The CTSB Knockout Raji Polyclonal Cells constitute a polyclonal knockout cell population generated by CRISPR/Cas9-mediated disruption of the CTSB gene in Raji human B lymphocytes. Cathepsin B, the encoded lysosomal cysteine protease, is absent in this heterogeneous pool, providing a robust model to dissect its roles in proteolysis, autophagy, apoptosis, and antigen processing. The product is supplied as a versatile tool for advanced cellular and molecular analyses.
The Raji cell line is an EBV-positive B lymphocyte model derived from Burkitt??s lymphoma, featuring rapid proliferation and constitutive NF-??B signaling. It is extensively employed to study B-cell biology, antigen presentation, and EBV-associated oncogenesis, offering a disease-relevant system for evaluating cathepsin B function in lymphoma.
CTSB encodes a lysosomal cysteine protease that is transcriptionally regulated by Sp1 and NF-Y and induced by TNF-??, IL-6, and LPS. Cathepsin B activates pro-uPA, pro-MMPs, and caspases, and degrades collagen and laminin, linking it to ECM remodeling and apoptosis. Its activity is inhibited by cystatin C and stefin B, and subcellular localization involves LAMP1, LAMP2, and Annexin II. The protease functions in autophagy by mediating lysosomal degradation of autophagic cargo downstream of mTOR/TFEB signaling, and also participates in antigen processing and NF-??B pathway modulation.
In Raji cells, CTSB knockout disrupts lysosomal proteolysis and autophagic flux, potentially altering apoptosis sensitivity and drug response. Impaired antigen processing due to cathepsin B deficiency may affect immune recognition, while aberrant ECM degradation could modify tumor invasion. These changes are particularly relevant in EBV-driven lymphoma, where lysosomal function and autophagy influence viral persistence and immune evasion, providing a model to study CTSB-dependent survival and microenvironmental interactions.
Researchers can employ this polyclonal knockout population for Western blotting, activity assays, and autophagy flux measurements (LC3 turnover) to verify cathepsin B disruption. Co-immunoprecipitation with LAMP1/2 or cystatin C, antigen presentation assays, and immunofluorescence for LAMP1 and LC3 enable mechanistic studies. Drug sensitivity testing, apoptosis assays, and RNA-seq further elucidate CTSB??s role in lymphoma biology and therapeutic resistance. The cells are also suitable for exploring EBV biology and tumor microenvironment crosstalk. For detailed inquiries, contact Ascent Research.
