Tsc1 Conditional Knockout mouse models
Hamartin, the product of Tsc1 (mouse ortholog of human TSC1), stabilizes tuberin and TBC1D7 within the TSC complex, the RHEB-directed GTPase-activating module that clamps mTORC1 at the lysosomal surface; growth factor signaling through AKT, ERK, and RSK phosphorylates the complex to relieve this restraint, whereas AMPK reinforces it under energy stress. Loss-of-function alleles produce tuberous sclerosis complex with cortical tubers, subependymal giant cell astrocytoma, angiomyolipoma, and pulmonary lymphangioleiomyomatosis, all driven by constitutive S6K1 and 4E-BP1 phosphorylation. Since homozygous deletion is embryonic lethal from liver hypoplasia and neural tube defects, mechanistic work depends on floxed exons combined with Nestin, Emx1, Synapsin, or Pax8 Cre, while heterozygotes serve tumor predisposition studies. Critically, Tsc1 and Tsc2 are obligate partners rather than redundant paralogs, so hamartin loss destabilizes tuberin and no compound genetics can rescue; align allele class with rapamycin sensitivity or seizure and lesion endpoints.
Tissue restricted knockout of Tsc1 keeps wild type function everywhere else. Breeding is often more robust, and the setup mirrors patient biology where mutations arise in a subset of cells.
What Tsc1 Conditional Knockout mouse models are available?
ingenious targeting laboratory offers 1 distinct Tsc1 conditional 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 |
|---|---|---|---|---|---|
| Tsc1-Flox | Conditional Knockout | KO/CKO mice, disease model mice | live | CKO 200231 | Inquire |
Why this approach
Conditional knockout focuses the experiment on your target tissue while the rest of the animal keeps 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.
Pricing and quotes
The Tsc1 Conditional 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 Tsc1 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 Tsc1 Conditional Knockout mouse models are available?
When Tsc1 Conditional 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 Tsc1 knockout embryonic lethal in mice?
It depends on background and allele design. Some Tsc1 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 Tsc1 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 Tsc1?
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.