Cat. No. ARG44032
The PEAR1 Knockout MDCK Cell Line is a CRISPR/Cas9-edited canine epithelial cell line providing a defined loss-of-function model for the platelet endothelial aggregation receptor 1. Derived from normal Madin-Darby Canine Kidney cells, this line retains the well-characterized polarized monolayer formation critical for adhesion and transport studies. PEAR1 transduces cell-cell and ECM signals via Src, PI3K, and Akt to regulate integrin ITGB1 activation and Rac1-driven actin remodeling, influencing epithelial junction integrity and platelet aggregation. This knockout is ideal for dissecting adhesion, migration, barrier function (TEER), and signaling (phospho-Akt) in epithelial biology, as well as for thrombosis research and anti-platelet drug screening.
| Host Cell | MDCK |
| Sex of Donor | Female |
| Age | Adult |
| Derived From Site | Kidney |
| Gene Name | PEAR1 |
| Gene Identifier | NCBI Gene ID 490403 |
| Morphology | Epithelial-like |
| Growth Mode | Adherent |
| Storage | Liquid nitrogen (LN2) |
| Temperature | 37°C |
| Atmosphere | 5% CO₂ |
| Sterility testing | The bacterial, yeast, and fungi are not detected in these cells by daily monitor. |
| Mycoplasma testing | Negative for mycoplasma through PCR analysis |
Intended Use: This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.
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This product is provided "AS IS". For Research Use Only. Not for human or animal therapeutic use.
The PEAR1 Knockout MDCK Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the Madin-Darby Canine Kidney (MDCK) epithelial cell lineage. This engineered line carries a targeted disruption of the PEAR1 gene, creating a straightforward loss-of-function platform for investigating PEAR1-dependent cellular processes. The knockout was generated using CRISPR/Cas9-mediated gene disruption, ensuring stable and heritable elimination of PEAR1 protein expression.
MDCK cells are a widely used polarized epithelial model established from normal adult canine kidney tissue. They form robust monolayers with well-defined apical and basolateral domains, exhibiting high transepithelial electrical resistance (TEER) and vectoral transport. This system is a gold standard for studying epithelial cell adhesion, tight junction assembly, membrane trafficking, and contact-dependent signaling. The non-transformed origin of MDCK cells makes them particularly suitable for dissecting signaling pathways without interference from oncogenic mutations.
PEAR1 is a type-1 transmembrane receptor that mediates cell-cell and cell-matrix interactions. Upon engagement by ligands such as integrin-binding ECM proteins, PEAR1 activates Src family kinases and PI3K, leading to Akt phosphorylation and downstream Rac1-dependent actin reorganization. This pathway promotes integrin activation (e.g., ITGB1) and focal adhesion dynamics, driving cell adhesion, spreading, and migration. PEAR1 associates with adaptors Shc and Grb2, forming signaling complexes that link to broader receptor tyrosine kinase-like cascades. In epithelial cells, PEAR1 tunes junctional stability and polarity, while in platelets and endothelium it governs aggregation and vascular integrity.
In the MDCK host, PEAR1 knockout enables direct study of its role in polarized epithelial biology. The non-transformed MDCK line forms tight monolayers, allowing clean evaluation of how PEAR1 loss affects barrier function, cell adhesion, and migration. Researchers can characterize changes in TEER, junctional protein localization, and actin dynamics without interference from oncogenic signaling. This model is thus ideal for dissecting PEAR1??s contribution to epithelial morphogenesis and wound healing.
This knockout line is suited for a wide range of assays: Western blotting and phospho-Akt profiling to confirm signaling deficits; immunofluorescence for junctional and cytoskeletal markers; co-immunoprecipitation to probe Src/PI3K complexes; and functional tests like TEER, scratch migration, and adhesion assays. Applications extend to platelet aggregation studies, thrombosis research, and drug screening for anti-platelet therapies. Cancer metastasis models also benefit from exploring how PEAR1 influences epithelial barrier breakdown. For further details, contact Ascent Research.
