DNAJC16 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the DNAJC16 gene in the Jurkat T lymphoblastoid cell line (Homo sapiens). This heterogeneous pool of edited cells lacks functional DNAJC16, providing a loss-of-function model to study its role in protein homeostasis.
Jurkat cells, derived from an acute T cell leukemia patient, are IL-2 independent and serve as a classic model for T cell signaling, activation, and apoptosis. Widely used in immunology and cancer research, their robust and well-characterized signaling networks make them an ideal host for investigating gene function in a T cell context. The DNAJC16 knockout in this background allows dissection of its specific contributions without altering other key pathways.
DNAJC16 encodes a co-chaperone of the DnaJ/Hsp40 family that regulates Hsp70 chaperone activity, primarily in protein folding and endoplasmic reticulum-associated degradation (ERAD). It interacts with HSPA5 (BiP) and other Hsp70 family members to recognize misfolded proteins, facilitating their refolding or targeting them for proteasomal degradation via VCP/p97, DERL1, and HRD1. Loss of DNAJC16 disrupts this quality control, leading to accumulation of ERAD substrates and activation of the unfolded protein response (UPR). Upstream regulators like XBP1, ATF6, and ATF4, induced by ER stress, modulate this pathway, while DNAJC16 acts downstream to mitigate proteotoxic stress.
In Jurkat T lymphoblastoid cells, DNAJC16 knockout creates a physiologically relevant system to examine proteostasis in hematologic malignancies. The high metabolic activity of leukemic T cells places a heavy demand on protein quality control, and perturbations can trigger UPR-mediated apoptosis or alter activation signaling. This model is valuable for studying how DNAJC16 deficiency impacts T cell leukemogenesis and for identifying vulnerabilities in protein homeostasis networks.
Applications include analysis of UPR markers (BiP, CHOP) by western blotting, monitoring XBP1 splicing via RT-qPCR, flow cytometry-based apoptosis assays, and co-immunoprecipitation of Hsp70 complexes. Proteasome activity measurements and RNA-seq transcriptomic profiling enable comprehensive functional dissection. This knockout cell population supports investigation of ER stress signaling, drug target validation for proteostasis-related therapies, and functional genomics of chaperone networks in T cell leukemia. For further information, contact Ascent Research.
