The GNA13 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human Burkitt lymphoma B lymphocyte line Raji. This product comprises a heterogeneous pool of cells with targeted disruption of GNA13, enabling loss-of-function studies without clonal selection, thus reflecting a more physiologically diverse model.
Raji is an Epstein-Barr virus (EBV)-positive lymphoblastoid B cell line established from a Burkitt lymphoma patient. It serves as a widely used model for B cell biology, lymphoma pathogenesis, and immune signaling, maintaining key surface markers and responding to chemokine and growth factor stimuli. Its robust proliferation and well-characterized signaling pathways make it ideal for investigating G protein-coupled receptor (GPCR) and Rho GTPase functions.
GNA13 encodes G??13, the ?? subunit of heterotrimeric G13. G??13 couples GPCRs activated by sphingosine-1-phosphate (S1P), lysophosphatidic acid (LPA), and CXCL12 to RhoA activation via RhoGEFs such as p115RhoGEF (ARHGEF1). Activated RhoA engages ROCK1/2, LIMK1/2, cofilin, and myosin light chain, regulating actin cytoskeletal reorganization, cell adhesion, and migration. This pathway is central to B cell development and malignant transformation.
In Raji cells, GNA13 knockout disrupts GPCR-driven RhoA activation, impairing cytoskeletal reorganization and migration essential for lymphoma cell dissemination. Loss of G??13 attenuates signaling downstream of S1P, LPA, and CXCL12, leading to reduced ROCK-mediated phosphorylation of myosin light chain and altered actin polymerization dynamics. Consequently, these polyclonal knockout cells provide a powerful tool to dissect the role of G??13 in B cell lymphoma pathogenesis, including chemokine-driven chemotaxis, B cell receptor signal modulation, and interactions with the tumor microenvironment. The model also permits exploration of G??13-dependent crosstalk with the PI3K/Akt and MAPK pathways.
Applications include screening of small-molecule inhibitors targeting the G??13?CRhoA axis, Transwell migration assays, F-actin staining with phalloidin, RhoA activation G-LISA, and quantitative phospho-Akt/phospho-ERK analysis. Transcriptomic profiling by RNA-seq and co-immunoprecipitation of G??13?CRhoGEF complexes support mechanistic investigations. For further technical details, please contact Ascent Research.
