The EHD2 Knockout A-549 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human lung adenocarcinoma A-549 cell line. This product provides a loss-of-function model for the EHD2 gene, which encodes an ATPase involved in caveolae-mediated endocytosis and actin cytoskeleton regulation. The polyclonal nature of this knockout population offers a heterogeneous gene-disrupted background suitable for studying EHD2-dependent processes without clonal selection biases.
The A-549 host cell line was originally established from a 58-year-old Caucasian male with lung adenocarcinoma and serves as a widely used model for human lung epithelial carcinoma. A-549 cells maintain key characteristics of adenocarcinoma, including the expression of alveolar type II epithelial markers, and are employed extensively in cancer research, drug testing, and studies of viral infection. Their adherent morphology and well-characterized signaling networks make them particularly amenable to genetic manipulation and phenotypic analysis.
EHD2 functions as a mechanosensitive ATPase that localizes to caveolae and regulates their stability and endocytic recycling. Biochemically, EHD2 interacts directly with caveolin-1 and cavin-1, linking caveolar structures to the actin cytoskeleton through nucleation factors such as the Arp2/3 complex and N-WASP. The activity of EHD2 is modulated by upstream signals including Src kinase and mechanical stress, while downstream it controls actin polymerization, focal adhesion dynamics, and Rho GTPase signaling via Rac1 and Cdc42. Through these interactions, EHD2 facilitates membrane tension buffering and contributes to cell migration and invasion.
In the context of A-549 cells, disruption of EHD2 is predicted to impair caveolae organization and the associated mechanoprotective responses, potentially altering migration and invasive behavior that are hallmark features of metastatic lung adenocarcinoma. Knockout of EHD2 in this lung cancer model allows investigation of the role of caveolae-mediated signaling in tumor progression and provides insight into the molecular mechanisms underlying EHD2-related pathologies such as cancer metastasis, muscular dystrophy, and cardiomyopathy.
This product is suited for a variety of research applications, including western blotting to confirm EHD2 ablation, immunofluorescence co-staining with caveolin-1 to examine caveolar integrity, transwell migration and invasion assays to assess metastatic potential, and co-immunoprecipitation to probe protein?Cprotein interactions within the caveolae?Cactin network. Additionally, phalloidin staining for F-actin and phospho-signaling analyses of Src and Rho GTPase pathways can be performed to dissect EHD2-mediated cytoskeletal regulation. For technical inquiries, please contact Ascent Research.
