The DNAJC10 Knockout K-562 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the DNAJC10 gene has been disrupted in the human K-562 chronic myelogenous leukemia cell line. This product provides a powerful loss-of-function model for investigating the role of the endoplasmic reticulum co-chaperone DNAJC10 (ERdj5) in protein homeostasis and ER stress signaling. The polyclonal format offers a heterogeneous knockout cell pool, suitable for functional studies without clonal selection artifacts.
The host K-562 cell line, derived from the pleural effusion of a CML patient in blast crisis, is a pluripotent hematopoietic progenitor capable of multi-lineage differentiation. It is widely used to study leukemia biology, drug sensitivity, and apoptotic signaling, and serves as a relevant model for investigating oncogenic drivers and stress response pathways in chronic myelogenous leukemia. The cells grow robustly in suspension, facilitating high-throughput screening and detailed mechanistic studies.
DNAJC10 encodes an ER-resident oxidoreductase that reduces disulfide bonds in misfolded glycoproteins to promote ER-associated degradation (ERAD). It acts downstream of ER stress sensors IRE1??, PERK, and ATF6, and is transcriptionally regulated by XBP1 and ATF6. DNAJC10 interacts with key ERAD components including BiP/GRP78, EDEM1, OS9, and the SEL1L-HRD1 complex, facilitating retrotranslocation, ubiquitination, and proteasomal degradation via p97/VCP. Loss of DNAJC10 disrupts ERAD, activating the unfolded protein response (UPR) and altering cell fate under proteotoxic stress.
In K-562 leukemia cells, which often exhibit elevated basal ER stress, DNAJC10 knockout provides a model to study the dependency of leukemogenesis on ERAD. Disruption of DNAJC10 may sensitize these cells to ER stress-inducing agents such as tunicamycin, uncovering potential therapeutic vulnerabilities. This system allows dissection of ER proteostasis and apoptosis regulation in hematologic malignancies.
These polyclonal knockout cells are suitable for Western blot monitoring of ER stress markers (BiP, CHOP), qRT-PCR analysis of XBP1 splicing, and flow cytometric apoptosis assays (Annexin V). Co-immunoprecipitation studies can characterize interactions with ERAD machinery, while proteasomal activity and ubiquitination profiling reveal functional consequences. Cell viability assays (MTT) with ER stressors assess chemosensitivity. These assays help delineate DNAJC10??s role in ER stress and drug response. For further details, please contact Ascent Research.
