The IKZF5 Knockout HT29 Polyclonal Cells product comprises a polyclonal population of Homo sapiens HT29 colorectal adenocarcinoma cells engineered via CRISPR/Cas9-mediated disruption of the IKZF5 gene. This targeted gene disruption generates a heterogeneous pool of cells carrying loss-of-function mutations at the IKZF5 locus, providing a versatile model for investigating IKZF5-dependent transcriptional regulation and tumor suppressor functions. The polyclonal format preserves diverse genetic backgrounds, making it suitable for functional genomics, pooled screening, and population-based assays where clonal homogeneity is not required.
The HT29 cell line is a well-characterized human colorectal adenocarcinoma line with epithelial morphology, originally derived from a primary colon tumor. HT29 cells are widely used in cancer biology and intestinal epithelial research due to their capacity to differentiate into enterocyte-like and mucin-secreting phenotypes under appropriate stimuli. They serve as a robust in vitro model for studying colorectal cancer signaling, intestinal barrier function, and drug responses, making them an ideal host for interrogating gene function in a colorectal cancer context.
IKZF5 encodes a member of the Ikaros family of zinc finger transcription factors, which orchestrate hematopoietic development and lymphocyte lineage commitment. Mechanistically, IKZF5 recruits chromatin remodeling complexes, including SIN3A and HDAC1/2, to repress or activate target gene expression. In the signaling network, IKZF5 operates downstream of IL7R, BCR/TCR signaling, CK2, and NOTCH1, while directly regulating downstream targets such as CD19, BCL2L1, CCND1, RAG1, and RAG2. IKZF5 also physically interacts with IKZF1, IKZF3, HDAC1, HDAC2, SIN3A, CTBP, and CK2, forming transcriptional regulatory complexes that integrate extracellular cues into gene expression programs.
In the HT29 colorectal cancer model, IKZF5 has been implicated as a tumor suppressor that may restrain cell proliferation and modulate differentiation programs. Disruption of IKZF5 in HT29 cells perturbs the normal Ikaros family transcriptional network, potentially altering the expression of key genes like CCND1 and BCL2L1, which control cell cycle progression and apoptosis. Consequently, this knockout model enables the functional dissection of IKZF5-dependent pathways in colorectal cancer biology, including its role in growth suppression, epithelial homeostasis, and interaction with the SIN3A-HDAC corepressor complex.
The IKZF5 Knockout HT29 Polyclonal Cells are ideally suited for a broad range of research applications, including colorectal cancer tumor suppressor studies, transcription factor functional analysis, and gene regulation profiling. Researchers can employ this model in proliferation and apoptosis assays, RNA-seq transcriptomic profiling, ChIP-qPCR analyses of chromatin occupancy, and co-immunoprecipitation studies to explore protein interaction networks. Additionally, flow cytometry and RT-qPCR enable quantitative assessment of downstream target genes like CD19 and BCL2L1. For detailed product specifications, technical support, or custom inquiries, please contact Ascent Research.
