In Stock Cell Lines
Homo sapiens (Human)
Brain
Adherent
The ATG4C Knockout T98G Cell Line offers a CRISPR/Cas9-edited human glioblastoma model with targeted disruption of ATG4C, a cysteine protease essential for processing LC3 family proteins during autophagy. This loss-of-function line enables precise investigation of autophagy-dependent processes in cancer, regulated by mTOR/AMPK/TFEB signaling. In T98G glioblastoma cells, ATG4C knockout impairs autophagosome formation and provides a platform for studying tumor cell survival, drug resistance, and autophagy flux using techniques such as LC3 western blotting and GFP-LC3 puncta analysis.
LEF1 Knockout A2780 Polyclonal Cells
Cat. No. ARG18904
ALKBH2 Knockout huh-7 Polyclonal Cells
Cat. No. ARG27876
C17orf80 Knockout jurkat Polyclonal Cells
Cat. No. ARG34046
ATAD3A Knockout TE1 Polyclonal Cells
Cat. No. ARG36839
CARD8 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG42308
LGR4 Knockout Hela Polyclonal Cells
Cat. No. ARG7523
The ATG4C Knockout T98G Cell Line is a CRISPR/Cas9-edited human glioblastoma cell line with targeted disruption of the ATG4C gene. This loss-of-function model abolishes expression of the cysteine protease ATG4C, providing a stable, renewable resource for autophagy research. Generated via CRISPR/Cas9, the knockout line avoids off-target silencing artifacts seen with transient methods. This knockout cell line serves as a robust tool for dissecting ATG4C??s role in autophagic pathways and for validating therapeutic targets.
The T98G parental line was established from a glioblastoma multiforme tumor and displays a hyperpentaploid karyotype. Commonly used in cancer studies, T98G cells model aggressive brain cancer with rapid growth, invasiveness, and apoptotic resistance, offering a clinically relevant backdrop for dissecting autophagy-related mechanisms in glioblastoma. Its hyperpentaploid genome recapitulates the genomic instability characteristic of glioblastoma, making it a suitable system for functional genomics and drug response studies.
ATG4C is a cysteine protease that cleaves LC3 family proteins (including MAP1LC3B and GABARAP) to enable their lipidation and membrane association during autophagosome biogenesis. Its activity is regulated by upstream kinases mTOR and AMPK, and by transcription factors TFEB and FOXO, which integrate nutrient and stress signals. ATG4C works within the LC3 lipidation system, interacting with ATG7 and ATG3, and is dependent on the PI3K class III complex. The enzyme functions downstream of the ULK1 complex and cooperates with the PI3K class III complex (Beclin-1/VPS34/ATG14) to produce LC3 lipidated forms. Disruption of ATG4C halts autophagy flux by blocking LC3 processing and autophagosome formation.
In glioblastoma, autophagy can sustain tumor survival under metabolic stress and therapy. The ATG4C knockout models autophagy deficiency in a cancer context, enabling investigation of how loss of ATG4C-dependent engulfment affects proliferation, drug sensitivity, and cellular homeostasis. This line is particularly suited for studies on therapy resistance where autophagy acts as a pro-survival mechanism. This knockout line also facilitates cross-talk studies between autophagy and apoptosis, two pathways that influence therapeutic outcome in glioblastoma.
Researchers can employ this knockout line in autophagic flux assays (LC3-I/II western blotting), immunofluorescence detection of GFP-LC3 puncta, RT-qPCR, and RNA-seq to monitor changes. Cell viability and proliferation assays help define the role of autophagy in glioblastoma growth. Combinatorial studies with mTOR inhibitors, starvation, or rapamycin further dissect ATG4C signaling. Additionally, the knockout line can be incorporated into high-throughput screens for autophagy modulators and used in functional assays to assess tumorigenic potential. For product inquiries, contact Ascent Research.
