The CCDC88B Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa human epithelial cell line. These cells carry a targeted disruption of the CCDC88B gene, resulting in a loss-of-function model that enables detailed investigation of actin cytoskeleton organization and immune-related signaling pathways. This polyclonal format provides a heterogeneous knockout population suitable for functional analyses without clonal selection artifacts.
HeLa cells are an immortalized cervical adenocarcinoma epithelial cell line widely employed as a robust and well-characterized host for gene perturbation studies. Their epithelial origin, rapid proliferation, and tractability for genetic manipulation make them a standard platform for examining cytoskeletal dynamics, cell migration, and signal transduction in a human cellular context.
CCDC88B encodes a coiled-coil domain-containing protein that bundles actin filaments and directly interacts with filamin A (FLNA), a key actin-crosslinking protein. Functioning downstream of T cell receptor (TCR) signaling and Rho family GTPases including RhoA and RAC1, CCDC88B integrates signals from integrin-mediated adhesion to modulate actin polymerization and focal adhesion dynamics. It also associates with ARPC2, a subunit of the Arp2/3 complex, thereby influencing branched actin network formation. Disruption of CCDC88B alters cytoskeletal rearrangement, cell motility, and immune cell activation, linking its function to inflammatory bowel disease (IBD) pathophysiology.
In the HeLa epithelial background, CCDC88B knockout provides a simplified yet physiologically relevant model to dissect actin-dependent processes independent of hematopoietic-specific factors. HeLa cells express core actin regulatory machinery, allowing for high-resolution imaging and biochemical studies of CCDC88B interactions with FLNA and F-actin. This system enables researchers to uncouple CCDC88B??s cytoskeletal functions from its immune-specific roles, facilitating mechanistic dissection of pathways common to epithelial and immune cell motility.
This knockout product supports a broad range of experimental approaches, including immunofluorescence localization of F-actin structures, western blotting to assess CCDC88B and FLNA levels, transwell migration and wound healing assays to quantify cell motility, co-immunoprecipitation of CCDC88B complexes, and flow cytometry for adhesion molecule expression. It serves as a valuable tool for drug target validation in IBD, studies of actin cytoskeleton regulation, and investigation of CCDC88B-related immune dysfunction. For further information, please contact Ascent Research.
