The DNAJC13 Knockout NCI-H1299 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population derived from the NCI-H1299 human non-small cell lung carcinoma cell line, featuring targeted disruption of the DNAJC13 gene. This polyclonal knockout product provides a heterogeneous pool of cells harboring diverse loss-of-function edits, enabling robust functional studies without clonal artifacts. The pool is designed for researchers investigating DNAJC13-dependent processes in a cancer cell background.
NCI-H1299 is an adherent epithelial cell line originally isolated from a lymph node metastasis of a lung carcinoma, widely used as a model for non-small cell lung cancer (NSCLC). These cells carry a TP53 mutation, which contributes to their transformed phenotype and makes them a relevant system for studying oncogenic signaling and metastatic mechanisms. The TP53-mutant background also influences endocytic trafficking and stress responses, providing a context for exploring how DNAJC13 integrates with tumor cell biology.
DNAJC13 encodes a DnaJ/Hsp40 family co-chaperone that recruits the Hsc70 chaperone (HSPA8) to endosomes, facilitating clathrin uncoating and retromer-mediated cargo sorting. DNAJC13 interacts with core retromer components VPS35 and sorting nexins SNX1/SNX2, and its activity is regulated by the unfolded protein response and Hsc70/Hsp70 activity. Downstream, it influences clathrin coat dynamics, retromer complex stabilization, and recycling of receptors such as those in the Wnt pathway. Disruption of DNAJC13 impairs endosomal trafficking, potentially altering the surface expression of key receptors involved in proliferation and migration.
In the NCI-H1299 NSCLC context, DNAJC13 knockout is expected to perturb endosomal sorting and receptor recycling, which may affect tumor cell migration, invasion, and signaling downstream of growth factor receptors. Given the TP53-mutant background, this model allows dissection of how endocytic dysfunction intersects with genomic instability and oncogenic pathways. Additionally, since DNAJC13 has been linked to Parkinson disease, these cells provide a cancer-based platform to study conserved trafficking mechanisms relevant to neurodegeneration.
Researchers can employ this polyclonal knockout pool in a variety of assays, including western blotting and RT-qPCR to confirm loss of DNAJC13 expression, immunofluorescence to visualize endosomal marker redistribution, and clathrin-mediated endocytosis assays to measure cargo uptake deficits. Co-immunoprecipitation and flow cytometry can determine alterations in receptor surface levels and retromer complex assembly. Migration and invasion assays can assess the functional impact on metastatic behavior. For further information or technical support, please contact Ascent Research.
