The ABHD14B Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HT29 colorectal adenocarcinoma cells. This loss-of-function model targets ABHD14B, a lysine deacetylase involved in Wnt/??-catenin signaling. The polyclonal pool contains a heterogeneous array of CRISPR-mediated gene disruptions, enabling population-level functional studies of ABHD14B in a colorectal cancer context. This product is supplied as a ready-to-use tool for investigating the role of ABHD14B in Wnt pathway regulation and tumor biology.
The host HT29 cell line is a well-characterized human colorectal adenocarcinoma model with epithelial morphology, capable of enterocytic differentiation under defined conditions. This line provides a physiologically relevant system for studying intestinal epithelial biology and colorectal cancer. HT29 cells carry mutations in APC, p53, and BRAF, resulting in constitutive Wnt signaling, thus offering a context in which ABHD14B-mediated modulation of ??-catenin can be examined against an oncogenic background.
ABHD14B functions as a lysine deacetylase that removes acetyl groups from ??-catenin at Lys-49, enhancing its transcriptional co-activator function. This deacetylation promotes ??-catenin interaction with TCF/LEF transcription factors and drives expression of Wnt target genes such as MYC, CCND1, and AXIN2. ABHD14B operates within the canonical Wnt cascade, downstream of receptor activation by WNT3A, Frizzled, and LRP5/6, and at the level of the ??-catenin destruction complex, where it counteracts acetylation-dependent regulation. Key pathway components include DVL, GSK3??, AXIN, APC, and ??-catenin, with ABHD14B serving as an epigenetic tuner of Wnt output.
In HT29 cells, constitutive Wnt activation due to APC truncation renders them dependent on ??-catenin signaling for proliferation. Disrupting ABHD14B in this background enables dissection of how deacetylase activity contributes to tumor cell growth and Wnt target gene expression. This knockout population is ideal for exploring whether ABHD14B loss alters ??-catenin acetylation status, transcriptional activity, and downstream oncogenic phenotypes, providing insight into deacetylase-mediated regulation in colorectal cancer maintenance.
This ABHD14B knockout tool supports diverse assays including Western blotting to measure ??-catenin acetylation, TOP/FOP luciferase reporters for Wnt activity, RT-qPCR for target gene profiling (e.g., MYC, CCND1, AXIN2), immunofluorescence to assess ??-catenin localization, and cell proliferation assays. Applications include Wnt pathway dissection, colorectal cancer research, epigenetic regulation of oncogenic signaling, and deacetylase target validation. For additional information or technical consultation, please contact Ascent Research.
