The EFCAB14 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting EFCAB14 in the HT29 human colorectal adenocarcinoma cell line. This product provides a heterogeneous loss-of-function model generated through CRISPR/Cas9-mediated gene disruption, avoiding clonal selection to reflect diverse editing outcomes. The polyclonal format is particularly useful for studying gene function in a population context, mirroring cellular heterogeneity found in tumors. This model offers a valuable tool for investigating EFCAB14’s role in calcium signaling and colorectal cancer biology.
The HT29 cell line is a well-characterized epithelial model derived from a human colorectal adenocarcinoma. HT29 cells maintain epithelial morphology, functional polarity, mucus production, and tight junctions, making them suitable for intestinal mucosal biology and colorectal cancer research. These cells are widely used to study proliferation, differentiation, and oncogenic signaling. Disrupting EFCAB14 in this background allows direct investigation of calcium-responsive proteins in an epithelial tumor context relevant to colorectal cancer progression.
EFCAB14 encodes an EF-hand calcium-binding protein with a putative role in calcium-dependent signal transduction. Although its precise function remains uncharacterized, it likely integrates calcium signals through interactions with calmodulin and Ca2+/calmodulin-dependent protein kinase II (CaMKII), responding to calcium influx via plasma membrane channels. EFCAB14 is predicted to modulate downstream effectors such as the transcription factor NFAT, the calcium-dependent proteases calpains, and the transcription factor CREB. Through potential interactions with calmodulin, other EF-hand proteins, and cytoskeletal components, EFCAB14 may participate in the calmodulin?Ccalcineurin?CNFAT pathway and the calpain cascade, which regulate gene expression and cytoskeletal dynamics. Knockout of EFCAB14 disrupts calcium homeostasis, altering signaling to these effectors and influencing cellular processes like transcription, apoptosis, and motility.
In HT29 colorectal cancer cells, loss of EFCAB14 provides a direct approach to dissect its contribution to calcium-driven oncogenic pathways. Colorectal tumors frequently exhibit dysregulated calcium signaling that promotes unchecked proliferation and survival. This polyclonal knockout model enables investigation of how EFCAB14 disruption impacts cancer-relevant effectors, including NFAT, which can drive pro-tumorigenic gene expression, and calpains, which modulate cell adhesion and migration. By linking EFCAB14 to these downstream mediators, the model facilitates identification of novel signaling nodes and potential therapeutic targets, while preserving the epithelial characteristics essential for studying roles in differentiation and metastasis.
This product is suited for diverse applications, from functional characterization of EF-hand proteins to translational colorectal cancer research. Compatible techniques include RNA-seq and RT-qPCR for transcriptomic profiling, western blotting and immunofluorescence for protein detection, and flow cytometry for signaling quantitation. Functional studies can employ calcium imaging to monitor dynamic calcium responses, cell viability and apoptosis assays to evaluate survival, and migration, invasion, and colony formation assays to assess metastatic potential. These capabilities establish the EFCAB14 Knockout HT29 Polyclonal Cells as a versatile tool for advancing calcium signaling and oncology research. For further information, please contact Ascent Research.
