The ATG16L1 Knockout 769-P Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the 769-P human renal cell carcinoma line, with targeted disruption of the ATG16L1 gene. This gene-edited pool provides a heterogeneous loss-of-function model for investigating ATG16L1-dependent processes in a cancer-relevant epithelial background. The polyclonal format captures diverse genetic modifications across the cell population, enabling robust assessment of autophagy-related phenotypes without clonal selection bias.
The parental 769-P cell line originates from a primary clear cell renal cell carcinoma of a 63-year-old male, displaying characteristic epithelial morphology. As a widely used clear cell RCC model, 769-P cells retain key oncogenic and metabolic features of kidney cancer, making this knockout system valuable for exploring tumor cell biology, drug response, and autophagy-mediated survival mechanisms in a clinically relevant context.
ATG16L1 is a core component of the autophagy machinery that forms an essential complex with the ATG5-ATG12 conjugate. This complex functions as an E3-like ligase for LC3 lipidation, driving autophagosome elongation and closure. ATG16L1 integrates signals from upstream regulators including mTORC1, AMPK, ULK1, and TFEB, which respond to nutrient status, energy stress, and starvation. Downstream, ATG16L1 directly promotes LC3 lipidation, autophagosome formation, and subsequent lysosomal degradation of cargoes such as p62/SQSTM1. In addition to canonical autophagy, ATG16L1 interacts with NOD2 and WIPI2 and participates in xenophagy, MHC class II antigen presentation, and inflammasome regulation, linking degradation processes to innate immunity and inflammatory signaling.
In the context of renal cell carcinoma, ATG16L1 knockout in 769-P cells allows dissection of autophagy??s dual roles in tumor suppression and tumor promotion. Clear cell RCC is characterized by metabolic reprogramming and dysregulated signaling that may impose autophagy dependence, providing a platform to test autophagy-targeted therapies. Moreover, because ATG16L1 is implicated in Crohn??s disease and inflammatory bowel disease through defective NOD2 signaling and altered cytokine responses, this polyclonal knockout model can be used to study crosstalk between autophagy and inflammatory pathways in a cancer cell background. Researchers can examine how loss of ATG16L1 impacts proliferation, survival under stress, and inflammatory mediator production.
Typical applications include autophagic flux measurements using bafilomycin A1 treatment combined with LC3 and p62 immunoblotting, immunofluorescence detection of LC3 puncta, and co-immunoprecipitation of ATG16L1-interacting partners such as ATG5 and ATG12. This model is suited for drug screening for autophagy modulators, cell viability assays under starvation or ER stress, NOD2 signaling assays, and RT-qPCR profiling of autophagy-related gene expression. It also supports CRISPR-based rescue experiments to validate ATG16L1-specific phenotypes. For technical specifications, validation data, or ordering information, please contact Ascent Research.
