CCDC167 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population for functional interrogation of the CCDC167 gene in a human colorectal adenocarcinoma background. This loss-of-function model, generated through targeted gene disruption in the HT29 cell line, enables dissection of the biological significance of the largely uncharacterized coiled-coil domain-containing protein 167. The polyclonal format provides a heterogeneous pool of edited cells, offering a robust system for studying gene function without clonal selection artifacts. This product is ideal for exploratory studies seeking to uncover CCDC167-involved cellular processes.
The HT29 host cell line is a well-established human colorectal adenocarcinoma cell line that serves as a versatile intestinal epithelial model. HT29 cells harbor mutations in the tumor suppressor genes APC and TP53, reflecting common genetic alterations in sporadic colorectal cancers. These cells retain the ability to undergo enterocytic differentiation under appropriate culture conditions, making them suitable for studies of intestinal barrier function, epithelial polarization, and colorectal tumor biology. The intrinsic tumorigenic properties of HT29, combined with its capacity for differentiation, provide a physiologically relevant context for examining gene function in both undifferentiated and differentiated states.
CCDC167 is predicted to encode a coiled-coil domain-containing protein, a structural motif known to mediate protein?Cprotein interactions. While its precise molecular function and signaling network remain undefined, CCDC167 may act as a scaffold, facilitating multi-protein complex assembly. Its coiled-coil domain suggests potential interactions with cytoskeletal components, transcription factors, or signaling intermediaries. Knockout in HT29 cells may illuminate roles in proliferation, migration, and apoptosis. Given the absence of identified regulators, targets, or partners, this polyclonal knockout model is a critical tool for initial phenotypic characterization and pathway discovery.
In HT29 colorectal adenocarcinoma cells, CCDC167 disruption may unmask phenotypes amplified by the oncogenic background. HT29 cells model colorectal cancer progression; thus, altered proliferation, migration, or invasion upon CCDC167 loss could indicate a role in tumorigenesis or metastasis. The interaction between CCDC167 and the APC/TP53-mutant environment may be informative, as coiled-coil proteins often participate in cytoskeletal reorganization and cell adhesion??processes deregulated in cancer. This model provides a valuable platform for probing context-dependent gene functions.
This polyclonal CCDC167 knockout cell product enables diverse assays for functional characterization. Researchers can assess cell proliferation via colony formation or MTT assays, motility and invasion via wound healing and transwell assays, and global transcriptomic changes by RNA-seq. Western blotting verifies protein expression changes. These cells also support unbiased screening to identify interacting partners or signaling networks. For detailed specifications or custom applications, contact Ascent Research.
