The GTF2IRD1 Knockout HT29 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal cell population in which the GTF2IRD1 gene has been disrupted in the HT29 human colorectal adenocarcinoma cell background. This heterogeneous mixture of knockout cells enables robust loss-of-function studies without the limitations of single-clone selection. The gene encoding the GTF2IRD1 transcription factor, a member of the TFII-I family, is targeted to eliminate its regulatory function, offering a versatile model for dissecting its roles in transcriptional control and disease.
HT29 cells are an established epithelial line derived from a primary colorectal adenocarcinoma and are widely employed in intestinal biology and cancer research. They exhibit characteristic epithelial morphology and retain the capacity to differentiate into enterocyte-like cells under appropriate culture conditions, making them a valuable platform for investigating differentiation programs, drug responses, and oncogenic signaling in a colorectal context.
GTF2IRD1 functions as a transcriptional regulator with critical roles in craniofacial development, neurodevelopment, and muscle differentiation. It operates within a network involving interactions with TFII-I family members, including GTF2I, and is modulated by the SUMO ligase PIAS3 and histone deacetylase (HDAC) complexes. Downstream, GTF2IRD1 transcriptionally regulates key targets such as HOXD cluster genes and MYOD1, and participates in retinoid signaling pathways. Its activity influences the expression of muscle-specific and developmental genes, with implications for Williams-Beuren syndrome pathogenesis.
In the HT29 background, disruption of GTF2IRD1 alters the transcriptional landscape, potentially affecting pathways relevant to colorectal cancer biology and intestinal cell homeostasis. Given that HT29 cells can be induced to differentiate, this knockout model facilitates the examination of GTF2IRD1??s contribution to epithelial differentiation and its interplay with retinoid signaling. Moreover, it allows the study of how loss of this transcription factor impacts proliferation, migration, or response to therapeutic agents in a colorectal adenocarcinoma setting.
This polyclonal knockout population is suitable for a range of functional assays, including ChIP-qPCR to assess target gene promoter occupancy, RT-qPCR and Western blotting to quantify downstream effector changes, and RNA-seq transcriptomic profiling to capture global gene expression shifts. It can be applied in cell differentiation assays, reporter gene experiments, and pathway analyses focused on TFII-I family signaling, retinoid responses, or Williams-Beuren syndrome mechanisms. For further technical details, please contact Ascent Research.
