The DPP8 Knockout HT29 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal cell population in which the DPP8 gene has been disrupted to create a loss-of-function model. This knockout product is generated in the HT29 colorectal adenocarcinoma background and provides a genetically defined platform for interrogating DPP8-dependent signaling pathways. The polyclonal format reflects a mixed population of edited cells, enabling robust representation of knockout phenotypes without clonal selection.
The HT29 cell line was originally derived from a human colorectal adenocarcinoma and exhibits an epithelial morphology. HT29 cells are widely employed as a model for intestinal epithelial biology, including studies of drug absorption, barrier function, and colorectal cancer pathogenesis. Their ability to differentiate into enterocyte-like phenotypes under specific conditions further expands their utility for investigating physiological and pathological processes in the gut.
DPP8 is a cytoplasmic serine protease and a critical negative regulator of the NLRP1 inflammasome. Its constitutive expression prevents spontaneous NLRP1 activation, thereby inhibiting ASC speck formation and downstream caspase-1 cleavage. Inflammatory cues such as IFN-?? and TNF-?? can upregulate DPP8 expression, linking it to immune signaling. Upon gene disruption, loss of DPP8 function leads to uncontrolled NLRP1 inflammasome assembly, resulting in gasdermin D-mediated pyroptosis and the release of IL-1?? and IL-18. Beyond inflammasome control, DPP8 modulates T-cell proliferation and cytokine production, likely through processing substrates with proline or alanyl penultimate sequences, and may engage the proteasome complex, indicating broader regulatory roles in cellular protein homeostasis.
In HT29 intestinal epithelial cells, DPP8 knockout offers a physiologically relevant context to examine NLRP1-driven pyroptosis and its crosstalk with apoptosis and cell proliferation. This model is particularly valuable for colorectal cancer research, as dysregulated inflammasome signaling and immune evasion are hallmarks of the tumor microenvironment. By disrupting DPP8 in these cells, investigators can dissect how intestinal epithelial cells balance cell death modalities and inflammatory output, and how these processes influence tumorigenesis, chemoresistance, and immune cell recruitment.
These polyclonal knockout cells are suited for diverse assays: Western blot to verify DPP8 ablation and monitor NLRP1, caspase-1, and GSDMD cleavage; ELISA and LDH release assays to measure IL-1??/IL-18 secretion and pyroptosis; immunofluorescence to detect ASC specks; and flow cytometry to discriminate pyroptosis from apoptosis. Beyond signaling studies, they enable high-throughput DPP8 inhibitor screening, cell proliferation and colony formation assays, and migration experiments. Thus, DPP8 Knockout HT29 Polyclonal Cells serve as a versatile tool for exploring NLRP1 inflammasome biology and immunogenic cell death in colorectal cancer and intestinal epithelium. For further information, contact Ascent Research.
