The GPANK1 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human HT29 colorectal adenocarcinoma cell line. This product provides a heterogeneous pool of cells carrying targeted disruptions in the GPANK1 gene, enabling loss-of-function studies without the selective pressures and clonal artifacts associated with monoclonal isolates. The polyclonal format retains the genetic diversity of an edited population, making it suitable for robust functional assays and screening applications where bulk-knockout responses are desired.
The host cell line HT29 is a widely used epithelial intestinal model originally isolated from a 44-year-old female with colorectal adenocarcinoma. HT29 cells grow adherently, form tight junctions, and express mutant p53, recapitulating key features of colorectal tumor biology. They are extensively employed in studies of drug absorption, mucus production, and colorectal cancer progression. The availability of GPANK1 knockout in this background provides a clinically relevant platform for examining the interplay between tumor cell-intrinsic pathways and immune-related gene functions.
GPANK1 encodes a protein with G-patch and ankyrin repeat domains that likely functions as a scaffold for protein-protein interactions, with the G-patch domain potentially binding RNA-processing factors and the ankyrin repeats engaging diverse partners. Positioned in the MHC class III region, GPANK1 neighbors immune genes such as TNFA, LTA, LTB, and NFKBIL1. It is induced by inflammatory cytokines like TNF-?? and IFN-??, suggesting it operates downstream of immune stimuli. Through its scaffold role, GPANK1 may influence pathways like NF-??B, contributing to immune response modulation. Disruption of GPANK1 facilitates dissection of its signaling role and its implication in autoimmune disease pathogenesis.
In the context of HT29 cells, GPANK1 knockout provides a means to explore the intersection of colorectal cancer biology and immune regulation. Given the gene’s genetic linkage to autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis, this model can be used to investigate how intestinal epithelial cells modulate local and systemic immune responses. The presence of mutant p53 in HT29 cells also permits studies on how GPANK1 loss affects tumor-cell behavior under genotoxic stress or inflammatory conditions. Consequently, the knockout cells serve as a tool to examine the contribution of MHC class III genes to cancer-associated inflammation and the tumor microenvironment.
Researchers can apply this polyclonal knockout model in diverse experimental workflows, including co-immunoprecipitation to identify GPANK1-interacting proteins, immunofluorescence to assess subcellular localization changes, western blotting for expression profiling, RT-qPCR and RNA-seq for transcriptomic analysis, and flow cytometry to evaluate immune marker expression. These assays facilitate studies on protein interaction networks, cytokine signaling, and the molecular mechanisms of autoimmune susceptibility. The polyclonal format is particularly advantageous for high-throughput screens and functional genomics approaches that require population-level responses. For additional product details, please contact Ascent Research.
