Programmed cell death is a mechanism that causes defective and potentially harmful cells to destroy themselves. It serves a number of purposes in the body, including the prevention of malignant tumor growth. Now, researchers at Technische Universität München (TUM) have discovered a previously unknown mechanism for regulating programmed cell death. They have also shown that patients with lymphoma often carry mutations in this signal pathway.
Fluorescence microscopy image showing the ubiquitin ligase FBXO25 (green) and the “life-preserving” protein (red) in a cancer cell that is currently undergoing programmed cell death. The yellow signal indicates instances where both proteins are at the same location.
Credit: Picture F. Bassermann / TUM
Original publication: Baumann U., Fernández-Sáiz V., Rudelius M., Lemeer S., Rad R., Knorn A.M., Slawska J., Engel K., Jeremias I., Li Z., Tomiatti V., Illert A.L., Targosz B.S., Braun M., Perner S., Leitges M., Klapper W., Dreyling M., Miething C., Lenz G., Rosenwald A., Peschel C., Keller U., Kuster B., and F. Bassermann, Disruption of the PRKCD–FBXO25–HAX-1 axis attenuates the apoptotic response and drives lymphomagenesis, Nature Medicine, 20, 1401-1409 (2014). DOI: 10.1038/nm.3740