The CCDC102B Knockout HEK293T Polyclonal Cells represent a pooled population of human embryonic kidney HEK293T cells in which the CCDC102B gene has been disrupted using CRISPR/Cas9-mediated gene editing. This polyclonal knockout pool is generated by introducing guide RNAs targeting the CCDC102B locus, resulting in a heterogeneous mixture of edited alleles across the cell population. Unlike clonal isolates, this product provides a broad loss-of-function model that more closely reflects the genetic diversity inherent in pooled screening approaches and is suitable for studying gene function in a versatile and widely used cellular background. The polyclonal nature allows researchers to assess overall phenotypic trends while mitigating clonal artifacts that can arise from single-cell expansion.
HEK293T cells are a well-established cell line derived from human embryonic kidney tissue and transformed with sheared adenovirus type 5 DNA. These cells constitutively express the SV40 large T antigen, which enables episomal replication of transfected plasmids containing the SV40 origin of replication, leading to high-level protein expression. As a result, HEK293T cells are extensively employed in transient and stable transfection, lentiviral and retroviral packaging, and recombinant protein production. Their robust growth, ease of transfection, and well-characterized proteome make them a preferred host for gene knockout studies, particularly for exploring signaling pathways, protein interactions, and cell biological functions.
CCDC102B encodes a protein predicted to contain coiled-coil domains, structural motifs known to mediate protein-protein interactions and often found in scaffold proteins that organize multiprotein complexes. Although the precise molecular role of CCDC102B remains largely uncharacterized, its domain architecture suggests engagement in cytoskeletal organization or signal transduction cascades. The lack of identified upstream regulators, downstream targets, or interaction partners highlights the need for functional studies. By removing CCDC102B in a controlled cellular system, researchers can begin mapping its contributions to protein networks, with possible links to Rho GTPase signaling, actin dynamics, or kinase scaffolds, based on the presence of coiled-coil domains that frequently associate with these processes.
In the HEK293T context, loss of CCDC102B may perturb protein scaffold complexes that interface with the cytoskeleton or modulate intracellular signaling. Given the cell line??s flat, epithelial-like morphology and rapid proliferation, phenotypic outcomes can include altered cell shape, adhesion, migration, or growth kinetics. Since HEK293T cells are also widely used for studying cancer-related signaling, this knockout model offers a relevant platform to investigate whether CCDC102B plays a role in pathways commonly dysregulated in malignancy. Indeed, limited GWAS evidence has pointed to potential associations with breast cancer, though functional validation is needed; thus, this model may serve initial experiments to explore oncogenic or tumor-suppressive functions.
This polyclonal CCDC102B knockout product is designed for a range of research applications, including functional characterization of the gene, interactome mapping via co-immunoprecipitation and mass spectrometry, and phenotypic assays such as cell proliferation, migration, and invasion tests. The cells can be used in Western blotting and immunofluorescence to confirm protein loss, RNA-seq to assess transcriptomic changes, and high-throughput screening to identify small molecules or genetic rescue elements that modulate the knockout phenotype. By providing a ready-to-use pool of edited cells, this product expedites hypothesis-driven and discovery-based studies of CCDC102B. Please contact Ascent Research for further information.
