Ace Therapeutics specializes in providing custom Lmx1b mutant mouse models to support glaucoma research. Our genetic mouse models are robust tools that enable researchers to explore the molecular mechanisms of glaucoma and develop innovative therapeutics.
The Significance of Lmx1b in Glaucoma
Glaucoma is commonly linked to elevated intraocular pressure (IOP), primarily caused by impaired aqueous humor outflow through the trabecular meshwork (TM). LMX1B is a LIM-homeodomain transcription factor that is indispensable for the proper development and function of this anterior segment outflow pathway. Mutations in the human LMX1B gene are linked to inherited conditions such as Nail-Patella Syndrome (NPS), with approximately 30–40% of NPS patients developing elevated IOP and primary open-angle glaucoma (POAG). Mutations in Lmx1b can lead to structural abnormalities of the TM and cornea, leading to impaired aqueous humor outflow, elevated IOP, and contributing to the pathogenesis of glaucoma.
Fig.
1 Deletion of Lmx1b in the periocular mesenchyme leads to multiple phenotypes in ocular anterior segment.
(Liu P and Johnson R L, 2010)
Custom Lmx1b Mutant Mouse Models for Glaucoma Research
Ace Therapeutics offers Lmx1b mutant mouse models that recapitulate glaucoma-related phenotypes found in humans.
Lmx1b Conditional Knockout Mouse Models of Glaucoma
To overcome the limitations of embryonic lethality, our scientific team is dedicated to establishing Lmx1b conditional knockout models. We employ Cre-loxP–mediated conditional knockout strategies, including tissue-specific promoter-driven inducible systems, to achieve cell-type–specific and temporally controlled deletion of Lmx1b. Our conditional knockout models serve as powerful tools for investigating the impacts of Lmx1b deficiency on ocular anterior segment development at different stages.
Ocular-specific knockout of Lmx1b
We can generate lens- or cornea-specific Lmx1b knockout mouse models that recapitulate human NPS-associated glaucoma phenotypes and retain normal postnatal viability.
Adult-inducible knockout of Lmx1b
We offer inducible Lmx1b knockout mouse models that enable targeted gene deletion in adult mice, supporting studies on its role in maintaining the structure and function of mature anterior segment tissues, including the cornea and TM.
Mouse Models with Dominant-Negative Lmx1b Mutations
Our mouse models with dominant-negative Lmx1b mutations recapitulate human glaucoma-associated variants and exhibit spontaneous glaucoma-like phenotypes, including elevated IOP, anterior segment defects, and optic nerve damage.
Comprehensive Preclinical Services Supported by Lmx1b Mutant Mouse Models
Our preclinical services leverage Lmx1b mutant mouse models to help researchers investigate glaucoma pathogenesis and evaluate therapeutic efficacy.
Lmx1b Mutant Mouse Model Evaluation Services
| Services | Details |
|---|---|
| Ocular phenotyping | Detailed non-invasive and invasive assessments, including slit-lamp microscopy, gonioscopy, and IOP measurement. | Histopathology & microscopy | Microscopic evaluation of anterior segment morphology, TM structure, and developmental defects. | Glaucomatous neurodegeneration assessment | Quantification of optic nerve damage and retinal ganglion cell (RGC) loss. |
Drug Efficacy Evaluation Services
We utilize Lmx1b mutant mouse models to evaluate the efficacy of novel glaucoma therapeutics, including IOP-lowering agents, neuroprotective compounds, and other disease-modifying strategies.
With deep expertise in custom Lmx1b mutant mouse models and integrated preclinical capabilities, Ace Therapeutics provides the critical tools and support to facilitate your glaucoma research. Contact us today to discuss your glaucoma projects with our scientists!
Reference
- Liu P and Johnson R L. Lmx1b is required for murine trabecular meshwork formation and for maintenance of corneal transparency. Dev Dyn, 2010, 239(8): 2161-2171.