The DNAAF2 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human ovarian serous adenocarcinoma cell line MES-OV, featuring targeted disruption of the DNAAF2 gene. This loss-of-function model is designed to abolish DNAAF2 protein expression, enabling studies of ciliary biology in an epithelial ovarian cancer context. As a polyclonal pool, these cells provide a heterogeneous population suitable for bulk assays examining global effects of DNAAF2 depletion on ciliogenesis and signaling.
The MES-OV cell line was established from a patient tumor of ovarian serous adenocarcinoma and is widely used as an adherent in vitro model for ovarian cancer biology and drug response profiling. MES-OV cells retain key characteristics of high-grade serous carcinoma, including epithelial morphology and relevant oncogenic pathways, providing a physiologically relevant platform for investigating ciliary dysfunction in a cancer-relevant system.
DNAAF2 encodes a cytoplasmic protein critical for the preassembly of axonemal dynein arm complexes. It functions as an HSP90 co-chaperone, stabilizing and folding dynein heavy chains such as DNAH5 and DNAH11, along with intermediate chains like DNAI1, prior to their intraflagellar transport into cilia. DNAAF2 cooperates with assembly factors DNAAF1 (LRRC50) and DNAAF3, and its expression is regulated by RFX family transcription factors RFX2 and RFX3 and the master ciliogenic factor FOXJ1, which integrate inputs from Notch, Wnt, and Hedgehog signaling pathways. Disruption of DNAAF2 leads to defective dynein arm assembly, immotile cilia, and impaired mucociliary clearance, recapitulating phenotypes of primary ciliary dyskinesia and Kartagener syndrome.
In MES-OV cells, primary cilia are emerging as modulators of oncogenic signaling, particularly Hedgehog and Wnt pathways, which are frequently dysregulated in ovarian cancer. DNAAF2 knockout in this background allows dissection of how ciliary dysfunction influences cancer cell proliferation, migration, and drug sensitivity. This model bridges ciliopathy research and cancer biology by providing a disease-relevant epithelial environment to study cilia-dependent signaling mechanisms.
This polyclonal knockout product is well-suited for diverse applications, including immunofluorescence analysis of ciliary markers (acetylated tubulin, ARL13B), co-immunoprecipitation to assess dynein arm assembly, transmission electron microscopy for ultrastructural examination, and functional assays such as ciliary beat frequency measurement and Hedgehog reporter assays. It supports modeling of primary ciliary dyskinesia, screening for cilia-modulating compounds, and investigation of ciliogenesis defects in ovarian cancer. Standard validation can be conducted via western blotting and RT-qPCR for DNAAF2 expression. For additional technical information, please contact Ascent Research.
