The DOCK11 Knockout Raji Polyclonal Cells provide a CRISPR/Cas9-edited heterogeneous knockout population derived from the human Raji B lymphocyte line, designed to disrupt the DOCK11 gene. This polyclonal product delivers a pooled loss-of-function model that faithfully recapitulates DOCK11 deficiency for functional studies of B cell signaling and actin dynamics, avoiding clonal selection bias.
The host Raji line is an Epstein-Barr virus?Ctransformed lymphoblastoid cell line from a Burkitt lymphoma, exhibiting mature B cell features including antibody production, humoral immunity, and antigen presentation. Its robust B cell receptor (BCR) signaling machinery and reproducible growth render it an ideal platform for investigating lymphocyte biology and lymphomagenesis.
DOCK11 acts as a specific guanine nucleotide exchange factor for CDC42, promoting the GTP-bound active state. BCR engagement and chemokine receptor activation trigger upstream kinases (SRC, SYK, PI3K) that signal to the DOCK11?CELMO (ELMO1/2/3) complex, leading to CDC42 activation. Active CDC42 then stimulates PAK1, which phosphorylates WASP, driving ARP2/3-mediated actin nucleation and polymerization. Thus, DOCK11 serves as an essential link between extracellular cues and cytoskeletal reorganization in lymphocytes. Knockout of DOCK11 abolishes this signaling axis, impairing actin remodeling, migration, and immune synapse formation.
In the Raji B cell context, loss of DOCK11 disrupts BCR-dependent actin dynamics, offering a model for DOCK11 deficiency??a primary immunodeficiency with autoimmunity and early-onset inflammatory bowel disease. Additionally, the Burkitt lymphoma origin of Raji cells enables exploration of DOCK11’s contribution to lymphoma cell migration and proliferation. The polyclonal knockout population ensures representation of diverse edits, mimicking heterogeneous gene inactivation.
Key applications include western blot and RT-qPCR verification of knockout, analysis of CDC42 activation via G-LISA and phospho-PAK1 ELISA, and assessment of BCR signaling by phospho-flow cytometry. Actin polymerization assays, F-actin immunofluorescence, and transwell migration assays quantify cytoskeletal and motility defects. The cells are suitable for co-immunoprecipitation studies of DOCK11?CELMO interactions and for screening regulators of the CDC42 pathway. For additional information, please contact Ascent Research.
