The EFCAB7 Knockout AGS Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population targeting the EFCAB7 gene in the AGS human gastric adenocarcinoma cell line. This polyclonal pool offers a ready-to-use loss-of-function model without requiring single-cell cloning, enabling researchers to interrogate the functional consequences of EFCAB7 disruption across a heterogeneous genetic background. CRISPR/Cas9-mediated gene disruption generates a knockout model suitable for studying ciliary biology and tumorigenesis. This product is designed for advanced biomedical research applications focusing on ciliary motility, intraflagellar transport, and oncogenic signaling pathways modulated by EFCAB7.
The AGS host cell line is a widely utilized adherent epithelial model derived from a human gastric adenocarcinoma. It is a well-characterized system for investigating gastric cancer biology, Helicobacter pylori infection, and drug metabolism. AGS cells retain key epithelial features and are amenable to a wide range of assays, including immunofluorescence, proliferation and migration studies, and signaling pathway analyses. This cellular context provides a relevant platform for examining the interplay between ciliary function and gastric cancer pathogenesis, as well as for evaluating candidate therapeutic agents in a disease-relevant setting.
EFCAB7 encodes an essential subunit of the nexin-dynein regulatory complex (N-DRC), a macromolecular assembly critical for ciliary motility and intraflagellar transport. EFCAB7 physically interacts with DRC1, DRC2, DRC3, DRC4, dynein heavy chains, and intraflagellar transport proteins, acting downstream of master ciliogenic transcription factors FOXJ1 and RFX family members, and Hedgehog pathway components. Disruption of EFCAB7 is expected to impair ciliary beat frequency and alter downstream signaling outputs, including Hedgehog pathway activation mediated through SMO and GLI1, and Wnt pathway activation involving CTNNB1. This mechanistic network positions EFCAB7 at the nexus of ciliary mechanics and signal transduction.
In the AGS gastric cancer cell line, EFCAB7 knockout provides a powerful tool to dissect the role of primary cilia in tumor cell biology. Ciliary dysfunction often leads to aberrant Hedgehog and Wnt signaling, which are frequently dysregulated in gastric adenocarcinoma and contribute to proliferation, migration, and epithelial-mesenchymal transition. This model enables exploration of the ciliopathy-tumorigenesis link by allowing researchers to assess how loss of EFCAB7 affects these oncogenic pathways and cellular behaviors. The polyclonal knockout cells facilitate population-level studies of ciliary defects in a gastric cancer microenvironment.
This product finds application in gastric cancer ciliary biology research, primary ciliary dyskinesia modeling, and drug screening for cilia-targeted therapies. Typical experimental workflows include immunofluorescence staining for ciliary markers, Western blotting to confirm EFCAB7 knockout, RT-qPCR profiling of Hedgehog and Wnt target genes, and functional assays such as cell proliferation, apoptosis, migration, and invasion analyses. Ciliary beat frequency measurements can further quantify the motility defect. For more information on integrating this knockout model into your research program, contact Ascent Research.
