The PDLIM1 Knockout Raji Polyclonal Cells product provides a CRISPR/Cas9-mediated gene-disrupted polyclonal cell population derived from the Raji B lymphoblastoid line, with targeted disruption of the PDLIM1 gene. This polyclonal pool comprises a heterogeneous mixture of edited cells carrying various loss-of-function alleles, enabling robust functional studies of PDLIM1 in a lymphoid context without clonal selection bottlenecks. The knockout model serves as a powerful tool for dissecting PDLIM1-dependent cytoskeletal and signaling networks.
The Raji host cell line is an Epstein-Barr virus (EBV)-positive Burkitt lymphoma line that exhibits characteristics of germinal-center-derived B lymphocytes. These cells are immortalized and retain key B-cell receptor (BCR) signaling machinery, making them a widely used model for humoral immunity, lymphomagenesis, and integrin-mediated adhesion studies. Their robust growth in suspension and semi-adherent cultures facilitates high-throughput applications.
PDLIM1 encodes a PDZ-LIM domain adaptor protein that orchestrates actin cytoskeleton dynamics and focal adhesion assembly. It directly interacts with alpha-actinin (ACTN1/ACTN4) via its PDZ domain, crosslinking actin stress fibers to integrin-based adhesion complexes. PDLIM1 functions downstream of mechanical cues, RhoA/ROCK, and integrin ligation, and is regulated by TGF-?? signaling. It forms complexes with palladin and enigma family members, and influences focal adhesion kinase (FAK) and Src kinase activation, ultimately modulating NF-??B transcriptional responses. Through these interactions, PDLIM1 controls cell adhesion, spreading, and migration.
In Raji B cells, PDLIM1 knockout is expected to disrupt the linkage between actin filaments and focal adhesions, impairing integrin-dependent spreading and adhesion dynamics. This disruption may attenuate crosstalk between integrin and BCR pathways, thereby dampening downstream NF-??B signaling, which is critical for B-cell survival and proliferation. Consequently, this polyclonal knockout model provides a physiologically relevant system to investigate how cytoskeletal adaptors regulate lymphoma cell behavior, migration, and signal transduction.
Researchers can employ this PDLIM1 knockout cell population in a broad range of assays, including Western blotting and RT-qPCR for knockout confirmation, RNA-seq for transcriptomic profiling, immunofluorescence and phalloidin staining to visualize actin remodeling, cell adhesion and Transwell migration assays to assess functional consequences, and phospho-FAK ELISA or NF-??B reporter assays to probe signaling alterations. It is suitable for drug screening efforts targeting cytoskeletal pathways and phenotypic analyses in lymphoma biology. For further information, please contact Ascent Research.
