The KIF13A Knockout NCI-H1975 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the KIF13A gene in the human NCI-H1975 cell line. This product provides a mixed population of cells carrying genetic disruptions at the target locus, offering a loss-of-function model for studying KIF13A-dependent processes without clonal isolation. The polyclonal format retains genetic heterogeneity while enabling robust functional studies, suitable for assays where population-level effects are assessed.
The host cell line NCI-H1975 is a well-characterized human non-small cell lung adenocarcinoma line harboring activating EGFR mutations (L858R and T790M), commonly used to model acquired resistance to first-generation tyrosine kinase inhibitors. These cells exhibit epithelial morphology and serve as a relevant in vitro system for investigating signaling pathways, drug responses, and metastatic mechanisms in lung cancer. Their genetic background makes them particularly valuable for studying how KIF13A-mediated trafficking influences oncogenic signaling and therapeutic sensitivity.
KIF13A encodes a plus-end-directed kinesin-3 motor protein that transports cargo along microtubules, playing critical roles in endosomal trafficking, melanosome distribution, and regulation of Wnt signaling. The motor interacts with the AP-1 adaptor complex and BLOC-3 to tether melanosomal cargoes such as TYRP1, while Rab GTPases (including Rab11) and phosphoinositides regulate its recruitment to membranes. KIF13A also facilitates the trafficking of endosomal receptors and cell adhesion molecules, linking it to pathways that govern cell migration and intercellular communication. Disruption of KIF13A is therefore expected to impair cargo delivery, altering the subcellular localization of key proteins and downstream signaling events.
In the NCI-H1975 background, knockout of KIF13A may significantly impact intracellular transport dynamics, potentially dysregulating melanogenesis-related signaling??though these cells are not melanocytic, kinesin-mediated trafficking is broadly implicated in cancer cell motility and metastasis. Given the role of KIF13A in Wnt signaling modulation, its loss could influence ??-catenin-dependent transcription and associated pro-metastatic programs. This model thus allows dissection of how microtubule-based transport contributes to lung adenocarcinoma progression, particularly in processes such as cell adhesion turnover, invadopodia formation, and response to EGFR-targeted therapies.
Researchers can employ this polyclonal knockout population in a variety of experimental contexts. Immunofluorescence imaging of organelle markers can reveal altered distributions of endosomes or lysosomes, while live-cell imaging of fluorescently tagged cargo provides real-time trafficking analysis. Migration and invasion assays, such as wound healing and Transwell assays, help assess the role of KIF13A in cell motility. Biochemical approaches, including western blotting for cargo proteins like TYRP1 and co-immunoprecipitation of motor-adaptor complexes, validate molecular interactions. Furthermore, this model is suitable for trafficking-based drug screening to identify compounds that modulate kinesin activity. For detailed technical specifications and ordering information, please contact Ascent Research.
