Title data
Gertz, Melanie ; Fischer, Frank ; Wolters, Dirk ; Steegborn, Clemens:
Activation of the lifespan regulator p66Shc through reversible disulfide bond formation.
In: Proceedings of the National Academy of Sciences of the United States of America.
Vol. 105
(2008)
Issue 15
.
- pp. 5705-5709.
ISSN 1091-6490
DOI: https://doi.org/10.1073/pnas.0800691105
Abstract in another language
Cell fate and organismal lifespan are controlled by a complex signaling network whose dysfunction can cause a variety of aging-related diseases. An important protection against these failures is cellular apoptosis, which can be induced by p66(Shc) in response to cellular stress. The precise mechanisms of p66(Shc) action and regulation and the function of the p66(Shc)-specific N terminus remain to be identified. Here, we show that the p66(Shc) N terminus forms a redox module responsible for apoptosis initiation, and that this module can be activated through reversible tetramerization by forming two disulfide bonds. Glutathione and thioredoxins can reduce and inactivate p66(Shc), resulting in a thiol-based redox sensor system that initiates apoptosis once cellular protection systems cannot cope anymore with cellular stress.
Further data
Item Type: | Article in a journal |
---|---|
Refereed: | Yes |
Additional notes: | PubMed-ID: 16051147 |
Institutions of the University: | Faculties > Faculty of Biology, Chemistry and Earth Sciences > Department of Chemistry > Chair Biochemistry > Chair Biochemistry - Univ.-Prof. Dr. Clemens Steegborn Faculties Faculties > Faculty of Biology, Chemistry and Earth Sciences Faculties > Faculty of Biology, Chemistry and Earth Sciences > Department of Chemistry Faculties > Faculty of Biology, Chemistry and Earth Sciences > Department of Chemistry > Chair Biochemistry |
Result of work at the UBT: | No |
DDC Subjects: | 500 Science > 540 Chemistry |
Date Deposited: | 16 Apr 2015 11:24 |
Last Modified: | 05 Sep 2022 07:39 |
URI: | https://eref.uni-bayreuth.de/id/eprint/10293 |