Appenzeller-Herzog, Christian ORCID: 0000-0001-7430-294X, Banhegyi, Gabor, Bogeski, Ivan ORCID: 0000-0001-9879-7174, Davies, Kelvin J. A., Delaunay-Moisan, Agnes, Forman, Henry Jay, Goerlach, Agnes, Kietzmann, Thomas ORCID: 0000-0003-0242-8636, Laurindo, Francisco, Margittai, Eva, Meyer, Andreas J., Riemer, Jan, Rutzler, Michael ORCID: 0000-0001-5597-8880, Simmen, Thomas, Sitia, Roberto ORCID: 0000-0001-7086-4152, Toledano, Michel B. and Touw, Ivo P. (2016). Transit of H2O2 across the endoplasmic reticulum membrane is not sluggish. Free Radic. Biol. Med., 94. S. 157 - 161. NEW YORK: ELSEVIER SCIENCE INC. ISSN 1873-4596

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Abstract

Cellular metabolism provides various sources of hydrogen peroxide (H2O2) in different organelles and compartments. The suitability of H2O2 as an intracellular signaling molecule therefore also depends on its ability to pass cellular membranes. The propensity of the membranous boundary of the endoplasmic reticulum (ER) to let pass H2O2 has been discussed controversially. In this essay, we challenge the recent proposal that the ER membrane constitutes a simple barrier for H2O2 diffusion and support earlier data showing that (i) ample H2O2 permeability of the ER membrane is a prerequisite for signal transduction, (ii) aquaporin channels are crucially involved in the facilitation of H2O2 permeation, and (iii) a proper experimental framework not prone to artifacts is necessary to further unravel the role of H2O2 permeation in signal transduction and organelle biology. (C) 2016 Elsevier Inc. All rights reserved.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Appenzeller-Herzog, ChristianUNSPECIFIEDorcid.org/0000-0001-7430-294XUNSPECIFIED
Banhegyi, GaborUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Bogeski, IvanUNSPECIFIEDorcid.org/0000-0001-9879-7174UNSPECIFIED
Davies, Kelvin J. A.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Delaunay-Moisan, AgnesUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Forman, Henry JayUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Goerlach, AgnesUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Kietzmann, ThomasUNSPECIFIEDorcid.org/0000-0003-0242-8636UNSPECIFIED
Laurindo, FranciscoUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Margittai, EvaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Meyer, Andreas J.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Riemer, JanUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Rutzler, MichaelUNSPECIFIEDorcid.org/0000-0001-5597-8880UNSPECIFIED
Simmen, ThomasUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Sitia, RobertoUNSPECIFIEDorcid.org/0000-0001-7086-4152UNSPECIFIED
Toledano, Michel B.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Touw, Ivo P.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-277641
DOI: 10.1016/j.freeradbiomed.2016.02.030
Journal or Publication Title: Free Radic. Biol. Med.
Volume: 94
Page Range: S. 157 - 161
Date: 2016
Publisher: ELSEVIER SCIENCE INC
Place of Publication: NEW YORK
ISSN: 1873-4596
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
PROTEIN-TYROSINE PHOSPHATASES; AQUAPORIN-11 KNOCKOUT MICE; GLUTATHIONE-PEROXIDASE 7; HYDROGEN-PEROXIDE; DNA-DAMAGE; REDOX REGULATION; NOX4; RECEPTOR; INACTIVATION; VACUOLIZATIONMultiple languages
Biochemistry & Molecular Biology; Endocrinology & MetabolismMultiple languages
Refereed: Yes
URI: http://kups.ub.uni-koeln.de/id/eprint/27764

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