Myc Knockout mouse models
Myc, the mouse ortholog of human MYC, encodes a basic helix-loop-helix leucine zipper transcription factor that heterodimerizes with Max to occupy E-box CACGTG elements, recruiting Trrap, Gcn5, and P-TEFb to release paused RNA polymerase II and thereby amplifying the existing transcriptional program rather than imposing a single target signature; it also represses through Miz1. Protein stability is governed by a phosphodegron in which Erk-driven Ser62 phosphorylation primes Gsk3-mediated Thr58 phosphorylation, creating the Fbxw7 recognition site, while Aurora kinase A binding and Usp28 oppose turnover. Homozygous nulls die at mid-gestation, so conditional deletion is required, and allele class maps to distinct questions: a Thr58Ala knockin isolates degradation control, tetracycline-regulated or Lox-Stop-Lox overexpression tests reversibility and tumor maintenance, and humanization supports epitope-dependent reagents. Mycn and Mycl are paralogs with restricted expression that can substitute when knocked into the Myc locus, so dosage and driver choice determine the phenotype observed.
Whole body loss of Myc gives the clearest readout when the question is whether the gene is required at all. Follow up tissue work can still move to a conditional allele if lethality or compensation appears.
What Myc Knockout mouse models are available?
ingenious targeting laboratory offers 1 distinct Myc knockout catalog mouse model. 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 |
|---|---|---|---|---|---|
| Myc-KO | Knockout | KO/CKO mice | sperm cryopreservation | KO 225067 | Inquire |
Designing a Myc Knockout allele
A germline Myc null is a developmental reagent, not a cohort. Homozygotes arrest around embryonic day 9.5 to 10.5 with defective yolk sac vasculature, failed primitive erythropoiesis, and cardiac and neural tube abnormalities, and the vascular defect is largely non-cell-autonomous, which means embryo phenotypes cannot be read as a direct cell-intrinsic requirement. The heterozygote is the more interesting animal and is often overlooked: reduced dosage yields smaller mice with altered metabolic and inflammatory profiles and extended median lifespan, which makes it a clean tool for asking what tonic Myc levels cost an organism. If a homozygous null cell is what you need, derive it rather than breed it, using inducible deletion in cultured fibroblasts or stem cells so the acute transcriptional collapse can be captured before compensation. Score embryos by precise somite staging and whole-mount vascular labeling, not gross morphology.
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 Myc 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 Myc 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 Myc Knockout mouse models are available?
When Myc 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 Myc knockout embryonic lethal in mice?
It depends on background and allele design. Some Myc 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 Myc 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 Myc?
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.
Citations
- MYCT1-IFITM2/3 interaction links endothelial endolysosomal trafficking to white adipose tissue expansion
- The X-Linked Helicase DDX3X Is Required for Lymphoid Differentiation and MYC-Driven Lymphomagenesis.
- Myc-induced nuclear antigen constrains a latent intestinal epithelial cell-intrinsic anthelmintic pathway
- The Myc 3′ Wnt-responsive element regulates homeostasis and regeneration in the mouse intestinal tract.