• Hight Throughput Gene Editing
    CRISPR Cas9

Mouse Models

ASC is one of the earliest service providers of CRISPR/Cas9 technology, and has successfully delivered >500 CRISPR mouse models in as little as 3 months. Our animal model portfolio offers competitive pricing and turnaround times for generating CRISPR knockout, conditional knockout, locus-specific/ safe harbor knock-in, controlled gene expression and gene correction, and more.

  • Most up-to-date CRISPR designing strategies and protocols
  • 100% target-site cutting efficiency using optimized, proprietary gRNA validation methods
  • Animal IP belongs to researchers
  • Project management and scientific support to discuss your project needs and suitable strategic options to fit your budget
  • NEW! Downstream electrophysiology and behavioral assessments for your mouse models
Mouse Models Categories

CRISPR 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.

CRISPR Conditional Knockout
Mouse Models

CRISPR Knockout, Knock-in,
Point Mutation Mouse Models

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

CRISPR Knockout, Knock-in,
Point Mutation Mouse Models

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

With our expanded facility and newly optimized CRISPR mouse model generation protocols, ASC is offering

  • Steep price-reduction
  • Full money-back guarantee
  • Upgraded and optimized high efficiency protocols
  • Fast turnarounds for F1 mice (germline transmission guaranteed)
  • Mouse models generated in facilities operated under the strict AAALAC, SPF and IACUC guidelines and shipped worldwide

In recent years, CRISPR/Cas9 has become a powerful, precision tool to generate genetically engineered mouse or rat models with point mutation(s), small reporter gene insertions, conditional knockout or constitutive knockout. The CRISPR mouse models have paved a novel way for in vivo gene-gene interactions and phenotype association studies, for disease modeling, proof-of-concept gene and cell therapy studies, as well as for preclinical drug efficacy and safety studies.

Applied StemCell (ASC) is one of the first and most experienced provider of the CRISPR-Cas9 Technology. Our expert team of scientists have extensively researched and upgraded the CRISPR system to optimize the efficiency of Cas9 cutting, modification efficiency, and even improve birth rate of mice. With more than 11 years’ experience in mouse model genetic engineering, ASC is a leader in CRISPR mouse model generation service:

Generate a wide variety of mutations to fit your research’s specifications#:




CRISPR Knockout Mouse Models

Constitutive knockout of gene of interest either by frame shift mutation or targeted fragment deletion

  • Study main function of gene/ protein
  • Disease modeling
  • Validate gene function
  • Drug/ target discovery
  • Drug specificity

CRISPR Conditional Knockout (cKO) Mouse Models

Insert LoxP sites to flank gene of interest (floxed allele); the gene of interest is deleted when the cKO mouse is mated with an appropriate Cre-deleter mouse line* which expresses the Cre recombinase under control of a tissue-specific promoter or a mouse line where Cre expression can be induced at a specific developmental stage of the mouse.


The cKO mouse models can also be used to generate constitutive germline knockout mice when mated with a

mouse line expressing Cre under control of a ubiquitous promoter.

  • Study gene function in a specific tissue or specific developmental stage
  • Physiologically relevant disease modeling for late-onset or organ/ tissue-specific diseases
  • Overcomes problems such as embryonic lethality, developmental abnormalities and sterility, seen in germline deletion of critical genes1
  • One cKO mouse line enables comparison of gene function in several tissues using hundreds of commercially available Cre-deleter mouse lines*
  • Allows for better understanding of sporadic cancer development, cancer biology and translational oncology2,3

CRISPR Knock-in Mouse Models

Insert a gene of interest or target sequence at a specific genetic locus or a safe harbor locus


Reporter genes/ tags, gene/ promoter replacement; humanized gene knock-in; inducible/ conditional expression; gene overexpression mouse models

  • Study promoter regulation, gene expression, stimulus response
  • Modeling human genetics, biology or disease without mouse orthologues
  • Drug development and screening applications
  • Proof-of-concept gene and cell therapy studies
  • Preclinical drug efficacy and safety testing

CRISPR Point Mutation Mouse Models

Substitute one or more nucleotide in the targeted region to result in amino acid change.

  • Study role of nucleotides and amino acids gene and protein function(s) and regulation
  • Clinically relevant mutations for disease modeling
  • Pharmacogenomic screening with cancer relevant mutations

* Cannot find a specific Cre mouse line? We can generate custom Cre mouse line(s) for you using our TARGATT™ site-specific knock-in technology

1 Tratar, U. L., Horvat, S., & Cemazar, M. (2018). Transgenic mouse models in cancer research. Frontiers in oncology, 8.

2 Kersten, K., de Visser, K. E., van Miltenburg, M. H., & Jonkers, J. (2017). Genetically engineered mouse models in oncology research and cancer medicine. EMBO molecular medicine, 9(2), 137-153.

3 Deng, C. X. (2014). Conditional knockout mouse models of cancer. Cold Spring Harbor Protocols, 2014(12), pdb-top074393.

For large fragment knock-in mouse models, our proprietary site-specific, knock-in technology, TARGATT™ has a unique advantage and higher insertion efficiency over CRISPR/Cas9.

Comprehensive Technology Platform for Gene Editing


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


  • 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.


CRISPR Mouse/ Rat Models:  Knock-in, Knockout, and Conditional Knockout 

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

  • Park, J., Jung, E., Lee, S. H., & Chung, W. S. (2020). CDC50A dependent phosphatidylserine exposure induces inhibitory post-synapse elimination by microglia. bioRxiv.
  • Ramachandra Rao, S., Fliesler, S. J., Kotla, P., Nguyen, M. N., & Pittler, S. J. (2020). Lack of Overt Retinal Degeneration in a K42E Dhdds Knock-In Mouse Model of RP59. Cells9(4), 896.
  • Beurg, M., Barlow, A., Furness, D. N., & Fettiplace, R. (2019). A Tmc1 mutation reduces calcium permeability and expression of mechanoelectrical transduction channels in cochlear hair cells. Proceedings of the National Academy of Sciences116(41), 20743-20749.
  • Goldring, A. C., Beurg, M., & Fettiplace, R. (2019). The contribution of TMC1 to adaptation of mechanoelectrical transduction channels in cochlear outer hair cells. The Journal of physiology.
  • Hwang, S., He, Y., Xiang, X., Seo, W., Kim, S. J., Ma, J., ... & Kunos, G. (2019). Interleukin‐22 ameliorates neutrophil‐driven nonalcoholic steatohepatitis through multiple targets. Hepatology https://doi.org/10.1002/hep.31031.
  • Dumesic, P. A., Egan, D. F., Gut, P., Tran, M. T., Parisi, A., Chatterjee, N., ... & Dou, F. (2019). An Evolutionarily Conserved uORF Regulates PGC1α and Oxidative Metabolism in Mice, Flies, and Bluefin Tuna. Cell metabolism.
  • Liang, T., Zhang, H., Xu, Q., Wang, S., Qin, C., & Lu, Y. (2019). Mutant Dentin Sialophosphoprotein Causes Dentinogenesis Imperfecta. Journal of dental research, 0022034519854029.
  • Qian, W., Miner, C. A., Ingle, H., Platt, D. J., Baldridge, M. T., & Miner, J. J. (2019). A human STAT1 gain-of-function mutation impairs CD8+ T cell responses against gammaherpesvirus-68. Journal of virology, JVI-00307.
  • Kweon, S. M., Chen, Y., Moon, E., Kvederaviciutė, K., Klimasauskas, S., & Feldman, D. E. (2019). An Adversarial DNA N6-Methyladenine-Sensor Network Preserves Polycomb Silencing. Molecular Cellhttps://doi.org/10.1016/j.molcel.2019.03.018
  • 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.

Mouse/ Rat Models: Homologous Recombination Conditional Knockout Mouse 

  • Geraets, R. D. (2019). Neuronal Ceroid Lipfuscinosis: A Tailored Animal Model of CLN2 Disease and Evaluation of Select Personalized Therapies (Doctoral dissertation, ProQuest Dissertations Publishing).
  • 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 reports26(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 therapy. Human Molecular Genetics, 24(1), 185–196. http://doi.org/10.1093/hmg/ddu428.

For more journal references, please visit our comprehensive list of citations and reference publications.

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