The KDM1B Knockout HT29 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout population of HT29 colorectal adenocarcinoma cells with targeted disruption of the KDM1B gene, offering a versatile loss-of-function system for epigenetic research. This polyclonal pool contains a heterogeneous mix of edited alleles, minimizing clonal selection artifacts and enabling robust functional analyses.
The HT29 cell line is a well-characterized model of human colorectal adenocarcinoma, originally established from a primary tumor of a 44-year-old Caucasian female diagnosed with Dukes?? stage B colorectal cancer. These epithelial cells retain features of intestinal epithelium, including the ability to form polarized monolayers and undergo differentiation in culture. HT29 cells are widely employed in cancer research to study signal transduction pathways, drug sensitivity, and mechanisms of tumor progression, making them a relevant host for investigating colorectal cancer epigenetics.
KDM1B, also known as lysine-specific demethylase 1B, is a histone H3K4 demethylase that catalyzes the removal of mono- and dimethyl groups (H3K4me1/me2), leading to transcriptional repression of target genes. It functions as a core component of the CoREST transcriptional corepressor complex, where it interacts with HDAC1/2, BHC80, and the homologous demethylase LSD1 (KDM1A). KDM1B is recruited to chromatin via transcription factors such as REST and SP1, and its demethylase activity modulates H3K4 methylation at regulatory regions of genes involved in cellular differentiation, proliferation, and development. Downstream transcriptional effects are mediated through factors including MEF2, linking KDM1B activity to broader gene regulatory networks that govern cell identity and growth.
Within the colorectal cancer context, KDM1B plays a significant role in maintaining epigenetic states that influence tumor cell behavior. In HT29 cells, KDM1B knockout allows researchers to probe how loss of H3K4me1/me2 demethylation affects chromatin structure, gene expression programs, and key malignant properties such as uncontrolled proliferation and impaired differentiation. This model is particularly relevant for exploring the epigenetic underpinnings of colorectal adenocarcinoma progression and for testing the functional consequences of altered histone methylation dynamics. Given KDM1B??s links to developmental and neurodevelopmental disorders, this knockout system also offers a platform for investigating broader disease mechanisms in an epithelial cancer background.
This polyclonal knockout product is suitable for a range of molecular and cellular assays. Chromatin immunoprecipitation with quantitative PCR (ChIP-qPCR) can be used to map changes in H3K4me1/me2 occupation at target loci, while RNA sequencing (RNA-seq) reveals global transcriptional shifts. Western blotting and RT-qPCR serve to validate KDM1B depletion. Functional studies may include proliferation assays, colony formation, and immunofluorescence to assess cell phenotype. The model supports research into colorectal cancer epigenetics, drug target identification, and gene expression profiling. For additional product details or technical inquiries, please contact Ascent Research.
