A novel cell line has been developed by using AAV gene targeting to effectively delete a segment of the FADD genomic locus in HCT116 colon cancer cells obtained from ATCC. This precise method resulted in cells that completely lack FADD protein expression, while still maintaining normal cell viability under basal conditions. Two independently derived clones have been thoroughly characterized, demonstrating significant resistance to apoptosis triggered via the extrinsic pathway without any evidence of spontaneous necrosis. This tool offers a reliable model for investigating apoptosis and related cell death mechanisms in a controlled in vitro setting.
Description
This technology is differentiated by its ability to achieve a complete knockout of FADD expression, as opposed to previous approaches that only reduced protein levels through truncated overexpression or RNA interference. The use of AAV gene targeting vectors, sourced from renowned research groups, ensures high specificity and reproducibility. Its unparalleled capability to completely disrupt FADD function provides an innovative platform to explore therapeutic resistance in cancer treatments, making it a valuable resource for both basic research and drug development applications.
Applications
- Cancer drug screening platform
- Therapeutic resistance testing model
- Apoptosis pathway evaluation tool
- Preclinical cancer research reagent
Advantages
- Provides a unique, complete knockout of FADD, ensuring the absence of residual protein expression unlike knockdown methods.
- Offers a robust model for studying the mechanisms of extrinsic pathway-induced apoptosis in colon cancer.
- Enables investigation of resistance mechanisms to apoptosis, enhancing research on therapeutic resistance.
Aids in drug development research by providing a clear background free from spontaneous necrosis effects.
IP Status
Research Tool
