The PDGFRB Knockout Raji Polyclonal Cells product offers a CRISPR/Cas9-edited polyclonal population of Raji B lymphocytes with targeted disruption of the PDGFRB gene. This polyclonal knockout model avoids clonal artifacts and preserves population heterogeneity, providing a robust system for loss-of-function studies. Loss of the PDGFRB receptor tyrosine kinase eliminates PDGF-induced signaling, enabling dissection of this pathway in a lymphoma context.
Raji cells, derived from a human Burkitt lymphoma, are an EBV-positive, suspension B-lymphoblast line widely used in immunology and oncology research. Their rapid proliferation and well-characterized signaling landscape make them a suitable host for gene editing. The polyclonal nature of this product reflects the genetic diversity of the edited pool, supporting experiments that require a representative cell population rather than a single clone.
PDGFRB encodes the beta-type receptor for platelet-derived growth factor. Upon activation by ligands such as PDGF-BB and PDGF-DD, the receptor autophosphorylates and recruits adaptors including Grb2, Shc, and SHP2, triggering downstream cascades. Central pathways include the MAPK/ERK module (Grb2?CSos?CRas?CRaf?CMEK?CERK1/2) and the PI3K/AKT/mTOR axis, with additional contributions from PLC??/PKC and JAK/STAT signaling involving STAT3 and STAT5. The receptor also interacts with Cbl, Src, and RasGAP, fine-tuning signal output. Disruption of PDGFRB abrogates these signaling networks, halting ligand-driven proliferation, survival, and migration.
In the Raji B-cell lymphoma model, PDGFRB knockout allows investigation of this receptor’s role in lymphocyte biology and oncogenesis. It provides a platform to study how PDGF signaling intersects with pathways dysregulated in Burkitt lymphoma, such as MYC-driven proliferation. Researchers can assess phenotypic changes including altered cell growth, apoptosis resistance, and response to kinase inhibitors, thereby validating PDGFRB as a therapeutic target in hematologic malignancies.
Applications include Western blotting for PDGFRB and phospho-proteins (e.g., phospho-ERK, phospho-AKT), RT-qPCR for transcript analysis, and flow cytometry for surface receptor expression. Functional assays such as proliferation and apoptosis tests, along with drug sensitivity screens using PDGFR inhibitors like imatinib, are directly applicable. This polyclonal knockout population is a valuable tool for target validation and signal pathway analysis in B-cell contexts. For additional details, please contact Ascent Research.
