The CRISPR/Cas9-edited DNAJC7 Knockout Raji Polyclonal Cells represent a loss-of-function model generated by CRISPR/Cas9-mediated disruption of the DNAJC7 gene in the human Raji B lymphocyte cell line. This polyclonal knockout cell population provides a heterogeneous pool of gene-edited cells, enabling the study of DNAJC7-dependent functions without clonal selection artifacts. The knockout product format is suitable for pooled screening approaches and population-level biochemical analyses.
Raji cells are a widely used suspension cell line derived from a Burkitt’s lymphoma patient, characterized by their Epstein-Barr virus (EBV)-positive status and B lymphocyte lineage. They retain features of mature B cells, including the capacity for immunoglobulin secretion and roles in immune surveillance. Their rapid proliferation and well-characterized signal transduction networks make them an excellent model for dissecting oncogenic and stress-responsive pathways in lymphoid malignancies.
DNAJC7 encodes a co-chaperone that cooperates with Hsp70 and Hsp90 to facilitate the folding, stabilization, and degradation of client proteins, including steroid hormone receptors such as the glucocorticoid receptor and androgen receptor. DNAJC7 directly interacts with RIPK1 and IKBKG (NEMO), and it regulates NF-??B signaling by modulating the IKK complex. Its activity is induced by upstream signals including heat shock factor 1 (HSF1), cellular stress (e.g., heat shock, oxidative stress), and inflammatory cytokines like TNF-??. Downstream, DNAJC7 modulates RIPK1 kinase activity, IKK complex function (IKBKB and IKBKG), and consequently NF-??B transcriptional responses mediated by RELA and NFKBIA. It also chaperones diverse Hsp70/Hsp90 clients, linking proteostasis to inflammatory and apoptotic pathways.
In the Raji B-cell context, loss of DNAJC7 is expected to disturb chaperone networks and impair NF-??B activation in response to stress and cytokines. Since Burkitt’s lymphoma cells rely on constitutive NF-??B activity for survival and proliferation, this knockout model may uncouple proteotoxic stress responses from pro-survival signaling. The resulting phenotype can reveal vulnerabilities in proteostasis and stress signaling that are relevant to B-cell malignancies, as well as neurodegenerative diseases where DNAJC7 mutations are linked to amyotrophic lateral sclerosis and frontotemporal dementia.
This polyclonal knockout model is suitable for investigating chaperone-mediated control of NF-??B in B-cell lymphomas, studying protein aggregation and unfolded protein response pathways, and performing functional analyses of Hsp70/Hsp90 co-chaperones. Typical experimental readouts include Western blotting for DNAJC7, Hsp70, and Hsp90; co-immunoprecipitation of chaperone complexes; NF-??B reporter and DNA-binding assays; annexin V-based apoptosis detection; RT-qPCR for NF-??B target genes; and heat shock protein induction profiling. The model is also a valuable tool for drug target discovery in lymphoma and ALS. For additional technical details, please contact Ascent Research.
