The PEPD Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji human B lymphocyte cell line, featuring targeted disruption of the PEPD gene. This loss-of-function model enables investigation of prolidase activity in a lymphoblastoid context. The polyclonal format provides a heterogeneous population of edited cells, facilitating studies of PEPD-dependent phenotypes without clonal selection bias.
The Raji cell line, originating from an EBV-positive Burkitt lymphoma, is widely used as a model of B lymphocyte biology, including antibody production, antigen presentation, and adaptive immunity. As a suspension cell line with robust growth characteristics, Raji cells are amenable to large-scale culture and high-throughput assays. Their lymphoblastoid origin preserves many features of normal B cells, making them a relevant platform for probing immune cell metabolism and tumor biology.
PEPD encodes prolidase, a homodimeric dipeptidase that specifically hydrolyzes imidodipeptides containing C-terminal proline or hydroxyproline, derived primarily from collagen degradation by matrix metalloproteinases (MMPs). This enzyme functions downstream of TGFB1 signaling and is transcriptionally regulated by AP-1 transcription factors. Prolidase-mediated proline liberation supports amino acid recycling, protein synthesis, and collagen biosynthesis. Consequently, PEPD is essential for ECM remodeling and proline homeostasis. Loss of PEPD impairs these processes, leading to reduced free proline availability and disrupted collagen turnover, which are hallmarks of prolidase deficiency.
In the Raji B lymphocyte context, PEPD disruption may significantly alter cellular metabolism and function. Proline is a critical amino acid for protein synthesis and energy production; its deficiency can impact antibody secretion and proliferative capacity. Additionally, ECM remodeling is increasingly recognized in lymphoma progression and immune cell interactions within tumor microenvironments. This knockout model therefore permits dissection of how prolidase deficiency contributes to immune dysfunction, as observed in prolidase deficiency patients who suffer from recurrent infections and impaired wound healing alongside connective tissue defects.
Typical applications include disease modeling for prolidase deficiency, investigation of ECM remodeling in B cell lymphomas, and metabolic profiling of amino acid utilization in transformed lymphocytes. The cells are suitable for prolidase activity assays, quantitative PCR, Western blotting, collagen degradation assays, cell proliferation measurements, and flow cytometry-based apoptosis analyses. Their lymphoblastoid nature renders them compatible with high-throughput drug screening aimed at identifying modulators of proline metabolism or ECM interactions in hematological malignancies. For detailed product specifications and support, please contact Ascent Research.
