Trp53 Conditional Knockout mouse — liver specific context
Trp53 is the guardian of the genome. Stress signals push this tumor suppressor toward cell cycle arrest, senescence, or apoptosis, so the pathway sits at the center of cancer biology. Mouse models let you test somatic mutation timing, cooperation with Kras or Myc, and therapeutic windows in DNA damage driven disease. Conditional alleles matter because complete loss can reshape development while adult onset deletion better mirrors human oncology. Humanized and point mutant variants support antibody and small molecule programs where epitope fidelity matters.
Conditional deletion of Trp53 limits genetic change to the lineage you choose. That precision matters for oncology, immunology, and metabolic work where systemic loss would confound interpretation. After you confirm your Cre specificity, crossing to Trp53 floxed stock yields interpretable cohorts. For liver work, plan Cre specificity, reporter crosses, and baseline phenotyping before you scale.
Catalog options
Conditional knockout keeps liver as the experimental theater while the rest of the animal retains a wild type allele. That pattern mirrors somatic mutation in patients and avoids systemic compensation that can erase subtle phenotypes. It is often preferred when a germline null is lethal, weak, or confounded by developmental rescue.
| Model | Type | Category | Availability | Catalog # | |
|---|---|---|---|---|---|
| Trp53-Frox | Conditional Knockout | KO/CKO mice, disease model mice | sperm cryopreservation | CKO 190067 | Inquire |
| Trp53-Flox/Kras-LSL-G12D | Conditional Knockout | KO/CKO mice,point mutantion mice | live | CKO 233079 | Inquire |
| Trp53-Flox | Conditional Knockout | KO/CKO mice, disease model mice | live | CKO 18005 | Inquire |
Why this approach
Conditional knockout keeps neuron as the experimental theater while the rest of the animal retains a wild type allele. That pattern mirrors somatic mutation in patients and avoids systemic compensation that can erase subtle phenotypes. It is often preferred when a germline null is lethal, weak, or confounded by developmental rescue.
Build timeline and pricing
Expect roughly twenty six weeks to study ready animals for many standard conditional crosses after contract start. We return quotes in about twenty four hours and map milestones for genotyping, QC, and dispatch.
Open the request quote formFAQ
How long does a Trp53 conditional knockout project take?
Most custom conditional knockout projects run near twenty six weeks from contract activation to study ready animals when breeding is straightforward. Complex humanization or multi allele stacks can add time. We return detailed quotes within about twenty four hours so you can align cohort start dates with grant or IND milestones.
Is Trp53 knockout embryonic lethal in mice?
Lethality depends on genetic background and exact allele design. Some Trp53 germline knockouts are viable, others require conditional alleles or mixed backgrounds. We review publications and our own experience, then recommend floxed versus null approaches before you commit.
Which Cre driver is best for liver specific focused experiments?
Driver choice depends on onset timing, recombination efficiency, and known leak patterns. We map your organ and cell type to a short list of proven Cre lines, then discuss reporter crosses and controls. Your query highlights liver specific as a primary axis, which we treat as the starting point for driver selection.
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 custom project with cryo or live dispatch options depending on cohort timing and geography.
How do I request a quote for Trp53?
Use the catalog inquire buttons or the request quote form with 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.