Transgenic Mice: How They Are Made and Why They Matter
By Dr. Zubair Khalid, DVM, MS, PhD ·
Key Takeaways
- Transgenic mice are created by introducing foreign DNA (transgenes) into the germline, enabling heritable genetic alterations for studying gene function and disease modeling.
- Key methods for generating transgenic mice include pronuclear microinjection for random integration, embryonic stem cell-based homologous recombination for precise gene targeting (knockouts/knock-ins), and CRISPR/Cas9 for rapid, targeted genome editing.
- Conditional and inducible systems, such as Cre-loxP and Tet-On/Tet-Off, allow for spatiotemporal control of gene manipulation, crucial for studying essential genes or developmental processes without causing embryonic lethality.
- Transgenic mice serve as indispensable models for human diseases like cancer, neurodegenerative disorders (e.g., Alzheimer's, Parkinson's), and metabolic diseases (e.g., diabetes), facilitating preclinical drug development and target validation.
- Ethical considerations and stringent regulations, guided by the 3Rs principle (Replacement, Reduction, Refinement), govern the creation and use of transgenic mice to ensure animal welfare and scientific integrity.
- Technical challenges such as position effects, insertional mutagenesis, and genetic background variability necessitate careful experimental design and interpretation of results to accurately attribute phenotypes to the intended genetic modification.
What Are Transgenic Mice?
Definition and Basic Concept
A transgenic mouse is a laboratory mouse whose genome has been permanently altered through the deliberate introduction of foreign DNA. The term "transgenic" specifically refers to the stable integration of an exogenous DNA sequence—called a transgene—into the animal's germline, meaning the alteration is heritable and will be passed to subsequent generations. This is distinct from transient genetic modifications, where foreign DNA is expressed for a short period but not integrated into the chromosomes.
The transgene can originate from any species, including humans, bacteria, or even synthetic sequences designed in a computer. Once integrated, the transgene is replicated along with the mouse's own DNA during every cell division, and it is expressed according to regulatory elements (promoters and enhancers) that are either included in the construct or co-opted from the host genome at the integration site. The result is a living organism that carries a defined genetic alteration, allowing researchers to observe the consequences of that alteration in the context of a whole, developing, and behaving animal.
The purpose of creating transgenic mice is straightforward: to answer biological questions that cannot be addressed in cell culture or simpler organisms. A transgene can be designed to express a human protein implicated in disease, to knock out a gene of interest, or to report when a specific gene is active. Because mice are mammals with physiology, immune systems, and organ systems that closely parallel our own, they serve as the most practical bridge between molecular biology and human medicine.
Why Use Mice for Genetic Studies?
Mice are the dominant model organism in mammalian genetics for several concrete reasons. First, their generation time is short: a mouse reaches sexual maturity at 6–8 weeks, and a pregnancy lasts only about 19–21 days. This allows researchers to produce multiple generations within a single year, which is essential for breeding transgenic lines to homozygosity or for crossing multiple mutations together.
Second, mice are small and relatively inexpensive to house compared to larger mammals. A standard mouse facility can maintain thousands of animals, enabling statistically meaningful experiments. Third, the mouse genome is extensively characterized. The complete genome sequence has been available since 2002, and over 95% of mouse genes have a direct human ortholog—meaning they share a common evolutionary ancestor and often perform similar functions. This genetic conservation is why a mutation in a mouse gene can faithfully model a human disease caused by the equivalent mutation.
Fourth, mice have a well-developed reproductive biology that permits precise embryo manipulation. Fertilized eggs can be harvested, microinjected, cultured, and re-implanted into surrogate mothers with high success rates. Finally, the mouse immune system, hematopoietic system, and nervous system are sufficiently similar to humans that many therapeutic responses observed in mice—both positive and adverse—are predictive of human outcomes. This is why the vast majority of preclinical drug testing is performed in mice before any human trial begins.
A Brief History of Transgenic Mouse Technology
Early Discoveries
The conceptual foundation for transgenic animals was laid in the 1960s and 1970s, when researchers first demonstrated that foreign DNA could be introduced into mammalian cells in culture. The key breakthrough came in 1980, when Jon Gordon and Frank Ruddle reported the first successful production of transgenic mice by microinjecting foreign DNA into the pronucleus of a fertilized mouse egg. The injected DNA—a construct containing the herpes simplex virus thymidine kinase gene—was found to be integrated into the mouse genome and transmitted to offspring.
This landmark experiment was rapidly followed by the demonstration that transgenes could be expressed in a tissue-specific manner. In 1982, Richard Palmiter and Ralph Brinster created the famous "growth hormone mouse" by injecting a construct linking the mouse metallothionein promoter to the rat growth hormone gene. The resulting mice grew up to twice the normal size, proving that a foreign gene under the control of an appropriate promoter could be expressed at biologically meaningful levels. This experiment captured the imagination of both the scientific community and the public, and it established the basic paradigm of pronuclear microinjection that remains in use today.
The next major milestone came in 1987 with the development of gene targeting in embryonic stem (ES) cells. Mario Capecchi, Martin Evans, and Oliver Smithies independently developed methods to introduce precise mutations into specific genes in ES cells using homologous recombination—a process where the cell's own DNA repair machinery exchanges sequences between the introduced targeting vector and the corresponding chromosomal locus. These modified ES cells could then be injected into mouse blastocysts to generate chimeric animals, some of which would transmit the mutation through their germline. This technology enabled the creation of knockout mice, in which a specific gene is permanently inactivated, and it earned Capecchi, Evans, and Smithies the 2007 Nobel Prize in Physiology or Medicine.
Advancements in Gene Editing
The field was revolutionized again in 2013 with the application of CRISPR/Cas9 to mouse embryos. CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats) is a bacterial adaptive immune system that uses a guide RNA to direct the Cas9 nuclease to a specific DNA sequence, where it introduces a double-strand break. The cell then repairs this break either by error-prone non-homologous end joining (NHEJ), which typically introduces small insertions or deletions that disrupt the gene, or by homology-directed repair (HDR), which can incorporate a donor template carrying a desired mutation or transgene.
The power of CRISPR lies in its simplicity and speed. Whereas traditional ES cell targeting required months to construct targeting vectors and screen clones, CRISPR can generate a knockout mouse in a single step by injecting Cas9 protein, guide RNA, and a donor template directly into fertilized eggs. This has reduced the time required to generate a new transgenic line from over a year to as little as 6–8 weeks. CRISPR has also made it feasible to create complex modifications—such as introducing multiple point mutations simultaneously or tagging endogenous proteins with fluorescent markers—that were previously impractical.
How Transgenic Mice Are Created
Pronuclear Microinjection
Pronuclear microinjection is the classical method for creating transgenic mice that overexpress a foreign gene. The procedure begins with the collection of fertilized eggs from a donor female mouse that has been superovulated by hormone injection. At this stage, the egg contains two pronuclei—one from the mother and one from the father—which have not yet fused. The larger male pronucleus is the target for injection.
The DNA construct is prepared as a linear fragment containing the gene of interest, a promoter to drive its expression, and often a polyadenylation signal for mRNA stability. The construct is dissolved in a buffer (typically 10 mM Tris-HCl, 0.1 mM EDTA, pH 7.4) at a concentration of 1–5 ng/µL. Using a fine glass micropipette with a tip diameter of about 0.5 µm, the researcher injects approximately 1–2 picoliters of this solution directly into the pronucleus. The injected eggs are then cultured briefly to confirm viability and implanted into the oviduct of a pseudopregnant surrogate female.
The success rate is low—typically 10–30% of injected eggs develop into live pups, and of those, only 10–20% carry the transgene. The transgene integrates randomly into the genome, often as a concatemer (multiple copies arranged head-to-tail) at a single chromosomal site. Because integration is random, the expression level of the transgene depends on the site of integration—a phenomenon called position effect. Some integration sites are transcriptionally silent, while others produce very high expression. For this reason, multiple founder lines are generated and screened to select one with appropriate expression levels.
Embryonic Stem Cell Method
The ES cell method is the standard approach for creating precise genetic modifications, particularly knockouts and knock-ins. Embryonic stem cells are derived from the inner cell mass of a mouse blastocyst (a 3.5-day-old embryo) and can be maintained indefinitely in culture while retaining the ability to contribute to all tissues of an adult mouse, including the germline.
The process begins with the construction of a targeting vector—a piece of DNA containing a mutated version of the gene of interest flanked by regions of homology to the target locus. The vector also typically contains a positive selection marker, such as the neomycin resistance gene (neo), and a negative selection marker, such as the herpes simplex virus thymidine kinase gene (tk), positioned outside the homology arms.
The targeting vector is introduced into ES cells by electroporation, a procedure that uses a brief electrical pulse to create transient pores in the cell membrane. Cells that have incorporated the vector are selected using the drug G418, which kills cells lacking the neo gene. The negative selection with ganciclovir eliminates cells that have integrated the vector randomly rather than by homologous recombination, because random integrants retain the tk gene and are killed, while homologous recombinants have lost it.
Correctly targeted ES cell clones are identified by Southern blotting or PCR, then injected into a host blastocyst. The injected blastocyst is implanted into a surrogate mother, and the resulting pups are chimeras—mice composed of a mixture of cells derived from the host blastocyst and the injected ES cells. Chimeric males are bred to wild-type females, and offspring that inherit the modified gene from the ES cell-derived germline are identified by coat color markers or by genotyping. These heterozygous mice are then intercrossed to produce homozygous knockouts.
CRISPR/Cas9 Gene Editing
CRISPR/Cas9 has largely superseded both previous methods for many applications because of its speed and versatility. The core components are the Cas9 endonuclease and a single-guide RNA (sgRNA) that contains a 20-nucleotide sequence complementary to the target DNA, followed by a scaffold sequence required for Cas9 binding. The target sequence must be immediately followed by a protospacer adjacent motif (PAM), which for Streptococcus pyogenes Cas9 is the sequence NGG.
For generating a knockout, the Cas9 protein and sgRNA are injected into the cytoplasm or pronucleus of a fertilized egg. Cas9 introduces a double-strand break at the target site, which is repaired by NHEJ. This repair pathway frequently introduces small insertions or deletions (indels) that shift the reading frame and create a premature stop codon, effectively inactivating the gene. The resulting founder mice are screened by PCR and sequencing to identify those carrying frameshift mutations.
For generating a knock-in or a point mutation, a single-stranded oligodeoxynucleotide (ssODN) or a plasmid donor template is co-injected. This donor carries the desired sequence flanked by homology arms of 40–100 bases (for ssODN) or longer (for plasmid donors). The cell repairs the double-strand break by HDR, using the donor as a template and thereby incorporating the desired change. The efficiency of HDR is typically lower than NHEJ, often 5–20% of injected embryos, but this is still sufficient to generate founders in most cases.
One important advantage of CRISPR is that it can target multiple genes simultaneously by injecting several sgRNAs at once. This has enabled the rapid generation of mice carrying mutations in multiple genes, which would have required years of breeding using traditional methods. Additionally, CRISPR can be used to introduce large reporter constructs, such as a fluorescent protein gene, into a specific locus to track the expression of an endogenous gene.
Types of Transgenic Mice
Knockout Mice
Knockout mice have a specific gene permanently inactivated. The most common strategy is to replace a critical exon with a selection cassette, thereby deleting a portion of the coding sequence and preventing the production of a functional protein. Knockouts are used to determine the function of a gene by observing the phenotype that results from its absence.
The phenotypes can range from embryonic lethality—indicating the gene is essential for development—to subtle behavioral or metabolic changes that require careful assays to detect. For example, knockout of the p53 tumor suppressor gene results in mice that develop normally but are highly susceptible to spontaneous tumors, confirming p53's role as a guardian of the genome. Knockout of the ob gene, which encodes the hormone leptin, produces mice that are massively obese and diabetic, revealing the role of leptin in appetite regulation. The Knockout Mice resource provides a comprehensive overview of the various knockout strategies and their applications.
Knock-in Mice
Knock-in mice have a specific DNA sequence inserted into a defined location in the genome. This can be used to introduce a human disease-associated mutation into the corresponding mouse gene, creating a more faithful model of the human condition. For example, knock-in of the human APOE4 allele, a major risk factor for Alzheimer's disease, into the mouse Apoe locus produces mice that exhibit age-related cognitive deficits and amyloid pathology.
Knock-in technology is also used to tag endogenous proteins with fluorescent markers or epitope tags, allowing researchers to visualize protein localization and dynamics in living tissues. A common approach is to insert the sequence encoding green fluorescent protein (GFP) in frame with the target gene, so that a GFP-fusion protein is produced under the control of the endogenous promoter. This preserves the natural regulation of the gene while providing a visual readout of its expression.
Conditional and Inducible Systems
Conditional transgenic mice allow gene modification to be restricted to specific tissues or developmental time points. The most widely used system is the Cre-loxP recombination system. Cre is a bacteriophage-derived enzyme that recognizes specific 34-base-pair DNA sequences called loxP sites and catalyzes recombination between them. If two loxP sites are placed flanking a critical exon of a gene (creating a "floxed" allele), Cre-mediated recombination will delete that exon, inactivating the gene.
To achieve tissue-specific knockout, a researcher generates two mouse lines: one carrying the floxed allele and another expressing Cre under the control of a tissue-specific promoter. When the two lines are crossed, the gene is deleted only in cells where the promoter is active. For example, crossing a floxed Trp53 mouse with a mouse expressing Cre under the Albumin promoter (active only in hepatocytes) results in liver-specific p53 knockout, allowing the study of p53's role in liver cancer without the confounding effects of whole-body knockout.
Inducible systems add a temporal dimension. The most common is the CreER system, in which Cre is fused to a mutated estrogen receptor ligand-binding domain. This fusion protein is inactive until tamoxifen is administered, at which point it translocates to the nucleus and catalyzes recombination. This allows the researcher to inactivate a gene at a chosen time—for example, in adult mice—avoiding developmental compensation or embryonic lethality. The Tet-On/Tet-Off system is another inducible approach, where gene expression is controlled by doxycycline in the drinking water.
Applications of Transgenic Mice in Research
Disease Models
Transgenic mice have become indispensable for modeling human diseases. Cancer models are among the most advanced. The MMTV-PyMT mouse, which expresses the polyomavirus middle T antigen under the mouse mammary tumor virus promoter, develops metastatic mammary tumors with a predictable time course, making it a standard model for breast cancer research. Similarly, APC mutant mice develop intestinal polyps and are used to study colorectal cancer and to test chemopreventive agents.
Neurodegenerative disease models have been particularly valuable. Transgenic mice expressing the human APP gene with familial Alzheimer's disease mutations (such as the Swedish mutation, K670N/M671L) develop amyloid plaques and cognitive deficits. Mice expressing the human SNCA gene with the A53T mutation, associated with familial Parkinson's disease, develop Lewy body-like pathology and motor dysfunction. These models have been used to test potential therapies, including antibodies against amyloid-beta that have advanced to clinical trials.
Cardiovascular and metabolic disease models include the ApoE knockout mouse, which develops severe hypercholesterolemia and atherosclerosis when fed a high-fat diet, and the db/db mouse, which carries a mutation in the leptin receptor and serves as a model of type 2 diabetes. These models are used to study disease mechanisms and to evaluate new drugs before human testing.
Gene Function Studies
Beyond disease modeling, transgenic mice are fundamental tools for understanding basic gene function. The ability to knock out a gene and observe the resulting phenotype provides direct evidence of that gene's role in development, physiology, and behavior. Large-scale projects, such as the International Knockout Mouse Consortium, have generated knockout mice for nearly every gene in the mouse genome, providing a public resource for the scientific community.
Transgenic reporter mice are used to map gene expression patterns with cellular resolution. For example, mice expressing GFP under the control of the Nestin promoter label neural stem cells, allowing researchers to track their proliferation and differentiation in the adult brain. Lineage tracing experiments, in which a Cre-expressing mouse is crossed with a reporter mouse that permanently labels Cre-expressing cells and their descendants, have revealed the developmental origins of many cell types.
Drug Development and Testing
The pharmaceutical industry relies heavily on transgenic mice for target validation and preclinical efficacy studies. Before a drug candidate enters human trials, it must demonstrate efficacy in an animal model of the disease. Transgenic models provide the most relevant platforms for this testing because they recapitulate the genetic basis of the disease.
For example, the NOD/SCID mouse, which lacks functional T and B cells, is used to engraft human tumors for testing anticancer drugs. Humanized mice, which carry human immune system components, are used to evaluate immunotherapies such as checkpoint inhibitors. Transgenic mice expressing human drug-metabolizing enzymes, such as CYP3A4, are used to predict drug metabolism and toxicity in humans more accurately than wild-type mice.
Ethical Considerations and Regulations
Animal Welfare
The creation and use of transgenic mice raises significant ethical concerns that must be carefully weighed against the potential scientific and medical benefits. The primary concern is animal welfare. Some transgenic modifications cause pain, distress, or reduced quality of life. For example, mice engineered to develop aggressive tumors or severe neurodegeneration may experience significant suffering. Researchers are ethically and legally obligated to minimize this suffering through appropriate housing, analgesia, and humane endpoints—criteria that define when an animal must be euthanized to prevent prolonged distress.
The "3Rs" principle—Replacement, Reduction, and Refinement—guides the ethical use of animals in research. Replacement refers to using alternative methods where possible, such as cell culture or computer models. Reduction means using the minimum number of animals necessary to obtain statistically valid results. Refinement involves modifying procedures to minimize pain and distress. Transgenic mouse research must continually strive to meet these principles, for example by using non-invasive imaging to monitor disease progression rather than sacrificing animals at multiple time points.
Regulatory Oversight
In most countries, research involving transgenic mice is subject to strict regulation. In the United States, the Animal Welfare Act and the Public Health Service Policy on Humane Care and Use of Laboratory Animals require that all institutions receiving federal funding establish an Institutional Animal Care and Use Committee (IACUC). The IACUC reviews all animal protocols, inspects facilities, and ensures compliance with standards for housing, veterinary care, and experimental procedures.
In the European Union, Directive 2010/63/EU sets similar requirements, including a project authorization system that requires researchers to demonstrate the scientific justification for their work and to implement the 3Rs. Genetically modified animals are specifically addressed, and the creation of new lines requires approval from competent authorities. Additionally, the release of transgenic animals into the environment is regulated under separate legislation, such as the Cartagena Protocol on Biosafety, though in practice laboratory mice are never released.
Common Pitfalls and Misconceptions
Transgenic vs. Knockout
A frequent confusion is the distinction between "transgenic" and "knockout." While all knockout mice are genetically modified, not all are transgenic in the strict sense. A knockout created by deleting a mouse gene without inserting foreign DNA is not transgenic—it is a gene-targeted mouse. The term "transgenic" is properly reserved for animals carrying DNA from another species or synthetic DNA that is not naturally present in the mouse genome. In practice, however, the terms are often used loosely, and many knockout mice are also transgenic because the targeting vector leaves behind a selection cassette (such as neo) that is of bacterial origin.
Technical Challenges
Several technical pitfalls can compromise transgenic experiments. Position effects from random transgene integration can cause variable or absent expression. This is often addressed by generating multiple founder lines and selecting those with appropriate expression, but it remains a source of experimental variability. Insertional mutagenesis—where the transgene integrates into an endogenous gene and disrupts its function—can produce phenotypes unrelated to the transgene itself. This is a particular concern in pronuclear injection, where integration sites are random.
For knockout mice, the choice of which exons to delete is critical. Deleting a single exon may not completely inactivate the gene if alternative splicing produces a functional protein from the remaining exons. Similarly, the presence of a neo cassette can disrupt the expression of neighboring genes, confounding the phenotype. This is why modern approaches often use the Cre-loxP system to remove the selection cassette after targeting, leaving behind only a single loxP site.
Misinterpretation of Results
A common scientific pitfall is the assumption that a phenotype observed in a knockout mouse is directly caused by the loss of the target gene. In reality, compensatory mechanisms may mask the true function of the gene, or the phenotype may be influenced by genetic background. The strain of mouse used can dramatically affect the phenotype; for example, the ApoE knockout phenotype is more severe on a C57BL/6 background than on a 129 background. Researchers must therefore use appropriate controls, including littermates and mice on a defined genetic background.
Another misconception is that transgenic mice are "humanized" in the sense that they fully recapitulate human biology. In reality, a mouse carrying a human gene is still a mouse, and the physiological context differs substantially from humans. For example, a mouse expressing the human CFTR gene with the common ΔF508 mutation does not spontaneously develop the lung pathology seen in cystic fibrosis patients, because mouse lung physiology differs from human lung physiology. Researchers must therefore interpret results with caution and validate findings in multiple models.
Summary and Future Directions
Future of Transgenic Mouse Research
The future of transgenic mouse research lies in increasing precision and complexity. CRISPR-based technologies continue to improve, with base editing and prime editing allowing single-nucleotide changes without introducing double-strand breaks, reducing off-target effects. Large-scale projects are generating comprehensive resources, such as mice carrying conditional alleles for every gene, which will enable systematic studies of gene function across all tissues.
The development of humanized mouse models is advancing rapidly. Mice with human immune systems, human liver cells, or human gut microbiota are being used to study infectious diseases, cancer immunotherapy, and drug metabolism with unprecedented relevance to human health. The combination of transgenic technology with advanced imaging, single-cell genomics, and computational modeling promises to provide an even deeper understanding of how genes control physiology and disease.
As the technology evolves, so too will the ethical considerations. The ability to introduce multiple human genes into mice raises questions about the boundaries between species, and the potential for germline editing in humans—informed by mouse studies—demands careful public discourse. What is certain is that transgenic mice will remain an essential tool for translating genetic knowledge into medical practice for decades to come.
Frequently Asked Questions
What is the meaning of transgenic mice?
Transgenic mice are mice that have had foreign DNA deliberately inserted into their genome. This foreign DNA, called a transgene, is stably integrated into the mouse's chromosomes and is passed on to offspring. The transgene can come from another species, such as a human gene, or it can be a synthetic sequence designed in the laboratory.
What are transgenic mice used for?
Transgenic mice are used to study gene function, model human diseases, and test new therapies. By introducing a human disease-associated gene into mice, researchers can create animal models that mimic the human condition. Transgenic mice are also used to determine what a gene does by observing the effects of its overexpression or inactivation.
How are transgenic mice created?
There are three main methods. Pronuclear microinjection involves injecting DNA into the pronucleus of a fertilized egg. The embryonic stem cell method involves modifying ES cells in culture and injecting them into blastocysts. CRISPR/Cas9 gene editing involves injecting Cas9 protein and guide RNA directly into fertilized eggs to introduce precise changes at specific genomic locations.
Can you give examples of transgenic mice?
The "growth hormone mouse" created in 1982 carried a rat growth hormone gene and grew to twice normal size. The Oncomouse, developed in the 1980s, carried an activated oncogene and was predisposed to cancer. Modern examples include mice carrying human APP mutations for Alzheimer's disease research and mice expressing human CFTR mutations for cystic fibrosis studies.
What is the difference between transgenic and knockout mice?
A transgenic mouse carries foreign DNA inserted into its genome, often at a random location. A knockout mouse has a specific endogenous gene inactivated. Knockout mice are created by gene targeting or CRISPR and may or may not be transgenic, depending on whether foreign DNA remains in the genome. All knockout mice are genetically modified, but not all are transgenic in the strict sense.
Are transgenic mice genetically modified organisms (GMOs)?
Yes, transgenic mice are genetically modified organisms. They contain DNA that has been altered using genetic engineering techniques. As such, they are subject to regulations governing the creation, housing, and use of GMOs in research.
Do transgenic mice have health problems?
Some transgenic mice do have health problems, depending on the nature of the genetic modification. Mice engineered to develop diseases, such as cancer or neurodegeneration, will show symptoms of those diseases. However, many transgenic mice are healthy and show no obvious abnormalities. The health status of each line must be carefully monitored, and humane endpoints must be established to prevent unnecessary suffering.
Key Takeaways
- Transgenic mice carry foreign DNA stably integrated into their genome, enabling the study of gene function in a whole mammalian organism.
- The three main methods for creating transgenic mice are pronuclear microinjection, embryonic stem cell manipulation, and CRISPR/Cas9 gene editing.
- Knockout mice have a gene inactivated, knock-in mice have a specific sequence inserted, and conditional systems allow tissue-specific or time-controlled modifications.
- Transgenic mice are essential for modeling human diseases, studying gene function, and preclinical drug testing.
- Ethical use of transgenic mice requires adherence to the 3Rs principle and compliance with institutional and governmental regulations.
- Technical challenges include position effects, insertional mutagenesis, and genetic background effects that can confound results.
- Emerging technologies such as base editing and humanized mouse models are expanding the capabilities and applications of transgenic mouse research.
Further Reading
- Hickman-Davis JM, Davis IC. Transgenic mice. Paediatric respiratory reviews. 2006. PubMed 16473817
- Palmiter RD, Brinster RL. Transgenic mice. Cell. 1985. PubMed 298527480004-0)
- Babinet C, Morello D, Renard JP. Transgenic mice. Genome. 1989. PubMed 2698852
- Cory S, Adams JM. Transgenic mice and oncogenesis. Annual review of immunology. 1988. PubMed 2838049
- Kasatkina LA, Verkhusha VV. Transgenic mice encoding modern imaging probes: Properties and applications. Cell reports. 2022. PubMed 35613592
- Crawley JN et al. Galanin overexpressing transgenic mice. Neuropeptides. 2002. PubMed 12359505