The IP6K2 Knockout HEK293T Polyclonal Cells product offers a human polyclonal knockout cell population derived from the HEK293T cell line, in which the IP6K2 gene has been disrupted using CRISPR/Cas9-mediated genome editing. This polyclonal knockout population, comprising a mixture of edited cells, provides a loss-of-function model for investigating IP6K2 cellular roles in inositol pyrophosphate metabolism and downstream signaling. The IP6K2 knockout cells serve as a tool for dissecting inositol pyrophosphate metabolism and its downstream signaling networks in a human cell context.
The host HEK293T line is a widely employed human embryonic kidney (HEK) epithelial cell type immortalized by stable integration of adenovirus type 5 DNA, conferring expression of the SV40 large T antigen. HEK293T cells, derived from HEK293, exhibit high transfectability and robust protein expression, making them a standard platform for recombinant protein production and signal transduction studies. The SV40 large T antigen interferes with p53 and Rb proteins, impacting cell cycle and apoptosis??relevant for studying IP6K2, a p53 interactor. These characteristics make HEK293T a well-characterized background for genetic knockouts.
IP6K2 encodes a kinase that phosphorylates inositol hexakisphosphate (IP6) to produce 5-diphosphoinositol pentakisphosphate (5-IP7), a key inositol pyrophosphate second messenger. Functionally, IP6K2 is activated by DNA damage and growth factor signaling, with TP53 acting as a critical upstream regulator. Upon activation, IP6K2 interacts directly with and modifies the activity of TP53, promoting p53-mediated apoptosis. Additionally, IP6K2 modulates cell migration and survival through the PDK1/AKT pathway, influencing downstream targets such as BCL2 family proteins and caspases. Other interacting partners include casein kinase 2 (CK2), TNF receptor-associated factor 2 (TRAF2), and heat shock protein 90 (HSP90). Through these interactions, IP6K2 integrates signals from the inositol phosphate metabolism, p53 signaling, insulin signaling, and phosphatidylinositol systems.
In the HEK293T context, disrupting IP6K2 eliminates endogenous 5-IP7 production, enabling direct analysis of inositol pyrophosphate requirements in p53-mediated apoptosis, AKT-driven cell migration, and insulin secretion. The SV40 large T antigen-mediated p53 perturbation in these cells provides a controlled setting to study IP6K2-TP53 functional interactions, avoiding dominant-negative p53 effects that might obscure the kinase’s role. Thus, this knockout model is particularly useful for dissecting IP6K2-dependent mechanisms in stress responses, metabolic signaling, cell death, and for validating small-molecule IP6K2 inhibitors.
Researchers can apply these IP6K2 Knockout HEK293T Polyclonal Cells in cancer apoptosis assays, inositol phosphate profiling by HPLC, and insulin secretion pathway investigations. Typical techniques include Western blotting, RT-qPCR, immunofluorescence, cell viability and apoptosis assays, IP7 quantification, and co-immunoprecipitation with factors like TP53, CK2, or TRAF2. The polyclonal population supports high-throughput drug screening for IP6K2 modulators. Contact Ascent Research for detailed specifications.
