The ACBD6 Knockout HT29 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population for loss-of-function analysis of ACBD6 in a human colorectal adenocarcinoma model. This polyclonal pool, derived from the HT29 cell line, carries targeted disruption of the ACBD6 gene without clonal selection, preserving population-level heterogeneity while establishing a stable knockout background. The product is suitable for studying ACBD6-dependent lipid metabolism, peroxisomal function, and protein lipidation pathways in a disease-relevant epithelial context.
The parental HT29 cell line was established from a primary colorectal adenocarcinoma in a 44-year-old female and is widely utilized as a model of colorectal cancer. HT29 cells are adherent, capable of enterocytic differentiation under appropriate conditions, and retain key features of colon adenocarcinoma such as aberrant Wnt signaling and tumorigenic potential. This host background provides a physiologically relevant platform for investigating metabolic and oncogenic signaling pathways that may be modulated by ACBD6.
ACBD6 (Acyl-CoA Binding Domain Containing 6) encodes a protein that binds long-chain acyl-CoA esters with high affinity, thereby controlling their availability for peroxisomal ??-oxidation and protein N-myristoylation. ACBD6 function is influenced by upstream metabolic regulators including PPAR??, PPAR??, SREBP1, and insulin signaling. Downstream, ACBD6 interacts directly with N-myristoyltransferase 1 (NMT1) and modulates the activity of peroxisomal enzymes such as ACOX1, as well as broader fatty acid ??-oxidation processes. ACBD6 also engages peroxisomal membrane proteins like PEX19 and PEX5, linking acyl-CoA trafficking to peroxisome biogenesis and function.
In the HT29 colorectal adenocarcinoma background, loss of ACBD6 is predicted to disturb lipid homeostasis by altering the equilibrium between acyl-CoA sequestration and utilization. This perturbation may affect membrane composition, trafficking, and oncogenic signaling pathways that rely on protein myristoylation or peroxisomally derived lipid mediators. The polyclonal knockout model consequently enables exploration of how lipid metabolic reprogramming contributes to colorectal cancer cell proliferation, survival, and metastatic behavior.
This knockout cell population supports a wide array of functional and biochemical analyses. Typical applications include Western blotting for ACBD6 and downstream targets, LC?MS-based acyl?CoA profiling, immunofluorescence imaging of peroxisomal markers (e.g., PEX19, PEX5), proliferation assays (MTT or BrdU), apoptosis detection (Annexin V/7?AAD), and transwell migration and invasion assays. Global lipidomics approaches can further elucidate metabolic rewiring upon ACBD6 disruption. Researchers can apply this model to screen for metabolic vulnerabilities or to dissect the role of peroxisomal lipid processing in colon cancer. For further information, please contact Ascent Research.
