The DNAJC15 Knockout Raji Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal knockout cell population derived from Raji B lymphocytes, with targeted disruption of the DNAJC15 gene. This loss-of-function model enables investigation of DNAJC15-dependent processes without the bottlenecks of clonal selection, preserving population-level heterogeneity while ablating gene function across the cell pool.
The Raji cell line is an Epstein-Barr virus (EBV)-positive Burkitt lymphoma-derived B lymphocyte model widely used in immunology and cancer research. These cells retain key B-cell functions, including antibody production and antigen presentation, and serve as a robust platform for studying oncogenic signaling, viral latency, and adaptive immunity.
DNAJC15 encodes a mitochondrial J-domain co-chaperone that interacts with HSPA9/mortalin to stimulate its ATPase activity, driving protein translocation through the TIM23 translocon. DNAJC15 forms complexes with TIMM17A, TIMM23, and PAM16 to facilitate mitochondrial import. Upstream, DNAJC15 expression is regulated by estrogen receptor alpha (ESR1) and heat shock factor 1 (HSF1) in response to mitochondrial stress signals. Downstream, functional DNAJC15 is required for proper mitochondrial import of substrates, and its loss leads to altered levels of apoptotic regulators BAX and Bcl-2, thereby linking mitochondrial proteostasis to cell death pathways.
In Raji B lymphocytes, DNAJC15 disruption compromises mitochondrial protein import, triggering the mitochondrial unfolded protein response (UPRmt) and proteotoxic stress. This perturbation can shift the balance of pro- and anti-apoptotic factors, potentially altering the sensitivity of these lymphoma cells to chemotherapeutic agents. Given the role of mitochondrial chaperones in cancer cell survival, this knockout model provides a physiologically relevant system to dissect how DNAJC15-dependent mitochondrial homeostasis influences B-cell lymphoma progression and drug resistance.
Researchers can employ this polyclonal knockout pool in a variety of experimental workflows. Western blot and RT-qPCR can confirm DNAJC15 ablation and monitor UPRmt gene expression. Flow cytometry enables assessment of apoptosis markers and mitochondrial mass. Co-immunoprecipitation and mitochondrial isolation assays permit biochemical analysis of TIM23 complex integrity and protein import. Cell viability (MTT/CTG) and drug sensitivity screening are suitable for evaluating chemoresistance mechanisms. RNA-seq can provide unbiased transcriptomic insights into stress responses. This model is particularly suited for mitochondrial biology, cancer drug resistance profiling, and functional genomics in lymphomas. For technical assistance or custom modifications, please contact Ascent Research.
