In Stock Cell Lines
Homo sapiens (Human)
Uterus (cervix)
Adherent
The CLCC1 Knockout HeLa Cell Line is a CRISPR/Cas9-edited human knockout cell line targeting CLCC1, an ER chloride channel critical for ion homeostasis, calcium regulation, and protein folding. Disrupted in HPV-18 positive HeLa cervical adenocarcinoma cells, this loss-of-function model enables precise investigation of ER stress signaling and apoptosis. Upstream regulators include ATF4 and XBP1, with downstream coupling to calreticulin- and BAX/BAK-mediated pathways. Ideal applications encompass UPR marker analysis (BiP, CHOP), calcium imaging, and drug screening for ER stress modulators, supporting cancer and ER stress-related research.
KIF2A Knockout Raji Polyclonal Cells
Cat. No. ARG23915
AGFG2 Knockout HEK293T Polyclonal Cells
Cat. No. ARG25624
KMT2C Knockout A2780 Polyclonal Cells
Cat. No. ARG29331
ITPRIPL2 Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG30869
IMPACT Knockout SK-HEP-1 Polyclonal Cells
Cat. No. ARG32669
IKBKE Knockout Hela Polyclonal Cells
Cat. No. ARG37252
The CLCC1 Knockout HeLa Cell Line is a CRISPR/Cas9-edited knockout cell line designed to disrupt the human CLCC1 gene in HeLa cells. This loss-of-function model enables targeted investigation of the endoplasmic reticulum (ER) chloride channel CLCC1, a key regulator of ER ion homeostasis and protein folding. The knockout is achieved through CRISPR/Cas9-mediated gene disruption, providing a stable cell line for stringent functional analyses without introducing exogenous sequences.
The host HeLa line is an immortalized human cervical adenocarcinoma epithelial cell line (HPV-18 positive) originally derived from a female patient. Widely employed in cancer and cell biology research, HeLa cells offer a robust, proliferative epithelial system that naturally exhibits the high metabolic and protein-folding demands common to transformed cells. Their intrinsically active unfolded protein response (UPR) and well-defined apoptotic pathways make them particularly suited for investigating ER-related processes and drug-induced stress.
CLCC1 encodes an ER chloride channel that maintains luminal ion balance, which is crucial for ER calcium dynamics and chaperone-mediated protein folding. It interacts with calnexin and calreticulin to support oxidative protein maturation. Upstream, CLCC1 is induced by ER stress via ATF4 and XBP1, placing it within the UPR. Downstream, it modulates calcium release through IP3R and feeds into apoptotic signaling via BAX/BAK. Representative UPR components include PERK, ATF6, IRE1, BiP, and CHOP, which together govern the balance between adaptive and apoptotic ER stress responses.
In HeLa cells, CLCC1 knockout disrupts ER chloride homeostasis, impairing calcium regulation and protein folding, which triggers chronic UPR activation and heightened ER stress. This sensitizes the cancer cells to apoptosis, recapitulating pathophysiological conditions observed in ER stress-related disorders and malignancy. The model thus allows researchers to explore how ER ion channel loss influences tumor cell vulnerability and proteostatic collapse, serving as a relevant system for studying cancer cell adaptation to ER stress.
This knockout line supports multiple research applications, including dissection of UPR signaling (e.g., western blotting for BiP and CHOP), calcium imaging, and caspase activity assays. It is suitable for screening ER stress modulators in cell viability formats and for examining ER morphology via immunofluorescence. Functional studies of ER ion channels and validation of CLCC1 as a cancer target are also feasible. For further information, product specifications, or technical support, please contact Ascent Research.
