The GYPC Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting the GYPC gene in human A-549 lung adenocarcinoma cells. This heterogeneous pool, generated via CRISPR-mediated gene disruption, provides a loss-of-function model for studying glycophorin C without clonal selection, enabling robust population-level analysis of GYPC-dependent phenotypes.
A-549 cells, derived from a 58-year-old Caucasian male with lung carcinoma, are an adherent, hypotriploid line with an activating KRAS mutation and wild-type p53. Widely used as a type II alveolar epithelial model for lung adenocarcinoma, these cells express key erythrocyte membrane skeleton components, allowing GYPC functional studies in an epithelial context amenable to genetic manipulation.
GYPC encodes glycophorin C, a sialoglycoprotein that anchors the membrane skeleton to the lipid bilayer via interactions with EPB41 (band 4.1) and MPP1 (p55), linking to spectrin (SPTA1/SPTB) and ankyrin (ANK1). Upstream, GATA1 and KLF1 regulate GYPC transcription; downstream, GYPC facilitates SLC4A1 recruitment and cytoskeletal organization. Knockout disrupts this complex, impairing mechanical stability and deformability??phenotypes central to hereditary elliptocytosis and reduced Plasmodium falciparum invasion.
In the A-549 background, GYPC knockout enables investigation of membrane skeleton dynamics in epithelial cells, where EPB41 and MPP1 are expressed. This model supports studies on adhesion, signaling, and cell mechanics, and serves as a surrogate for erythrocyte invasion assays. The knockout population allows assessment of GYPC-dependent Plasmodium falciparum entry and screening of anti-malarial agents targeting receptor interactions, without reliance on primary red blood cells.
Typical applications include flow cytometry for glycophorin C expression, Western blotting for GYPC and partners, immunofluorescence of junctional complexes, and deformability or invasion assays. This polyclonal pool is ideal for proteomic analyses and high-content screens in malaria and hereditary elliptocytosis research. For further information or customized cell engineering, please contact Ascent Research.
