EFHD1 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa human cervical adenocarcinoma cell line. This product features targeted disruption of the EFHD1 gene, encoding a calcium-binding protein that regulates mitochondrial dynamics and apoptosis. The polyclonal format preserves a heterogeneous pool of edited alleles, enabling functional studies in a population context without single-cell cloning artifacts. This loss-of-function model is suitable for investigating EFHD1-dependent cellular processes in cancer biology and mitochondrial research.
HeLa cells are a widely used epithelial cell line originally derived from a cervical adenocarcinoma. These HPV18-positive cells exhibit robust growth and have been extensively characterized in biomedical research. The immortalized nature of HeLa cells provides a consistent background for studying oncogenic signaling, cell cycle regulation, and apoptosis. Their human origin and cervical cancer context make them particularly relevant for dissecting pathways involved in tumor progression and therapeutic resistance.
EFHD1 functions as a calcium-sensing protein that interfaces with mitochondrial fission and intrinsic apoptosis. It interacts with BAX and DRP1, key effectors of mitochondrial membrane permeabilization and fragmentation. EFHD1 is activated by calcium influx and apoptotic stimuli, and its activity is transcriptionally regulated by TP53. Downstream, it modulates mitochondrial membrane potential, cytochrome c release, and caspase-3 activation. Knockout of EFHD1 disrupts these interactions, impairing DRP1-mediated fission and altering BAX translocation, thereby shifting the balance toward apoptosis sensitization.
In the context of HeLa cells, EFHD1 disruption provides insights into mitochondrial dysfunction syndromes and cervical cancer pathogenesis. Given the HPV18-positive background, this model can be used to explore how viral oncoproteins intersect with mitochondrial apoptosis machinery. The knockout cells enable dissection of calcium-dependent signaling events that influence cell fate decisions, drug sensitivity, and metastasis. They also offer a platform to study the interplay between mitochondrial dynamics and cancer cell survival.
Typical applications include western blot analysis of cleaved caspase-3 to assess apoptosis induction, JC-1 assays for mitochondrial membrane potential, MitoTracker staining for morphological changes, and immunofluorescence to visualize BAX/DRP1 translocation. Additional uses encompass cell viability assays under apoptotic stimuli, calcium imaging, and co-culture studies. This knockout population is a valuable tool for cancer researchers, mitochondrial biologists, and those investigating calcium signaling. For further information or technical inquiries, please contact Ascent Research.
