The DNAJB4 Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-mediated gene-disrupted polyclonal cell population designed to eliminate DNAJB4 protein expression in Jurkat cells. This knockout model enables the study of loss-of-function effects of DNAJB4 in a T-cell context, providing a genetically defined background for investigating co-chaperone functions without the limitations of transient silencing approaches. The polyclonal format ensures population-level heterogeneity that reflects the diversity of editing outcomes, suitable for applications where clonal representation of the knockout phenotype is desired.
Jurkat cells are a widely utilized immortalized human T lymphocyte line derived from the peripheral blood of a 14-year-old male with T cell acute lymphoblastic leukemia. These suspension cells are extensively employed as a model system for dissecting T cell receptor signaling, apoptosis, and the molecular mechanisms underlying T cell malignancies. Their well-characterized signaling circuitry and responsiveness to stress stimuli make them an ideal host for studying the functional roles of co-chaperones in lymphocyte biology.
DNAJB4, a member of the Hsp40 family, functions as a co-chaperone that stimulates the ATPase activity of Hsp70 (HSPA1A) to facilitate protein folding, refolding, and translocation under both physiological and stress conditions. It is transcriptionally upregulated by heat shock factor 1 (HSF1) in response to heat stress and proteotoxic insults. Mechanistically, DNAJB4 interacts with Hsp70 and BAG3, and it participates in the regulation of key signaling nodes: it modulates the RAF1-MAPK1 cascade and influences NF-kB signaling via RELA. By controlling Hsp70 activity, DNAJB4 integrates stress signals into cell survival decisions, impacting MAPK pathway dynamics and NF-kB-dependent transcription.
In the Jurkat T-cell background, DNAJB4 knockout disrupts this co-chaperone network and is predicted to impair cellular responses to heat shock and other forms of proteotoxic stress. Given the reliance of leukemic T cells on altered stress signaling and survival pathways, loss of DNAJB4 may sensitize cells to apoptosis or alter the balance of MAPK and NF-kB signaling. This model thus provides a unique tool to dissect how co-chaperone-mediated protein quality control intersects with oncogenic signaling in T cell leukemia.
Researchers can leverage this polyclonal knockout population to examine the role of DNAJB4 in stress granule dynamics, heat shock survival, and phospho-signaling events through assays such as western blotting for downstream targets (e.g., phospho-MAPK1), RT-qPCR for NF-kB target genes, flow cytometry for annexin V-based apoptosis detection, and RNA-seq for transcriptomic profiling of perturbed pathways. Functional studies can probe the interaction of DNAJB4 with Hsp70 and BAG3 using co-immunoprecipitation. This product is ideally suited for investigations into the co-chaperone dependencies of T cell leukemia and signal integration between stress and survival pathways. For detailed protocols or technical support, please contact Ascent Research.
