Conventional / global / constitutive KO
We build the exact model your study needs.
Designed and delivered by ingenious targeting laboratory. Quote in 24 hours.
Browse 3 Tlr7 mouse models including conditional knockout, knockin, knockout variants — in stock and ready to ship from ingenious targeting laboratory. Available as Tlr7 conditional knockout mouse, Tlr7 knockin mouse, Tlr7 knockout mouse. Request a quote within 24 hours.
Tlr7 is the mouse ortholog of human TLR7 and encodes an endosomal receptor that requires UNC93B1 for trafficking and proteolytic maturation, then senses single-stranded RNA degradation products through two cooperating sites, one binding guanosine or synthetic agonists such as imiquimod and R848 and a second binding short uridine-containing oligoribonucleotides, with dimerization driving MyD88, IRAK4, and IRF7 dependent type I interferon in plasmacytoid dendritic cells. Dosage is central to disease logic: the Yaa locus duplication of Tlr7 accelerates murine lupus, human gain of function substitutions such as Y264H that increase guanosine affinity cause childhood systemic lupus erythematosus, and escape from X inactivation raises expression in females. Design accordingly, using conditional nulls to assign requirement to plasmacytoid dendritic cells or B cells, copy-number or point-mutant knockins for gain of function, and humanized alleles for agonist pharmacology. Tlr8 and Tlr9 overlap in nucleic acid sensing, so target autoantibody, interferon signature, or adjuvant endpoints.
ingenious targeting laboratory offers 3 distinct Tlr7 (TLR7) catalog mouse models, featuring conditional knockout, standard knockout, and knockin. Researchers can order pre-developed catalog lines or request a custom mouse model, including humanized, knockin, and transgenic variations with verified germline transmission.
| Model Availability | Allele Class Options |
|---|---|
| 3 Ready Catalog Lines | Conditional Knockout (cKO) |
| Custom Model Generation | Constitutive Knockout (KO) |
| Advanced Modifications | Humanized, Knockin, Transgenic |
Knockout
Conditional knockout
Knockin
Humanized
Transgenic / overexpression
Prefer the order form? Order. Need an allele that is not listed? Request a quote.
Knockout, conditional, knockin, humanized, and related paths for Tlr7 (human TLR7). Catalog lines ship when inventory exists. Everything else is a generation quote.
Specify tissue or Cre driver on quote
Convertible floxed allele pathway
Multi allele / compound knockout project
BAC scale deletion or targeting
LSL or conditional expression knockin
Domain or partial humanization scope
Checkpoint IO humanization when gene is a checkpoint target
Multi humanized / combination IO project
BAC transgenic or large fragment insert
Tamoxifen or dox inducible Cre
Dual recombinase breeding scheme
Flp or FRT derivative allele pairing
Catalog reporter lines not tied to a single gene allele
Specify rat on quote
Specify rabbit on quote
Background substrain on quote
Background strain on quote
3 Tlr7 lines with QC documentation and technical support. Tlr7 floxed mice use loxP flanked alleles for Cre dependent tissue specific knockout.
We have 3 Tlr7 models in stock — including Conditional Knockout, Knockin, Knockout types. In stock and ready to ship this week. All models come with full QC documentation, health certificates, and dedicated technical support.
Best pricing in the industry. Get a quote in 24 hours. Our team of PhD scientists is available to help you select the right model for your research.
Order catalog modelA Tlr7 knockout mouse has the Tlr7 gene permanently inactivated, enabling loss of function studies. A Tlr7 conditional knockout (floxed) mouse carries loxP sites flanking a critical exon of Tlr7, allowing Cre recombinase dependent deletion in specific tissues or at specific timepoints. Tlr7 knockin models carry a precisely inserted sequence at the Tlr7 locus, useful for reporter, tag, or humanization studies.
Jump to catalog backed pages for Tlr7 organized by modification type. Each URL is indexable and matches common search patterns.