The EFCAB14 Knockout NCI-H1299 Polyclonal Cells consist of a polyclonal population of the NCI-H1299 human lung epithelial carcinoma cell line that has been engineered via CRISPR/Cas9 to disrupt the EFCAB14 gene. This targeting generates a loss-of-function model appropriate for dissecting the biological roles of the EF-hand calcium-binding protein in a cellular context that retains genetic heterogeneity, thereby better mimicking the complexity of tumor tissues compared to clonal isolates. The product is formatted as a ready-to-use polyclonal knockout cell pool for immediate application in NSCLC-related research.
The host NCI-H1299 line was originally derived from a lymph node metastasis of a lung adenocarcinoma and has become a classic in vitro model for non-small cell lung cancer. These cells display robust proliferation, high motility, and epithelial carcinoma characteristics, and they are extensively employed to study oncogenic pathways, metastatic mechanisms, and drug sensitivities. The parental line??s well-documented behavior provides a stable reference point for evaluating phenotypic alterations that arise from EFCAB14 knockout.
EFCAB14 encodes a protein featuring EF-hand motifs that bind calcium ions, positioning it at the nexus of calcium signaling, microtubule dynamics, and cilium assembly. It interacts directly with tubulin and calmodulin, and its transcription is regulated by FOXJ1 and calcium/calmodulin-dependent kinases. Within the signaling network, EFCAB14 may function downstream of calcium influx to modulate calmodulin?CCaMKII and MAPK/ERK cascades, ultimately influencing the stability of microtubules and the composition of ciliary axonemal proteins. This functional integration suggests that EFCAB14 couples changes in intracellular calcium to cytoskeletal reorganization and cell motility.
In the NCI-H1299 background, loss of EFCAB14 is predicted to impair calcium-regulated microtubule functions and ciliary integrity, thereby affecting cell proliferation, migration, and invasion. This model provides a tractable system for exploring how calcium-binding scaffolds shape the malignant behavior of NSCLC cells and may uncover targetable dependencies related to calcium homeostasis or cilium-driven signaling. Moreover, because EFCAB14 has been associated with ciliopathies, the knockout can also inform broader studies on ciliary dysfunction and calcium-related disease mechanisms.
A wide array of assays can be deployed with these cells, including Western blotting and immunofluorescence to verify knockout efficiency and probe downstream targets such as tubulin and calmodulin, proliferation and migration/invasion assays to quantify tumor-relevant phenotypes, and calcium imaging to directly visualize alterations in calcium flux. These applications support research in lung cancer biology, calcium signaling, cilium function, and drug target identification. For additional technical details or ordering information, please contact Ascent Research.
