The GOLIM4 Knouckout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 colorectal adenocarcinoma cell line. This product is designed to disrupt the GOLIM4 gene, which encodes a Golgi integral membrane protein involved in protein glycosylation and vesicular trafficking. The polyclonal format comprises a heterogeneous pool of edited cells, reducing clonal bias and enabling population-level functional analyses. This knockout model serves as a versatile tool for dissecting the roles of Golgi-mediated processes in cancer biology.
The HT29 parental cell line is a well-characterized human colorectal adenocarcinoma model with epithelial morphology. Isolated from a primary colorectal tumor, HT29 cells are widely employed in studies of colorectal cancer pathology, including signal transduction, drug response, and tumor progression. Their adherent growth and reproducible behavior make them suitable for rigorous genetic perturbation experiments. Using this established line, the GOLIM4 knockout system provides a relevant context for examining Golgi-dependent mechanisms in colorectal cancer.
GOLIM4 localizes to the Golgi apparatus and functions as a key mediator of COPI-mediated retrograde transport and protein glycosylation. It interacts with the COPI coatomer complex and forms homodimers, which are essential for its correct subcellular distribution. GOLIM4 operates within a molecular network that includes the KDEL receptor and Golgi re-assembly stacking proteins, coordinating the trafficking of secretory and membrane glycoproteins. Knockout of GOLIM4 disrupts Golgi architecture and impairs glycosylation pathways, leading to altered processing of downstream targets such as cell surface receptors and secreted factors. This disruption is influenced by upstream regulators including stress-responsive transcription factors and signals controlling Golgi biogenesis.
In the HT29 colorectal cancer background, loss of GOLIM4 function has profound implications. Impaired glycosylation and trafficking can modify the expression and activity of membrane receptors critical for tumor cell proliferation, migration, and survival. Consequently, this polyclonal knockout model permits investigation of how Golgi dysfunction reshapes oncogenic signaling networks and contributes to colorectal adenocarcinoma pathogenesis. It offers an advanced platform for uncovering the contributions of post-translational modifications to malignant phenotypes and therapeutic vulnerabilities.
Typical applications of this knockout product include western blotting for glycosylation markers, immunofluorescence analysis of Golgi morphology, lectin-binding assays, flow cytometric quantification of surface receptor levels, and functional studies such as migration and drug sensitivity assays. Researchers can employ these cells to explore Golgi biology, glycoprotein secretion, cancer cell signaling pathways, and mechanisms of drug resistance. The polyclonal nature reinforces the reliability and translational relevance of the findings. For additional details or to discuss customized experimental designs, please contact Ascent Research.
