The GMIP Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Raji B lymphocytes harboring targeted disruption of the GMIP gene. This loss-of-function model enables detailed interrogation of GMIP??s regulatory roles in Rho GTPase signaling and actin cytoskeleton dynamics without endogenous gene expression. The polyclonal format captures a spectrum of CRISPR-mediated editing events, reflecting population-level effects and providing a versatile tool for functional assays requiring GMIP-deficient B cell models.
The Raji cell line, established from a Burkitt??s lymphoma patient, serves as a well-characterized human B lymphoblastoid system. Raji cells express hallmark B cell markers including CD19, CD20, and surface immunoglobulin, supporting studies of B cell receptor signaling, antigen presentation, and lymphoma biology. Their Epstein-Barr virus positivity and robust suspension growth facilitate large-scale experiments, and their malignant origin makes them directly relevant for investigating oncogenic pathways in B cell cancers.
GMIP encodes a Rho GTPase-activating protein that accelerates GTP hydrolysis on RhoA, leading to its inactivation and consequent downregulation of the Rho-associated coiled-coil kinase ROCK. This cascade reduces LIM kinase-mediated cofilin phosphorylation and myosin light chain phosphorylation, promoting actin filament depolymerization and decreased stress fiber formation. The GMIP PX domain binds phosphoinositide lipids, including PI3P, enabling membrane recruitment near phosphoinositide 3-kinase and receptor tyrosine kinase signals. Additionally, GMIP interacts with the GEM small GTPase, integrating upstream cues to modulate RhoA-dependent contractility and cytoskeletal organization.
In the Raji B lymphocyte context, GMIP knockout is predicted to elevate RhoA activity, altering actin-based contractility and impacting processes such as cell migration, adhesion, and immune synapse assembly. These changes provide insights into how GMIP influences B cell activation and lymphoma progression. The polyclonal knockout model thus offers a physiologically accurate platform to dissect GMIP-specific contributions to lymphocyte behavior, potentially revealing vulnerabilities in Rho GTPase dysregulation that are relevant to lymphomagenesis.
Researchers can employ these cells in RhoA activation assays (G-LISA), Western blotting for phospho-MLC, and immunofluorescence analysis of F-actin stress fibers. Co-immunoprecipitation experiments can probe GMIP?CGEM interactions and their phosphoinositide dependence, while transwell assays assess migration and invasion. Flow cytometry enables quantification of cell size and morphology changes linked to cytoskeletal remodeling. The model also supports drug screening targeting Rho GTPase pathways. For further details or to request a quote, please contact Ascent Research.
