This product is a CRISPR/Cas9-edited polyclonal knockout K-562 cell population with targeted disruption of the CCPG1 gene. CCPG1 encodes a Golgin protein that mediates vesicle tethering at the Golgi apparatus, and its knockout provides a loss-of-function model to dissect Golgi-dependent intracellular trafficking pathways. The polyclonal nature ensures a heterogenous mix of edits at the target locus, making the population well-suited for bulk biochemical and functional assays while minimizing artifacts associated with clonal selection. This format is particularly useful for studying global trafficking effects and non-clonal protein secretion phenotypes.
K-562 is a chronic myelogenous leukemia cell line established from the pleural effusion of a 53-year-old female in blast crisis. It contains the Philadelphia chromosome t(9;22), resulting in the BCR-ABL fusion oncogene that drives leukemic proliferation. The cells are erythroleukemic and retain the ability to differentiate into erythrocytic, granulocytic, and monocytic lineages upon appropriate stimuli, offering a multifaceted hematopoietic model. K-562’s suspension growth and well-characterized signaling landscape facilitate scalable experimental designs, including high-throughput screening and drug combination studies.
CCPG1 functions as a homodimeric Golgin localized to the cis-Golgi, where it tethers COPI and COPII transport vesicles through direct interactions with RAB GTPases such as RAB6A, and scaffold proteins including GCC2 and SEC23IP. The CCPG1 protein is regulated by stress-responsive pathways like the unfolded protein response and nutrient deprivation, which modulate its expression. Downstream, CCPG1 promotes Golgi ribbon maintenance, efficient secretory protein trafficking, and protein stabilization. Disruption of CCPG1 impairs ER-to-Golgi transport and leads to fragmented Golgi morphology, affecting protein secretion and cell surface receptor presentation. Additional interacting partners FAM131B and COPI/COPII subunits further underscore its central role in Golgi organization.
In the context of K-562 leukemia cells, CCPG1 knockout introduces specific secretory pathway perturbations that may intersect with aberrant BCR-ABL signaling. Malignant cells often rely on heightened protein secretion and surface receptor display to sustain growth and evade apoptosis, making the Golgi a potential vulnerability. Loss of CCPG1 can alter the trafficking of cancer-relevant proteins, potentially modulating leukemic cell proliferation, differentiation, and response to therapeutic agents. This model is therefore valuable for exploring how Golgi dysfunction influences cancer cell biology and for identifying trafficking-based therapeutic targets.
Representative assay applications include Western blotting for CCPG1 protein knockdown, RT-qPCR to quantify residual mRNA, immunofluorescence staining of Golgi markers like GM130 or giantin to assess morphological changes, and luminescence-based protein secretion assays. The model facilitates investigations of Golgi trafficking pathways in leukemia, screening for functional interactions with BCR-ABL inhibitors, and studying the contributions of Golgins to hematopoietic differentiation and cell growth. For additional product details or custom gene-editing inquiries, please contact Ascent Research.
