The DNAJC5 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphocyte cell line, engineered for loss-of-function studies of the DNAJC5 gene. This product provides a heterogeneous pool of cells carrying targeted disruptions in DNAJC5, eliminating the expression of cysteine string protein alpha (CSP??) and enabling investigation of its cellular roles without clonal selection. The polyclonal format preserves population-level variability, making it suitable for pooled functional assays and high-throughput screening approaches.
The Raji cell line is an Epstein-Barr virus (EBV)-positive human Burkitt lymphoma-derived B lymphocyte model widely used in immunology and cancer research. These cells retain key B-cell functions such as antibody production and antigen presentation, and they serve as a robust system for studying secretory pathways, immune signaling, and lymphomagenesis. Their B-cell identity offers a physiologically relevant context to examine CSP??-mediated exocytic mechanisms in professional secretory cells.
DNAJC5 encodes CSP??, a synaptic vesicle-associated co-chaperone that partners with the heat shock cognate 70 (HSC70/HSPA8) chaperone to regulate SNARE complex assembly and stability, thereby facilitating regulated exocytosis. CSP?? directly interacts with SNARE components SNAP-25, syntaxin-1, and VAMP2/synaptobrevin, and its activity is modulated by upstream signals including calcium influx and phosphorylation by protein kinase A (PKA) and protein kinase C (PKC). This molecular network ensures efficient vesicle docking and fusion, and loss of CSP?? disrupts SNARE complex integrity and impairs secretion.
Within Raji B lymphocytes, DNAJC5 knockout disrupts CSP??-dependent exocytic pathways, likely affecting immunoglobulin secretion and exosome release, which positions this model as a valuable tool for studying chaperone-controlled protein trafficking in immune cells. Moreover, because mutations in DNAJC5 are linked to adult-onset neuronal ceroid lipofuscinosis (ANCL), a neurodegenerative disorder characterized by protein aggregation, these cells provide a non-neuronal platform to dissect the underlying cell biology of CSP?? misfunction and its contribution to diseases involving secretory defects and proteotoxicity.
Researchers can employ these polyclonal knockout cells to investigate CSP?? function through a range of assays, including Western blotting and RT-qPCR to confirm gene disruption, ELISA to quantify secreted immunoglobulins, and exocytosis assays to measure vesicle fusion capacity. Co-immunoprecipitation and immunofluorescence can probe CSP?? interactions with HSC70 and SNARE proteins, while flow cytometry evaluates surface marker expression linked to secretory activity. Transcriptomic profiling via RNA-seq further enables exploration of pathway alterations following loss of DNAJC5. For additional technical specifications and support, please contact Ascent Research.
