The HDAC4 Knockout HT29 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the human HDAC4 gene in HT29 colorectal adenocarcinoma cells. This polyclonal product provides a heterogeneous loss-of-function model for investigating histone deacetylase 4 (HDAC4, Homo sapiens), generated through CRISPR/Cas9-mediated gene disruption without single-cell clonal selection. Researchers can leverage this model to explore gene function in a population-level context.
The HT29 cell line originates from a human colorectal adenocarcinoma and serves as a canonical epithelial model for colorectal cancer research. These cells carry a BRAF V600E oncogenic mutation, a TP53 tumor suppressor mutation, and are microsatellite stable (MSS). HT29 cells are frequently utilized to study intestinal epithelial biology, oncogenic signaling, and therapeutic responses, offering a well-defined genetic background for gene editing studies.
HDAC4 belongs to the class IIa histone deacetylase family and acts as a transcriptional repressor by deacetylating histone H3 and H4 tails, primarily at promoters of MEF2 transcription factor target genes. Its activity is regulated by upstream kinases including CaMKII and PKD, which phosphorylate HDAC4 to promote 14-3-3 protein binding and nuclear export, integrating calcium signaling and hypoxia cues. HDAC4 assembles with the N-CoR/SMRT corepressor complex and interacts with HDAC3, MEF2C, ANKRA2, and 14-3-3 proteins. Consequently, HDAC4 represses transcription of MEF2?dependent genes as well as RUNX2 and HIF?1?? targets, linking chromatin modification to cell cycle control and differentiation.
In HT29 colorectal cancer cells, disruption of HDAC4 is anticipated to cause histone hyperacetylation at MEF2-regulated loci and derepression of downstream targets, potentially altering cell proliferation and apoptosis. Given the BRAF V600E and TP53 mutations, this knockout model enables dissection of epigenetic regulation intertwined with oncogenic signaling. It is particularly suited for elucidating the role of HDAC4 in tumor suppressor gene regulation and testing epigenetic drugs.
Key applications include western blotting for global or site-specific histone acetylation, RT-qPCR for MEF2 target gene expression, and chromatin immunoprecipitation (ChIP) for mapping HDAC4 and histone marks. Functional assays such as proliferation, apoptosis, and migration assays can reveal phenotypic changes. Additional techniques like immunofluorescence for HDAC4 localization and RNA-seq for transcriptome profiling are also well-supported. For further inquiries, please contact Ascent Research.
