KDM5D Knockout HT29 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population originating from the HT29 human colorectal adenocarcinoma epithelial line. This product provides a heterogeneous pool of cells with targeted disruption of the KDM5D gene, enabling loss-of-function analyses without the selection biases associated with clonal isolation. The polyclonal format is well-suited for robust population-level studies in chromatin biology and cancer epigenetics.
The HT29 host cell line was established from a primary colorectal adenocarcinoma (Dukes’ stage B) in a 44-year-old female. These adherent epithelial cells serve as a standard intestinal model for investigating drug absorption, oncogenic signaling, and tumor biology. Their characteristic morphology and well-defined genetic background make them a reliable platform for studying colorectal cancer pathology and therapeutic responses.
KDM5D encodes a histone lysine demethylase that specifically removes methyl groups from H3K4me2 and H3K4me3, thereby repressing transcription. It functions within multiprotein complexes containing HDAC1, HDAC2, REST corepressor, CoREST, and SIN3A. Upstream, it is regulated by androgen receptor signaling. Its activity targets H3K4me3-marked promoters, including CDH1 and CDKN1A, and influences Y-chromosome gene expression. Knockout of KDM5D eliminates this demethylation, causing altered chromatin states and transcriptional derepression.
In the context of HT29 colorectal cancer cells, KDM5D knockout provides a focused model for examining how histone demethylation influences tumor-relevant phenotypes. Loss of KDM5D-mediated H3K4me3 removal may shift chromatin to a more active state, potentially affecting genes involved in proliferation, migration, and drug sensitivity. This system is valuable for dissecting the epigenetic mechanisms underlying colorectal cancer and for evaluating targeted epigenetic therapies.
This product is suitable for epigenetic drug screening, chromatin biology, and transcriptional regulation studies. Compatible assays include western blot, RT-qPCR, ChIP-qPCR for H3K4me3, immunofluorescence, and functional tests such as proliferation, migration, and drug sensitivity. It supports research on Y-linked spermatogenic failure, colorectal cancer, and developmental disorders. For further information, please contact Ascent Research.
