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| Image Credit: © Julian Nüchel, Center for Biochemistry Cologne |
Researchers from the UoC’s Center for Biochemistry at the Faculty of Medicine and the UoC CECAD Cluster of Excellence in Aging Research have discovered that an excessive immune response can be prevented by the intramembrane protease RHBDL4. In a study now published in Nature Communications under the title ‘RHBDL4-triggered downregulation of COPII adaptor protein TMED7 suppresses TLR4-mediated inflammatory signaling’, a previously unknown regulatory mechanism is described: The cleavage of a cargo receptor by a so-called intramembrane protease reduces the localization of a central immune receptor on the cell surface and thereby the risk of an overreaction of the immune system.
Intramembrane proteases are reactive proteins that reside in the cell membranes. They form a special group of proteases because they cut proteins within cellular membranes. Many of these unusual proteases have not yet been sufficiently characterized and only a few of the molecules they can cleave – the so-called substrates – and thus their functions are known. One of these intramembrane proteases is RHBDL4. It is located in the endoplasmic reticulum, a large intracellular membrane system that is responsible, among other things, for the correct folding of newly synthesized proteins that are fed into the secretory route.
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