The EFCAB7 Knockout A2780 Polyclonal Cells constitute a CRISPR/Cas9-edited knockout pool in the A2780 human ovarian carcinoma line, featuring targeted disruption of the EFCAB7 gene. EFCAB7 encodes CFAP45, a calcium-binding component of the nexin-dynein regulatory complex vital for ciliary motility. This pool is designed for studies of ciliary motility, calcium signaling, and ciliopathy mechanisms. The polyclonal format captures a spectrum of gene-editing events, providing a heterogeneous loss-of-function population suitable for functional genomic screens without clonal artifacts.
The A2780 cell line is derived from an untreated female patient with ovarian endometrioid adenocarcinoma and serves as a well-established epithelial ovarian cancer model. Although not prominently ciliated under standard culture, A2780 retains key ciliary motility regulators and can be induced to form cilia under specialized conditions. This knockout model therefore uniquely bridges ciliary biology and ovarian cancer pathobiology, enabling investigation of ciliary protein functions in a tumor-relevant context.
Molecularly, CFAP45 acts as a calcium-binding sensor within the nexin-dynein regulatory complex, translating intracellular calcium signals into changes in ciliary beat frequency. EFCAB7 transcription is driven by the ciliogenesis master regulators RFX2, RFX3, and FOXJ1. At the protein level, CFAP45 interacts directly with axonemal dynein heavy chain DNAH5, coiled-coil proteins CCDC39 and CCDC40, and dynein assembly factors DAI1 and DAI2. This complex cooperates with radial spoke heads RSPH9 and RSPH4A and the intermediate chain DNAI1 to modulate dynein arm activity. Disruption of EFCAB7 therefore severs calcium-dependent dynein regulation, producing hallmark ciliopathy motility defects.
Within the A2780 ovarian cancer system, EFCAB7 knockout provides a powerful tool to study the role of ciliary and calcium signaling in cancer cell behavior. Ciliary motility proteins have been implicated in cell migration and metastasis, processes central to ovarian cancer dissemination. By ablating CFAP45, researchers can evaluate how loss of the dynein regulatory complex alters cellular motility, calcium dynamics, and downstream signaling. The epithelial origin of A2780 makes it particularly relevant for investigating ciliated epithelial dysfunction in gynecological malignancies and for testing ciliopathy-associated phenotypes under ciliogenic conditions.
Researchers can utilize this polyclonal knockout population for ciliary beat frequency analysis, motility assays, calcium imaging, and immunofluorescence detection of dynein complex components such as DNAH5 and CCDC39. RT-qPCR profiling of RFX2/3/FOXJ1 targets supplements these functional readouts. These tools support studies of primary ciliary dyskinesia, sperm motility pathways, and ovarian cancer cell migration. The polyclonal knockout format ensures heterogeneous gene disruption, avoiding clonal selection artifacts. For additional information or technical support, please contact Ascent Research.
