GPM6A Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of human HEK293T cells carrying a targeted disruption of the GPM6A gene. This loss-of-function model is generated by introducing CRISPR/Cas9-mediated gene disruption into a heterogeneous pool of host cells, yielding a polyclonal knockout population suitable for functional studies. The product provides researchers with a ready-to-use tool for investigating GPM6A-dependent mechanisms without the clonal variability associated with single-cell-derived lines, thereby capturing population-level phenotypic effects of target-gene ablation.
HEK293T cells are an adherent human embryonic kidney epithelial line widely valued in biomedical research for their exceptional transfection efficiency, robust protein expression, and high-titer viral production capacity. The line was derived from HEK293 cells and stably expresses the adenovirus E1A/E1B gene products along with the SV40 large T antigen, which together support episomal replication of plasmids containing the SV40 origin. This transformed background confers rapid growth and compatibility with a broad range of expression and functional assays, making it a versatile host for studying gene function in a non-neuronal context.
GPM6A encodes a transmembrane glycoprotein that acts as a key mediator of actin cytoskeleton remodeling, filopodia formation, and neurite outgrowth. Its expression is positively regulated by neurogenic factors including NEUROD1, retinoic acid, thyroid hormone, NGF, and BDNF. Upon activation, GPM6A engages downstream small GTPases Rac1 and Cdc42, thereby driving localized actin polymerization and the extension of filopodial structures. Mechanistically, neurotrophin-triggered signaling through NGF/TrkA activates the MAPK/ERK pathway, which enhances GPM6A transcription; the newly synthesized GPM6A protein then organizes lipid raft membrane domains, homodimerizes or interacts with the related protein GPM6B, and facilitates Rac1/Cdc42-dependent actin reorganization to promote membrane protrusion and neurite elongation.
In the HEK293T host, GPM6A knockout is expected to abrogate filopodia formation and compromise actin-driven membrane dynamics, providing a clean genetic background for dissecting GPM6A contributions to cell morphology, migration, and intracellular signaling. Although HEK293T cells are not neuronal, their expression of key actin-regulatory machinery allows GPM6A-dependent pathways to be isolated and studied without confounding neuro-specific cues. The polyclonal nature of the knockout population preserves the full spectrum of editing outcomes, enabling robust, reproducible measurement of GPM6A loss-of-function phenotypes in a highly tractable cellular model.
This cell product is well suited for a variety of research applications including neuronal development modeling, filopodia quantification, cell migration assays, neurodevelopmental disorder investigation, and drug screening campaigns targeting GPM6A-related conditions. Representative experimental readouts include western blotting for target validation, immunofluorescence and phalloidin staining for cytoskeletal visualization, transwell migration assays, Rac1 activation assays, RT-qPCR for transcriptional analysis, and neurite outgrowth measurements. For further details and ordering information, please contact Ascent Research.
