Genome-edited Cells
Large intestine (colon)
A CRISPR/Cas9-edited knockout cell line of the Prkdc gene in the CT26 mouse colon carcinoma background. Prkdc encodes DNA-PKcs, the catalytic subunit of the NHEJ complex, which is recruited by Ku70/Ku80 to DNA breaks and phosphorylates key repair factors including XRCC4, Artemis, and DNA ligase IV. Loss of DNA-PKcs impairs DNA double-strand break repair, leading to genomic instability and hypersensitivity to DNA-damaging agents. This model enables investigation of NHEJ in colorectal cancer, assessment of DNA-PK inhibitors, and dissection of DNA damage responses. The syngeneic BALB/c origin supports in vivo tumor immunology studies. Representative assays include ??-H2AX foci imaging, clonogenic survival, and drug sensitivity profiling. Contact Ascent Research.
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The Prkdc Knockout CT26 Cell Line is a CRISPR/Cas9-edited mouse colon carcinoma model with targeted disruption of the Prkdc gene, encoding the DNA-dependent protein kinase catalytic subunit (DNA-PKcs). This loss-of-function line ablates DNA-PKcs expression, offering a defined system to study non-homologous end joining (NHEJ) DNA repair, V(D)J recombination, and genomic stability. It enables dissection of DNA damage responses without pharmacological intervention.
The parental CT26 line, a chemically induced BALB/c mouse colorectal adenocarcinoma, is an established syngeneic tumor model used in cancer biology and immunotherapy. Its adherent epithelial cells form aggressive tumors in immunocompetent BALB/c hosts, making it valuable for in vivo studies. The Prkdc knockout in this background creates a unique platform to investigate DNA repair deficiencies in colorectal cancer.
DNA-PKcs is the catalytic core of NHEJ, recruited to double-strand breaks by the Ku70/Ku80 heterodimer. Autophosphorylation activates its kinase activity, phosphorylating downstream effectors XRCC4, Artemis, and DNA ligase IV to execute repair. It also phosphorylates H2AX (??-H2AX) to amplify signaling and intersects with ATM/ATR pathways to regulate p53-mediated checkpoints and senescence. Accessory interactions with PNKP and APLF further coordinate ligation complex assembly. Thus, Prkdc centrally orchestrates DNA break repair and genome maintenance.
In CT26 cells, Prkdc knockout severely impairs NHEJ, causing genomic instability and radiosensitivity, reminiscent of SCID and cancer susceptibility syndromes. The increased mutational load and defective repair provide a model for studying colorectal cancer progression and response to DNA-damaging therapies. This line allows examination of synthetic lethality with DNA repair inhibitors (e.g., PARP, ATR) and tumor immunogenicity in syngeneic BALB/c mice, linking repair status to anti-tumor immunity.
Applications include Western blotting for DNA-PKcs ablation, ??-H2AX immunofluorescence for damage foci, clonogenic survival after radiation, comet assays for DNA breaks, and NHEJ reporter assays. High-throughput drug screening with DNA-PK inhibitors can be performed via viability assays. Transcriptome-wide RNA-seq and flow cytometric cell cycle analysis reveal downstream effects. These enable mechanistic exploration of DNA repair, therapeutic evaluation, and toxicology studies. For technical inquiries and customization options, please contact Ascent Research.
