In Stock Cell Lines
Homo sapiens (Human)
Lung
Adherent
The DNAJC10 Knockout NCI-H1975 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from NCI-H1975 lung adenocarcinoma cells. It disrupts DNAJC10, encoding an ER co-chaperone that regulates IRE1-alpha-mediated UPR signaling, providing a model to study ER stress in EGFR-mutant NSCLC. Applications include investigating protein folding, redox homeostasis, and ER-associated degradation, plus roles in drug resistance and apoptosis. Representative techniques are western blotting for GRP78 and CHOP, XBP1 splicing assays, and cell viability studies under ER stress.
CXCR4 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG16983
LITAF Knockout Raji Polyclonal Cells
Cat. No. ARG0965
ESYT1 Knockout Lovo Polyclonal Cells
Cat. No. ARG11713
GLCE Knockout A549 Polyclonal Cells
Cat. No. ARG10539
HDGF Knockout MES-OV Polyclonal Cells
Cat. No. ARG24514
MAP3K20 Knockout HEK293T Polyclonal Cells
Cat. No. ARG4396
The DNAJC10 Knockout NCI-H1975 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the human lung adenocarcinoma NCI-H1975 cell line. This model enables loss-of-function studies of DNAJC10, a gene encoding an ER co-chaperone involved in protein folding and the unfolded protein response (UPR). Disruption of DNAJC10 facilitates investigation of its role in ER stress signaling, redox homeostasis, and cancer cell biology.
NCI-H1975 is a non-small cell lung cancer (NSCLC) line established from a non-smoking female adenocarcinoma patient. It carries an activating EGFR double mutation (L858R/T790M) and wild-type KRAS, making it a key model for studying EGFR-targeted therapy resistance and ER proteotoxic stress in lung cancer. These cells provide an epithelial background to evaluate DNAJC10 function in a clinically relevant oncogenic setting.
DNAJC10 encodes an ER-resident protein containing a J-domain and a thioredoxin-like domain, functioning as a co-chaperone and oxidoreductase. It interacts with HSPA5/BiP and directly regulates IRE1-alpha (ERN1) signaling, a central UPR transducer. Under ER stress, ATF4 and XBP1 transcriptionally upregulate DNAJC10, which promotes protein folding and disulfide bond formation. Knockout of DNAJC10 impairs IRE1-alpha-mediated XBP1 splicing and alters downstream signaling, affecting CHOP/DDIT3 expression and ER-associated degradation (ERAD) through interactions with PDIA3 and ERAD components. This positions DNAJC10 at the intersection of ER quality control and redox maintenance.
In NCI-H1975 cells, DNAJC10 knockout allows dissection of how ER co-chaperone deficiency impacts UPR signaling in an EGFR-mutant NSCLC background. Such cancers often display high basal ER stress and depend on adaptive UPR pathways for survival. Loss of DNAJC10 may sensitize cells to ER stress-inducing agents or modulate drug resistance, providing a platform to study the balance between adaptive and pro-apoptotic UPR branches and to identify context-specific vulnerabilities.
This knockout cell line supports diverse research applications, including validation of UPR components as therapeutic targets, mechanistic studies of ER stress-induced apoptosis, and investigation of resistance mechanisms to chemotherapeutics or EGFR inhibitors. Representative assays include western blotting for GRP78, CHOP, and phospho-eIF2alpha; RT-qPCR for XBP1 splicing; cell viability and apoptosis assays following tunicamycin or thapsigargin treatment; co-immunoprecipitation of IRE1-alpha; immunofluorescence for ER morphology; and transcriptomic analysis under ER stress. For further details, please contact Ascent Research.
