In Stock Cell Lines
Homo sapiens (Human)
Uterus (cervix)
Adherent
The GSDMC Knockout Hela Cell Line is a CRISPR/Cas9-edited knockout cell line derived from human cervical adenocarcinoma, designed to eliminate GSDMC expression and study pyroptosis. GSDMC, a pore-forming protein cleaved by caspase-8 downstream of TNF-?? and other death signals, triggers inflammatory cell death and regulates IL-1?? release. Its expression is controlled by YAP/TAZ. This model enables research into pyroptosis mechanisms, cancer drug responses, and inflammatory diseases. Suitable for assays such as LDH release, IL-1?? ELISA, and caspase-8 activation, it supports drug screens, cell death studies, and tumor microenvironment investigations.
MEF2D Knockout HT29 Polyclonal Cells
Cat. No. ARG14675
MAP3K7 Knockout CAL27 Polyclonal Cells
Cat. No. ARG11573
ISG15 Knockout A2780 Polyclonal Cells
Cat. No. ARG29243
BAX Knockout CAL27 Polyclonal Cells
Cat. No. ARG35348
CNOT4 Knockout MES-OV Polyclonal Cells
Cat. No. ARG6773
BAP1 Knockout MeT-5A Cell Line
Cat. No. ARG0572
The GSDMC Knockout Hela Cell Line is a CRISPR/Cas9-edited knockout cell line in which the GSDMC gene has been disrupted to eliminate its protein expression. This loss-of-function model enables direct investigation of GSDMC-dependent pyroptosis and associated signaling in a well-defined human epithelial system. The stable genetic disruption avoids transient pharmacological manipulations, providing a reliable tool for long-term functional assays and drug screening applications.
HeLa cells are an immortalized human cervical adenocarcinoma line harboring HPV-18 sequences that inactivate p53 and Rb tumor suppressors. As a widely used model, HeLa offers robust growth, well-characterized signaling networks, and compatibility with high-throughput assays, making it ideal for genetic manipulation. This parental background provides a relevant context for studying GSDMC function within HPV-driven oncogenesis and tumor biology.
GSDMC is a pore-forming executor of pyroptosis, activated by caspase-8 cleavage downstream of death receptors (TNF-??, FasL, TRAIL) or chemotherapeutic stress (e.g., doxorubicin, hypoxia). Cleaved N-GSDMC oligomerizes in the plasma membrane, inducing membrane permeabilization, LDH and IL-1?? release, and NLRP3 inflammasome activation. Transcriptional regulation by YAP/TAZ links Hippo pathway signals to GSDMC expression, while the assembled death-inducing signaling complex (DISC) facilitates caspase-8 activation. In tumor settings, GSDMC can suppress or promote malignancy depending on stimulus context, making this knockout essential for dissecting its dual roles.
In the HeLa background, where p53 and Rb are inactivated, GSDMC knockout allows dissection of pyroptotic signaling independent of these classical tumor suppressor pathways. This model is particularly valuable for assessing how GSDMC loss impacts cell fate decisions, drug sensitivity, and inflammatory responses in a cervical cancer context, revealing therapeutic vulnerabilities or resistance mechanisms.
Researchers can utilize this knockout for mechanistic studies of pyroptosis, anti-cancer drug screening, and tumor microenvironment modeling. Typical assays include Western blotting, RT-qPCR, LDH release, IL-1?? ELISA, Annexin V/PI flow cytometry, caspase-8 activation, and drug sensitivity colony formation. The model also supports RNA-seq and functional assays like migration/invasion. For detailed characterization data or assistance with experimental design, please contact Ascent Research.
