The EHBP1 Knockout HeLa Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout population derived from HeLa cells, in which the EHBP1 gene has been disrupted to eliminate functional protein expression. This polyclonal pool serves as a versatile loss-of-function model, retaining a heterogeneous mixture of edited alleles that more closely mimics population-level genetic ablation while reducing clonal artifacts. The cells are generated by CRISPR/Cas9-mediated gene disruption, providing a reliable system for investigating EHBP1-dependent cellular functions.
HeLa cells, an immortalized human cervical adenocarcinoma epithelial line, are a cornerstone of cancer biology and intracellular trafficking research. They exhibit robust growth, well-characterized receptor tyrosine kinase signaling, and invasive characteristics, making them an ideal platform for studying oncogenic processes. Extensive genomic, transcriptomic, and proteomic resources available for HeLa cells further support the integration of this EHBP1 knockout model into advanced mechanistic studies and screening applications.
EHBP1 (EH domain-binding protein 1) functions as a critical endocytic adaptor that directly couples EHD family ATPases, particularly EHD1 and EHD2, to the actin cytoskeleton. It coordinates endosomal tubulation and the recycling of internalized receptors by linking EHD-mediated fission events to actin polymerization. EHBP1 operates downstream of receptor tyrosine kinase signaling and endocytic cargo, interacting with sorting nexins and actin filaments to orchestrate endocytic recycling. Disruption of EHBP1 impairs the recycling of receptors such as transferrin receptor, making this knockout model a powerful tool for dissecting the molecular machinery of endosomal transport, actin dynamics, and Rab GTPase-regulated pathways.
In HeLa cells, loss of EHBP1 leads to defective endocytic recycling, altering the surface expression and signaling of recycled receptors. This disruption can modulate actin cytoskeleton organization and cell migration??processes frequently dysregulated in cancer. Given the cervical adenocarcinoma origin of HeLa, the EHBP1 knockout model is particularly pertinent for investigating the molecular basis of cancer cell invasion and metastasis. It allows researchers to examine how EHBP1-dependent endosomal trafficking impacts oncogenic signaling downstream of receptor tyrosine kinases, and how EHBP1 loss may influence cell adhesion, motility, and proliferation, bridging endocytosis and tumor biology.
This polyclonal knockout cell population is suitable for a wide range of assays. Western blotting and immunofluorescence enable verification of EHBP1 loss and assessment of effects on interacting partners such as EHD1 and actin. Co-immunoprecipitation facilitates study of protein complexes, while transferrin uptake assays quantify endocytic recycling capacity. Migration and invasion assays evaluate the contribution of EHBP1 to cancer cell motility, and RT-qPCR allows transcript-level analysis of related pathways. The polyclonal format supports robust, population-based experiments and is compatible with high-content screening. For further information or to place an order, please contact Ascent Research.
