EFCAB7 Knockout NCI-H1975 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population specifically engineered to disrupt the EFCAB7 gene within the NCI-H1975 human lung adenocarcinoma cell line. This product is formulated as a heterogeneous pool of knockout cells, providing a loss-of-function model for studying the roles of the EF-hand calcium-binding protein EFCAB7 (also known as CFAP91) in a cancer-relevant epithelial background. The polyclonal format ensures representation of a range of editing events, and the polyclonal cell population is ready for immediate functional assays without the need for single-cell isolation.
The host cell line, NCI-H1975, is derived from a human non-small cell lung cancer (NSCLC) with adenocarcinoma histology. It is characterized by EGFR wild-type status and activating mutations in KRAS (G12D) and PIK3CA (E545K), making it a widely used model for oncogenic signaling studies in lung cancer. NCI-H1975 cells retain certain epithelial features and have been reported to express ciliary components, rendering them suitable for investigating the intersection between ciliary biology and cancer signaling.
EFCAB7 encodes an EF-hand calcium-binding protein that is a core component of the dynein regulatory complex (DRC) within motile cilia. EFCAB7/CFAP91 is transcriptionally regulated by the master ciliogenic factors FOXJ1 and RFX family transcription factors. At the protein level, it interacts directly with dynein heavy chains and other DRC subunits, including CFAP57 and CFAP43, and binds calmodulin in response to calcium influx. Functionally, EFCAB7 mediates calcium-dependent modulation of ciliary beat frequency and is implicated in cAMP?CPKA signaling downstream of G protein-coupled receptor activation. Disruption of EFCAB7 therefore impairs dynein regulatory complex assembly, ciliary motility, and calcium/calmodulin-dependent signaling cascades.
In the context of NCI-H1975 cells, knockout of EFCAB7 creates a unique model to dissect how ciliary dysfunction interacts with oncogenic pathways driven by KRAS and PIK3CA mutations. Since motile cilia are critical for airway epithelial homeostasis, loss of EFCAB7 in these lung cancer cells may reveal novel roles for ciliary components in tumor cell migration, invasion, or response to microenvironmental signals. This polyclonal knockout population thus bridges ciliopathy research and cancer biology, enabling the study of how primary ciliary dyskinesia-related genes influence tumor cell behavior.
Typical applications include immunofluorescence staining for cilia markers such as acetylated ??-tubulin and ARL13B to assess cilia morphology and frequency; measurement of ciliary beat frequency by high-speed video microscopy; calcium imaging using Fluo-4 AM to evaluate intracellular calcium dynamics; western blotting to quantify dynein heavy chains and DRC components; RT-qPCR for ciliogenesis-related gene expression; and migration or invasion assays to test the contribution of EFCAB7 to cancer cell motility. The polyclonal nature also supports pooled CRISPR screens and drug testing for ciliary modulators in a NSCLC background. For further details on validation data, quality control, and ordering information, please contact Ascent Research.
