The GPRIN2 Knockout HEK293T Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HEK293T human embryonic kidney cell line, designed to disrupt the GPRIN2 (G Protein-Regulated Inducer of Neurite Outgrowth 2) gene. This polyclonal product offers a heterogeneous pool of edited cells, providing a robust loss-of-function model for studying GPRIN2-mediated signaling and cellular processes without the limitations of clonal selection.
The HEK293T cell line is a widely used derivative of human embryonic kidney 293 cells, transformed with adenovirus type 5 DNA and stably expressing the SV40 large T antigen. These features confer high transfection efficiency and robust protein expression capacity, making HEK293T a preferred host for heterologous expression, viral production, and a broad array of cell biology applications. The immortalized nature and epithelial morphology of HEK293T cells provide a reliable platform for investigating signaling pathways, protein interactions, and subcellular dynamics.
GPRIN2 functions as a downstream effector in G protein-coupled receptor (GPCR) signaling, with a well-documented role in promoting neurite outgrowth and neuronal differentiation. It is regulated by GPCR ligands such as neurotrophic factors and neurotransmitters, acting through G??i/o proteins and cAMP-dependent cascades. GPRIN2 modulates cytoskeletal dynamics by interacting with actin and tubulin networks, and couples to key downstream effectors including ERK1/2 and CREB, thereby linking extracellular signals to gene expression programs. The protein interacts with G??i/o subunits and cytoskeletal regulatory proteins, and may intersect with Notch pathway components, positioning it at a signaling nexus that integrates multiple inputs to control cell morphology.
In HEK293T cells, GPRIN2 knockout is expected to attenuate GPCR-induced morphological changes and signaling outputs, as suggested by its mechanistic role. This polyclonal knockout model enables researchers to dissect the functional contribution of GPRIN2 to cytoskeletal reorganization and downstream transcriptional responses. HEK293T cells endogenously express components of the GPCR?CcAMP?CPKA?CCREB axis and MAPK/ERK pathway, making them suitable for reconstitution studies and examining how GPRIN2 loss impacts these cascades. The absence of neuron-specific context simplifies analysis, allowing focused investigation of core signaling modules.
Typical applications include Western blotting and RT-qPCR to confirm GPRIN2 disruption, immunofluorescence to visualize actin cytoskeletal changes, and GPCR reporter assays (cAMP, calcium) to assess signaling defects. Co-immunoprecipitation experiments can map GPRIN2 interaction networks, while cell morphology analyses provide functional readouts of neurite-like extensions in permissive conditions. This polyclonal product is also ideal for functional complementation assays, where GPRIN2 variants are reintroduced to rescue phenotypes. For additional details or to discuss custom research solutions, please contact Ascent Research.
