Short Communication Open Access
Volume 1 | Issue 1 | DOI: https://doi.org/10.33696/genetics.1.004

Constitutively Active Death Receptor Induces Apoptosis in Mammalian Cells

  • 1Department of Physiology and Developmental Biology, Brigham Young University, Provo UT, USA
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Corresponding Author

Dario Mizrachi, dario_mizrachi@byu.edu

Received Date: January 21, 2022

Accepted Date: February 16, 2022


poptosis is a physiological response in development and homeostasis of metazoans. Apoptosis is triggered during pathological events as a means to renew affected tissues and eliminate cancer cells. The immune system regulates the extrinsic pathway of apoptosis, where signals such as TNFα or displayed ligands on the surface of immune cells trigger signal cascades by death receptors present on targeted cells. Therapeutics, like Doxorubicin, lead to apoptosis successfully. In this article, we present a design for a constitutively active death receptor (CADRE) based on a single mutation within the transmembrane domain of Fas (CD95, Apo-1, TNFRSF6), a prototypical death receptor in the tumor necrosis factor receptor superfamily. Overexpression of CADRE in HEK-293 cells initially results in decreased proliferation. Upon closer inspection, CADRE overexpression in HEK-293 caused apoptosis, similar to the effects of Doxorubicin. Finally, using 10 different cancer cell lines, we report that CADRE induced apoptosis in all of them. CADRE is a new tool in the search for a single solution to fight cancer.

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