The MICALL2 Knockout Raji Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population in which the MICALL2 gene has been disrupted in the Raji B lymphocyte cell line. This heterogeneous polyclonal population retains the Raji cellular background while eliminating functional expression of MICALL2, providing a physiologically relevant loss-of-function model for studying B cell biology. The product is supplied as a ready-to-use polyclonal cell stock, suitable for downstream applications in immunology, cancer biology, and signal transduction research.
Raji cells are an EBV-positive Burkitt lymphoma-derived lymphoblastoid cell line that serves as a well-established model for human B lymphocytes. These cells exhibit an antigen-presenting cell phenotype and maintain key features of humoral immunity, including surface immunoglobulin expression and responsiveness to B cell receptor (BCR) stimulation. Their robust growth characteristics and ease of genetic manipulation make them particularly suited for gene-editing studies aimed at dissecting molecular mechanisms in B cell malignancies.
MICALL2 encodes a protein that orchestrates actin cytoskeleton dynamics and membrane trafficking, with critical roles in endocytic recycling and cell?Ccell junction stabilization. Mechanistically, MICALL2 functions downstream of Rho GTPases such as Rac1 and Cdc42, and directly interacts with Rab8, Rab13, cingulin, and actin to couple Rab GTPase signals to actin remodeling. This coupling facilitates the recycling of junctional adhesion molecules and tight junction components, thereby maintaining epithelial and endothelial barrier integrity. In the context of lymphocyte biology, MICALL2 is implicated in the regulation of antigen receptor internalization and immune synapse formation, linking receptor-mediated signaling to cytoskeletal reorganization.
In Raji B cells, disruption of MICALL2 is anticipated to impair endocytic trafficking and adhesion dynamics, potentially altering BCR surface expression, signaling output, and cell migration. Given the role of BCR signaling in B cell survival and proliferation, this knockout model provides a valuable tool to investigate how junctional and trafficking deficiencies influence lymphoma cell behavior. Furthermore, the polyclonal nature of the cell population allows for the analysis of heterogeneous cellular responses, mirroring the clonal diversity often observed in lymphoid malignancies.
This MICALL2 knockout polyclonal cell product is well-suited for a range of experimental applications, including BCR trafficking assays, endocytosis pathway analysis, and lymphoma cell adhesion and migration studies. Representative assays that can be performed include flow cytometry for surface marker expression, immunofluorescence staining of junctional proteins, transferrin uptake measurement, co-immunoprecipitation of interacting proteins, and phospho-signaling analysis following BCR activation. These functional studies can support drug target validation efforts for B-cell lymphomas and investigations into cancer metastasis and immune deficiency disorders. For additional technical information or assistance with experimental design, please contact Ascent Research.
