The DIAPH3 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-mediated polyclonal knockout cell population derived from the Raji B lymphocyte line, engineered for targeted disruption of the DIAPH3 gene. This product provides a heterogeneous pool of cells carrying loss-of-function mutations at the DIAPH3 locus, enabling robust functional studies of formin-dependent processes without clonal artifacts.
The Raji cell line originates from an EBV-positive Burkitt??s lymphoma and grows in suspension as B lymphocytes. These cells exhibit characteristic features of mature B cells, including surface immunoglobulin expression and the capacity for antigen presentation, and they serve as a widely employed model for studying B cell receptor signaling, immune synapse assembly, and lymphomagenesis.
DIAPH3 encodes a member of the diaphanous-related formin family that functions as a downstream effector of Rho GTPases, including RhoA, Rac1, and Cdc42, and is activated by integrin-mediated adhesion and mechanical cues. Upon activation, DIAPH3 promotes linear actin polymerization through its interaction with profilin and nucleates the formation of F-actin stress fibers, while also stabilizing microtubules via associations with plus-end tracking proteins such as EB1 and CLIP-170. Through these cytoskeletal remodeling activities, DIAPH3 regulates the subcellular localization and transcriptional activity of the mechanosensitive co-activators YAP and TAZ, as well as the SRF/MRTF pathway, thereby linking dynamic changes in the actin and microtubule networks to gene expression programs controlling cell adhesion, migration, and proliferation.
Disruption of DIAPH3 in the Raji B cell background eliminates formin-mediated actin polymerization and microtubule stabilization, offering a powerful system to dissect the role of these cytoskeletal processes in lymphocyte biology. Since B cell receptor activation and immune synapse formation require precise cytoskeletal rearrangements, the DIAPH3 knockout cells enable investigation of formin-dependent mechanisms controlling adhesion molecule dynamics, cell polarization, and antigen presentation. Furthermore, as Raji cells are derived from Burkitt??s lymphoma, this model provides a unique tool to explore the contribution of DIAPH3-regulated cytoskeletal pathways to lymphoma cell motility, invasiveness, and sensitivity to cytoskeleton-targeting agents.
Researchers can utilize these polyclonal knockout cells to investigate formin-mediated actin and microtubule dynamics in B lymphocyte adhesion, transwell migration, and immune synapse formation, employing techniques such as immunofluorescence for F-actin and tubulin, flow cytometry for surface adhesion markers, and live-cell imaging of cytoskeletal remodeling. The model also supports screening assays for small molecules or genetic regulators that modulate DIAPH3 activity, as well as transcriptomic analyses (RNA-seq) and RhoA activation pull-downs to map downstream signaling networks. Additionally, given the association of DIAPH3 mutations with autosomal dominant deafness 1 (DFNA1), these cells may serve as a hematopoietic platform to study DIAPH3-linked hearing loss mechanisms at the cellular level. Overall, the DIAPH3 Knockout Raji Polyclonal Cells provide a versatile resource for exploring formin-dependent pathways in lymphocyte function, lymphoma progression, and beyond. For further information regarding this product, please contact Ascent Research.
