App Knockout mouse models
App encodes amyloid precursor protein, the mouse ortholog of human APP, a type I transmembrane glycoprotein with E1 and E2 ectodomain modules that is either cleaved by ADAM10 within the Aβ sequence, precluding amyloid, or processed sequentially by BACE1 and the presenilin-containing γ-secretase complex to liberate Aβ40, Aβ42 and the AICD transcriptional fragment. Familial Alzheimer alleles act by shifting that competition: Swedish KM670/671NL enhances BACE1 cleavage, London V717I raises the Aβ42 to Aβ40 ratio, Arctic E22G accelerates protofibril assembly, and Icelandic A673T is protective. Rodent Aβ differs from human at three residues (Arg5, Tyr10, His13) and aggregates poorly, so humanizing the Aβ-coding exons in place, rather than transgenic overexpression, is the design that preserves endogenous promoter control and copy number. Aplp1 and Aplp2 compensate broadly, and App with Aplp2 double nulls die perinatally, so plan compound genetics when synaptic and neuromuscular endpoints accompany plaque and cerebral amyloid angiopathy readouts.
Global App deletion answers broad mechanism questions quickly. If timing or site matters, conditional alleles are a natural next step after the null is characterized.
What App Knockout mouse models are available?
ingenious targeting laboratory offers 1 distinct App 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 |
|---|---|---|---|---|---|
| App-KO | Knockout | KO/CKO mice, disease model mice | sperm cryopreservation | KO 190444 | Inquire |
Designing a App Knockout allele
A null tells you what APP does, not what amyloid does, and the two are routinely confused. Germline deletion is viable with reduced body weight, subtle gliosis, impaired long-term potentiation, and a lowered seizure threshold, phenotypes muted because Aplp1 and Aplp2 carry overlapping functions. Because deleting the gene removes the Abeta source entirely, this allele cannot model Alzheimer pathology; it is a loss-of-function and specificity resource. Its best uses are as an absolute negative control for anti-APP and anti-Abeta antibodies, for BACE1 and gamma-secretase substrate specificity work, and as the base for compound crosses with Aplp1 or a conditional Aplp2 allele. Delete the entire coding region so no secreted fragment remains, since soluble APP alpha is itself bioactive. Endpoints are fragment-level protein confirmation, hippocampal electrophysiology, grip and rotarod performance, and Aplp1 and Aplp2 compensation measured directly.
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 App 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 App 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 App Knockout mouse models are available?
When App 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 App knockout embryonic lethal in mice?
It depends on background and allele design. Some App 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 App 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 App?
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.
Related models and routes
Citations
- Spatial Mapping of CoQ10 Repletion by BPM31510 in a Genetic Mouse Model (Coq4F147C) of Coenzyme Q Deficiency
- Increased Neuronal Expression of the Early Endosomal Adaptor APPL1 Replicates Alzheimer's Disease-Related Endosomal and Synaptic Dysfunction with Cholinergic Neurodegeneration
- Six distinct NFκB signaling codons convey discrete information to distinguish stimuli and enable appropriate macrophage responses
- Caspase Activation and Caspase-Mediated Cleavage of APP Is Associated with Amyloid β-Protein-Induced Synapse Loss in Alzheimer’s Disease
- Multi-image color refinement with application to disparity estimation