Trp53 Knockout mouse models
Trp53, the mouse ortholog of human TP53, encodes the tetrameric transcription factor whose central DNA-binding core reads p53 response elements at Cdkn1a, Mdm2, Bbc3, Pmaip1, and Zmat3, coupling ATM and ATR phosphorylation of the amino-terminal transactivation domains to arrest, senescence, and mitochondrial apoptosis while MDM2 and MDM4 impose continuous ubiquitin-dependent turnover. Because most human alleles are missense rather than deleted, the design fork is decisive: conditional or germline nulls model pure suppressor loss and yield thymic lymphoma and sarcoma, whereas structural and contact hotspot knockins such as R172H and R270H (human R175H and R273H) confer dominant-negative and gain-of-function metastatic behavior that a null never reproduces. Lox-stop-lox and restorable alleles interrogate reactivation therapeutics, and humanized TP53 supports MDM2 inhibitor and mutant-reactivator pharmacology. Note that Trp63 and Trp73 share response elements and can buffer apoptotic output, so match allele class to tumor spectrum, latency, and drug response endpoints deliberately.
Trp53 null animals are straightforward to genotype and phenotype when survival is acceptable. They remain a standard background for pharmacology, biomarker, and rescue studies.
What Trp53 Knockout mouse models are available?
ingenious targeting laboratory offers 4 distinct Trp53 (TP53) knockout catalog mouse models. Researchers can order pre-developed catalog lines or request a custom mouse model, including humanized, knockin, and transgenic variations with verified germline transmission.
Catalog table
| Model | Type | Category | Availability | Catalog # | Action |
|---|---|---|---|---|---|
| Trp53-KO(2) | Knockout | KO/CKO mice, disease model mice | embryo cryopreservation | KO 191203 | Inquire |
| Trp53-KO(5) | Knockout | KO/CKO mice | live | KO 250665 | Inquire |
| Trp53-KO | Knockout | KO/CKO mice | live | KO 00011 | Inquire |
| Trp53-KO/Nf1-Flox | Knockout | KO/CKO mice | sperm cryopreservation | KO 242359 | Inquire |
Designing a Trp53 Knockout allele
Unlike most genes on this list, complete germline deletion of Trp53 is compatible with development, which makes the straight null the cheapest sensitizing background available and the correct choice when the question is suppressor dosage rather than tissue of origin. Homozygotes die of thymic lymphoma within roughly six months; heterozygotes live longer and develop osteosarcoma and soft tissue sarcoma after losing the remaining allele, which is the closest genetic mimic of Li-Fraumeni syndrome. Two caveats govern interpretation. Strain background shifts the spectrum substantially, so cohorts must be backcrossed and reported, and a fraction of female homozygotes show exencephaly, meaning expected Mendelian ratios at weaning are not a reliable genotyping check. Confirm loss of heterozygosity by sequencing or allele-specific PCR in heterozygote tumors, and report survival as a spectrum-annotated curve rather than a single median.
A conventional knockout answers whether the gene is required broadly. When your target tissue is the organ of interest, a global null can still be informative if viability is acceptable and you want the simplest genotype. If the null is harsh, a floxed allele with a regional Cre is the safer long term platform.
Pricing and quotes
The Trp53 Knockout lines listed above are catalog models. Send us the catalog number and our team confirms current availability, pricing, and whether the line ships cryopreserved or live.
If your study needs a Trp53 allele configuration that is not listed above, our scientific team designs and generates it. Model generation quotes return in about twenty four hours with project milestones and pricing.
FAQ
What Trp53 Knockout mouse models are available?
When Trp53 Knockout lines are in catalog, we ship from inventory. If your configuration is not listed, we design the allele to order. Common paths include conditional knockout, constitutive knockout, humanized, knockin, and transgenic options, with documented germline transmission and United States QC.
Is Trp53 knockout embryonic lethal in mice?
It depends on background and allele design. Some Trp53 germline knockouts are viable. Others need conditional alleles or mixed backgrounds. We review publications and our own experience, then recommend floxed versus null before you commit.
Which Cre driver is best for experiments?
Driver choice depends on onset timing, recombination efficiency, and known leak. We map your organ and cell type to a short list of proven Cre lines, then talk through reporter crosses and controls. We favor drivers with strong community validation for your tissue.
Do you ship live Trp53 animals?
When catalog lines are live, we ship with health certificates and QC documentation. If your exact combo is not listed, we quote a generation project with cryo or live dispatch depending on cohort timing and geography.
How do I request a quote for Trp53?
Use the catalog inquire buttons or the request quote form. Include your allele goal, Cre plan if any, strain background, and cohort size. A PhD led team responds with pricing, milestones, and the fastest path to experimental animals.