The ARL14EP Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population engineered for targeted disruption of the ARL14EP gene in Homo sapiens A-549 cells. This polyclonal pool offers a loss-of-function model generated through gene editing without selecting individual clones, preserving population-level heterogeneity. The product is intended for advanced biomedical research requiring ARL14EP deficiency in an epithelial context.
The A-549 cell line is a human lung adenocarcinoma model with epithelial-like characteristics, originally derived from alveolar basal epithelium. It is extensively employed in cancer biology, respiratory disease research, and drug development due to its stable growth and genetic tractability. A-549 cells retain key features of lung epithelium and are frequently used to study tumor-immune interactions, oncogenic signaling, and endosomal trafficking.
ARL14EP (ADP-ribosylation factor-like 14 effector protein) serves as a critical effector of the small GTPase ARL14, coupling it to myosin 1E (MYO1E) to mediate transport of MHC class II-containing vesicles in dendritic cells. ARL14EP is activated by upstream signals from BCR stimulation and CD40, leading to phosphorylation and recruitment of downstream partners such as SYK. Through its association with ARL14 and MYO1E, ARL14EP governs the dynamic redistribution of MHC class II compartments to the plasma membrane, thereby facilitating antigen presentation and shaping adaptive immune responses. The gene is a key node connecting vesicular trafficking to immune signaling pathways.
Within A-549 cells, ARL14EP knockout influences intracellular transport processes, potentially altering MHC class II distribution and vesicle trafficking. Given the lung epithelial origin, this model provides a unique system to investigate how immune-related trafficking machinery operates in non-hematopoietic cancer cells. It may reveal mechanisms of immune evasion in lung adenocarcinoma, particularly how disrupted antigen presentation components affect tumor recognition by the adaptive immune system.
Applications encompass immunology, dendritic cell biology, antigen presentation studies, B cell receptor signaling, vesicular trafficking, and primary immunodeficiency research, including common variable immunodeficiency and autoimmunity. Researchers can perform western blotting, co-immunoprecipitation, immunofluorescence, flow cytometry, MHC class II localization assays, RT-qPCR, and vesicle trafficking analyses. This polyclonal knockout population serves as a valuable tool for CRISPR validation, rescue experiments, and dissection of ARL14EP-dependent pathways. For further inquiries, please contact Ascent Research.
