The GPS2 Knockout HT29 Polyclonal Cells product comprises a population of HT29 human colorectal adenocarcinoma cells genetically modified using CRISPR/Cas9 to disrupt the GPS2 gene locus. This polyclonal knockout pool provides a loss-of-function model for analyzing GPS2-dependent mechanisms without single-cell clonal selection artifacts. The engineered cells retain the core characteristics of the parental HT29 line while enabling population-level studies of transcriptomic, proteomic, and functional changes associated with GPS2 ablation.
HT29 is a widely used human colorectal adenocarcinoma epithelial cell line derived from a primary tumor. It harbors well-characterized mutations in APC, TP53, and KRAS, is EGFR positive, and retains the capacity for enterocytic differentiation under appropriate culture conditions. These features make HT29 a versatile model for investigating colorectal adenocarcinoma biology, intestinal epithelial barrier integrity, drug transport, and therapeutic resistance mechanisms. The line??s predictable growth and signaling profiles render it an ideal host for gene editing and functional genomics studies.
GPS2 functions as a transcriptional corepressor within the NCOR1-HDAC3 complex, deacetylating histones to silence target gene expression. It directly interacts with NCOR1, HDAC3, TBL1, and TBLR1, and suppresses MAPK/JNK and NF-??B signaling by binding TAK1 and attenuating JNK1 phosphorylation. Upstream regulators including TNF-?? and insulin modulate GPS2 activity; downstream, GPS2 represses SREBF1-regulated metabolic genes, CYP7A1, ABCA1, ABCG1, and inflammatory cytokines. GPS2 also interfaces with PPAR??, p53, and RELA, linking nuclear receptor, stress, and inflammatory pathways.
In HT29 cells, GPS2 knockout permits examination of colorectal cancer mechanisms. Given the cell line??s mutant APC, TP53, and KRAS background, loss of GPS2 corepressor function can reveal impacts on proliferation, apoptosis, and inflammation. Enhanced NF-??B and JNK pathway activity may alter cytokine production and tumor microenvironment interactions. Moreover, GPS2??s role in nuclear receptor signaling may affect enterocytic differentiation and drug transporter regulation, making this model valuable for dissecting transcriptional control in oncogenic contexts.
These polyclonal knockout cells support diverse assays: western blotting and RT-qPCR for target validation, RNA-seq for transcriptomic analysis, co-immunoprecipitation for complex formation, NF-??B and nuclear receptor reporter assays, phospho-specific flow cytometry for JNK and NF-??B, proliferation and migration tests, and drug sensitivity screens. Applications include colorectal cancer biology, tumor microenvironment inflammation, metabolic regulation, and intestinal epithelial barrier function research. For technical inquiries, contact Ascent Research.
