The DIP2A Knockout HEK293T Polyclonal Cells are a genetically engineered polyclonal cell population derived from the HEK293T human embryonic kidney cell line. These cells harbor a CRISPR/Cas9-mediated disruption of the DIP2A gene, creating a loss-of-function model for investigating DIP2A-dependent signaling. As a polyclonal knockout population, this product reflects a heterogeneous mixture of edited alleles across the cell pool, providing a robust system to assess gene function without clonal selection bias.
The HEK293T parental line is a widely used human embryonic kidney cell model immortalized by stable expression of SV40 large T-antigen. This transformation confers high transfection efficiency and supports episomal replication of plasmids containing the SV40 origin of replication, making HEK293T a preferred host for protein expression, lentivirus production, and transient transfection studies. The cells exhibit adherent growth and lend themselves to a broad array of biochemical and cell-based assays, ensuring compatibility with standard laboratory workflows.
DIP2A encodes a transmembrane receptor that specifically binds the secreted glycoprotein follistatin-like 1 (FSTL1). Upon ligand engagement, DIP2A activates downstream signaling cascades including the PI3K/AKT and ERK/MAPK pathways. FSTL1-DIP2A signaling promotes cell survival and proliferation through phosphorylation-dependent activation of AKT and ERK, linking extracellular cues to transcriptional and metabolic responses. Dysregulation of this axis has been implicated in various cancers and neurodevelopmental disorders, highlighting the biomedical relevance of DIP2A as a signaling node.
In the HEK293T background, disruption of DIP2A eliminates the receptor??s capacity to transduce signals from exogenously added or autocrine FSTL1, enabling direct assessment of DIP2A contribution to AKT and ERK phosphorylation events and cellular outcomes. The high transfectability of HEK293T cells further facilitates reconstitution experiments, where wild-type or mutant DIP2A can be reintroduced to dissect structure-function relationships. This polyclonal model is particularly useful for screening and validation experiments that require consistent genetic ablation across a population while avoiding clonal artifacts.
Researchers can employ these DIP2A knockout cells to interrogate FSTL1-driven signaling in cancer biology, characterize downstream effects on cell viability and clonogenicity, and explore neurobiological pathways regulated by DIP2A. Typical assays include western blotting for phospho-AKT and phospho-ERK, co-immunoprecipitation of DIP2A interactors, cell viability assays following FSTL1 stimulation, and RT-qPCR to monitor transcriptional changes. The polyclonal format offers a cost-effective and reliable platform for drug target validation, pathway dissection, and functional genomics screens. For further details, purchasing information, or technical support, please contact Ascent Research.
