The KTN1 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the KTN1 gene has been disrupted. Targeted Cas9-mediated cleavage and subsequent repair produce a heterogeneous pool of KTN1 alleles, eliminating the requirement for single-cell cloning. This population provides an immediate and robust platform to investigate kinectin-dependent functions.
The HEK293T cell line is an adherent epithelial line derived from human embryonic kidney cells and stably expresses the SV40 large T antigen. These cells are favored for their high transfection efficiency, rapid proliferation, and exceptional capacity for protein overexpression and lentiviral production, making them an ideal host for CRISPR-based knockout models.
KTN1 codes for kinectin, a transmembrane kinesin receptor that anchors the kinesin-1 motor (KIF5B) to cargo vesicles, thus directing microtubule-dependent organelle transport. Kinectin also governs cell adhesion and spreading by coupling to integrin signaling through integrin-linked kinase and integrin ??1 at focal adhesions. Regulatory inputs include phosphorylation by Src kinase and modulation by kinesin light chain. Downstream, KTN1 controls organelle positioning, ER network architecture, and cell migration. Its interactome encompasses Rab GTPases, dynactin, and dynein, positioning kinectin at a critical junction between motor-based trafficking and adhesion dynamics.
KTN1 ablation in HEK293T cells provides a simplified model for dissecting microtubule-dependent transport and adhesion without the confounding variables of neuronal systems. The cells?? well-characterized ER and focal adhesion structures facilitate direct analysis of trafficking aberrations and motility defects. As a polyclonal knockout pool, this product reduces clone-specific artifacts and is well suited for transient rescue experiments with KTN1 mutants to map functional domains.
Researchers can confirm KTN1 disruption via western blotting and examine organelle distribution and focal adhesion composition by immunofluorescence. Functional assays like wound healing and Transwell migration enable quantitative motility assessment, while co-immunoprecipitation clarifies altered protein interactions. Live-cell imaging reveals kinetic defects in organelle dynamics. Given KTN1??s associations with cancer metastasis and neurodegeneration, this model supports disease-oriented research. For technical details or a quotation, please contact Ascent Research.
