The C19orf47 Knockout HT29 Polyclonal Cells product consists of a population of HT29 colorectal adenocarcinoma cells that have undergone CRISPR/Cas9-mediated disruption of the C19orf47 gene, generating a polyclonal knockout cell pool. This model provides a loss-of-function system to investigate the biological roles of C19orf47 in intestinal epithelial cells. The polyclonal format ensures genetic diversity within the knockout population, enabling robust and reproducible functional studies without clonal bias. These cells serve as a powerful tool for dissecting pathways regulated by C19orf47 in the context of colorectal cancer and inflammatory signaling.
The parental HT29 cell line is a well-characterized human colorectal adenocarcinoma model originally derived from a 44-year-old female. HT29 cells are widely used in cancer research to study intestinal epithelial biology, including barrier function, differentiation, and tumorigenesis. Their epithelial origin and responsiveness to inflammatory stimuli make them an ideal host for investigating the interplay between tumor cell signaling and innate immune pathways. This knockout model retains the foundational characteristics of HT29 cells while enabling targeted interrogation of C19orf47-dependent mechanisms.
C19orf47 functions as a negative regulator of the NLRP3 inflammasome, interacting with NLRP3 and autophagy receptors such as p62 to promote autophagic degradation of inflammasome components. It responds to upstream stimuli including TLR ligands, inflammatory cytokines, and lipid signals. Knockout of C19orf47 removes this inhibition, leading to heightened NLRP3-mediated caspase-1 activation and increased processing and secretion of IL-1?? and IL-18. The protein also participates in lipid metabolism regulation, linking inflammatory and metabolic pathways. This knockout model thus allows dissection of the interplay between NLRP3 inflammasome signaling, autophagy, and lipid metabolism.
In the HT29 colorectal adenocarcinoma background, C19orf47 loss-of-function enables investigation of NLRP3 inflammasome-driven inflammatory responses in intestinal epithelial cells. This is pertinent to colorectal cancer, where chronic inflammation and metabolic dysregulation contribute to tumorigenesis. The cells provide a platform to explore how C19orf47 impacts cytokine production, inflammasome assembly, and lipid metabolic shifts within a cancer cell context, supporting research on inflammatory diseases and metabolic disorders.
Typical research applications for these polyclonal knockout cells include inflammasome regulation studies, lipid metabolism analysis in colorectal cancer, and intestinal epithelial immunology. Researchers can perform functional assays such as western blotting for IL-1?? and cleaved caspase-1, ELISA quantification of secreted IL-1??, NLRP3 speck immunofluorescence to visualize inflammasome formation, and RT-qPCR for inflammatory gene expression profiling. Lipid profiling assays can be employed to investigate metabolic alterations upon C19orf47 loss. These cells support mechanistic studies, drug screening, and pathway validation experiments. For further information, including detailed protocols and order inquiries, please contact Ascent Research.
