The DNAJC1 Knockout Jurkat Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal population of Jurkat T lymphocytes with targeted disruption of the DNAJC1 gene (encoding ERdj1). This knockout model provides a genetically heterogeneous pool of edited cells, enabling robust evaluation of DNAJC1 loss of function without reliance on single-clone artifacts. The polyclonal format is particularly suited for pooled screening approaches and for assessing phenotype penetrance across a diverse genetic background.
The Jurkat cell line, originally derived from an acute T-cell leukemia patient, is a widely employed human T lymphocyte model for investigating T-cell receptor (TCR) signaling, adaptive immunity, and lymphocyte activation. Its well-characterized signaling cascades and ease of genetic manipulation make it an ideal host for studying the intersections between immune function and cellular stress responses.
DNAJC1 functions as an endoplasmic reticulum (ER)-resident co-chaperone that recruits the heat shock protein BiP (HSPA5) to nascent polypeptides during translocation, thereby facilitating protein folding and maintaining ER proteostasis. DNAJC1 is transcriptionally regulated by the unfolded protein response (UPR) sensors ATF6 and XBP1s and acts within a network involving the Sec61 translocon, ERdj3, and ERdj4. Under ER stress, DNAJC1 contributes to the activation of the IRE1???CXBP1 and PERK?CCHOP arms of the UPR, linking its activity to protein quality control and the heat shock response.
Disruption of DNAJC1 in Jurkat cells provides a powerful tool for dissecting how ER proteostasis influences T-cell biology. Given the sensitivity of TCR signaling to redox and nutrient states, loss of DNAJC1 may perturb the folding and assembly of nascent receptors and other secretory proteins, potentially altering lymphocyte activation thresholds. This model is therefore highly relevant for exploring the contribution of ER stress pathways in immune cell function and in T-cell leukemogenesis, where the UPR is often hijacked to support malignant proliferation.
The DNAJC1 Knockout Jurkat Polyclonal Cells enable a broad range of experimental applications in cancer biology and protein misfolding research. Researchers can employ this model to study UPR dynamics using Western blotting for key markers such as BiP and CHOP, monitor XBP1 splicing via RT-qPCR, visualize ER stress with immunofluorescence, and quantify apoptosis through flow cytometry. Protein-folding luciferase reporter assays can directly assess changes in cellular folding capacity. These cells also serve as a platform for drug discovery targeting proteostasis mechanisms. For additional information, please contact Ascent Research.
