The ABHD10 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to eliminate ABHD10 gene function in the HT29 human colorectal adenocarcinoma cell line. This engineered model provides a clean loss-of-function background for investigating ABHD10-dependent cellular processes, without the variability associated with transient silencing methods. The polyclonal format captures a diversity of genetic edits, enabling robust analysis of gene function across a heterogeneous cell pool.
HT29 is an established colon cancer cell line derived from a 44-year-old Caucasian female with primary colorectal adenocarcinoma. It harbors a mutation in the TP53 tumor suppressor gene and exhibits an intestinal epithelial-like morphology. HT29 cells are extensively used as a model for colorectal cancer biology, including studies of oncogenic signaling, therapeutic resistance, and intestinal barrier function.
ABHD10 functions as a serine hydrolase with depalmitoylase activity, catalyzing the removal of palmitate moieties from substrate proteins. Its two well-characterized targets are NSF and PRDX5. Depalmitoylation of NSF drives the disassembly of SNARE complexes, which include SNAP25 and syntaxin-1, thereby regulating synaptic vesicle exocytosis. Concurrently, depalmitoylation of PRDX5 enhances its peroxidase activity, directly contributing to the detoxification of reactive oxygen species. ABHD10 is itself under transcriptional control of NRF2, a master regulator of the antioxidant response, and its activity is counterbalanced by the palmitoyltransferases ZDHHC3 and ZDHHC7. This places ABHD10 at a critical nexus linking reversible palmitoylation to neuronal-like exocytic processes and cellular redox defense mechanisms.
In the HT29 colorectal cancer model, ABHD10 knockout enables dissection of its role in disease-relevant phenotypes. Given HT29??s intestinal epithelial origin, loss of ABHD10 may affect barrier integrity, cell migration, and survival under oxidative stress??processes implicated in tumor progression and metastasis. The knockout cells also permit evaluation of how depalmitoylation-dependent regulation of NSF and PRDX5 influences cancer cell exocytosis pathways and antioxidant capacity, providing insights into the interplay between protein acylation and oncogenic signaling.
This polyclonal knockout product is ideally suited for functional genomics, drug discovery, and pathway interrogation. Key applications include analysis of protein palmitoylation using ABE assays, co-immunoprecipitation of SNARE components, ROS quantification, and viability/apoptosis screening. The model is also valuable for studying intestinal epithelial biology and for evaluating depalmitoylase inhibitors. Compatible techniques: Western blotting, RT-qPCR, immunofluorescence, flow cytometry, MTT, and migration assays. For additional details or custom requests, please contact Ascent Research.
