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RELT induces cellular death in HEK 293 epithelial cells
John K Cusick1, Andrea Mustian, Kate Goldberg
1University of Colorado Denver School of Dental Medicine, Department of Craniofacial Biology, 12801 East 17th Avenue, Aurora, CO 80045, USA. john.cusick@ucdenver.edu
Tumor Necrosis Factor Receptor RELT and its homologues RELL1/RELL2 induce apoptosis in HEK 293 cells. This cell death pathway, characterized by DNA fragmentation, suggests RELT family members play a role in programmed cell death.
Area of Science:
- Cell Biology
- Molecular Biology
- Immunology
Background:
- RElT is a novel Tumor Necrosis Factor Receptor.
- RELL1 and RELL2 are human homologues of RELT.
Purpose of the Study:
- To investigate the role of RELT and its homologues in inducing cell death.
- To determine if RELT family members activate apoptotic pathways.
Main Methods:
- Transient transfection of RELT family members into HEK 293 and COS-7 cells.
- Observation of cellular morphology changes.
- Assessment of DNA fragmentation as an indicator of apoptosis.
Main Results:
- Transfection of RELT, RELL1, and RELL2 into HEK 293 cells induced cell death with DNA fragmentation, indicative of apoptosis.
- Overexpression of RELT in COS-7 cells caused cell rounding and lifting but no DNA fragmentation.
- The cellular response to RELT signaling varied between cell types.
Conclusions:
- RElT and its homologues can induce apoptosis in HEK 293 epithelial cells.
- The apoptotic effects of RELT signaling may be cell-type specific.
- RElT family members are implicated in the regulation of programmed cell death.
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