562.
  • Allocca, S., Ciano, M., Ciardulli, M. C., D’Ambrosio, C., Scaloni, A., Sarnataro, D., ... & Bonatti, S. (2018). An αB-Crystallin Peptide Rescues Compartmentalization and Trafficking Response to Cu Overload of ATP7B-H1069Q, the Most Frequent Cause of Wilson Disease in the Caucasian Population. International journal of molecular sciences, 19(7).
  • 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.

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

  • Zhao, M., Tao, F., Venkatraman, A., Li, Z., Smith, S. E., Unruh, J., ... & Marshall, H. (2019). N-Cadherin-Expressing Bone and Marrow Stromal Progenitor Cells Maintain Reserve Hematopoietic Stem Cells. Cell reports, 26(3), 652-669.
  • 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 therapyHuman Molecular Genetics24(1), 185–196. http://doi.org/10.1093/hmg/ddu428.
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