The GOLGA5 Knockout A-549 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of GOLGA5 in the A-549 lung adenocarcinoma cell line. This pooled format retains genetic heterogeneity and avoids clonal selection, providing a versatile loss-of-function model for studying golgin-84-dependent Golgi biology.
A-549 cells derive from a 58-year-old Caucasian male lung carcinoma and model alveolar type II epithelial cells. They are extensively used in lung adenocarcinoma research for investigating epithelial function, oncogenic signaling, and drug responses. Their robust growth and well-characterized transcriptome make them an ideal host for gene knockout studies.
GOLGA5 encodes golgin-84, a Golgi-resident transmembrane protein that tethers COPI vesicles via interactions with RAB1A and COPI coatomer, enabling retrograde intra-Golgi transport and stack maintenance. Its function is regulated by RAB1 GTPase, ARF1 GTPase, and protein kinase D. GOLGA5 cooperates with GM130 (GOLGA2) and GRASP65 (GORASP1) to preserve Golgi architecture. Disruption abolishes these tethering events, leading to disorganized stacks, impaired glycosylation, and secretion defects.
In A-549 cells, GOLGA5 knockout helps elucidate the contribution of Golgi integrity to lung adenocarcinoma phenotypes, including altered glycoprotein secretion that may affect receptor signaling, migration, and apoptosis. This model also enables exploration of Golgi stress responses relevant to cancer and autoimmune diseases like Sj?gren’s syndrome, where anti-golgin autoantibodies are detected.
Research applications include immunofluorescence staining for Golgi markers (GM130, giantin), VSV-G ts045 trafficking assays, Golgi ribbon morphology analysis, apoptosis assays, co-immunoprecipitation with RAB1, and western blotting for Golgi-associated proteins. The polyclonal population supports drug screening and mechanistic studies of Golgi-targeted therapeutics. For more information, contact Ascent Research.
