dc.creator | Sanzo-Machuca, Ángela | es |
dc.creator | Monje Moreno, José Manuel | es |
dc.creator | Casado-Navarro, Rafael | es |
dc.creator | Karakuzu, Ozgur | es |
dc.creator | Guerrero Gómez, David | es |
dc.creator | Fierro-González, Juan Carlos | es |
dc.creator | Swoboda, Peter | es |
dc.creator | Muñoz, Manuel J. | es |
dc.creator | Miranda Vizuete, Antonio | es |
dc.date.accessioned | 2019-08-20T11:02:59Z | |
dc.date.available | 2019-08-20T11:02:59Z | |
dc.date.issued | 2019-06 | |
dc.identifier.citation | Sanzo-Machuca, Á., Monje Moreno, J.M., Casado-Navarro, R., Karakuzu, O., Guerrero Gómez, D., Fierro-González, J.C.,...,Miranda Vizuete, A. (2019). Redox-dependent and redox-independent functions of Caenorhabditis elegans thioredoxin 1. Redox Biology, 24, 101178-1-101178-8. | |
dc.identifier.issn | 2213-2317 | es |
dc.identifier.uri | https://hdl.handle.net/11441/88465 | |
dc.description.abstract | Thioredoxins (TRX) are traditionally considered as enzymes catalyzing redox reactions. However, redox-independent functions of thioredoxins have been described in different organisms, although the underlying molecular mechanisms are yet unknown. We report here the characterization of the first generated endogenous redox-inactive thioredoxin in an animal model, the TRX-1 in the nematode Caenorhabditis elegans. We find that TRX-1 dually regulates the formation of an endurance larval stage (dauer) by interacting with the insulin pathway in a redox-independent manner and the cGMP pathway in a redox-dependent manner. Moreover, the requirement of TRX-1 for the extended longevity of worms with compromised insulin signalling or under calorie restriction relies on TRX-1 redox activity. In contrast, the nuclear translocation of the SKN-1 transcription factor and increased LIPS-6 protein levels in the intestine upon trx-1 deficiency are strictly redox-independent. Finally, we identify a novel function of C. elegans TRX-1 in male food-leaving behaviour that is redox-dependent. Taken together, our results position C. elegans as an ideal model to gain mechanistic insight into the redox-independent functions of metazoan thioredoxins, overcoming the limitations imposed by the embryonic lethal phenotypes of thioredoxin mutants in higher organisms. | es |
dc.description.sponsorship | NIH Office of Research Infrastructure P40 OD010440 | es |
dc.description.sponsorship | Spanish Ministry of Economy and Competitiveness BFU2015- 64408-P | es |
dc.description.sponsorship | Fondo Social Europeo BFU2015- 64408-P | es |
dc.description.sponsorship | National Institute of Allergy and Infectious Diseases of the National Institutes of Health R01AI076406 | es |
dc.format | application/pdf | es |
dc.language.iso | eng | es |
dc.publisher | Elsevier | es |
dc.relation.ispartof | Redox Biology, 24, 101178-1-101178-8. | |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject | Caenorhabditis elegans | es |
dc.subject | Dauer | es |
dc.subject | Food-leaving | es |
dc.subject | Lips-6 | es |
dc.subject | Longevity | es |
dc.subject | Male | es |
dc.subject | Redox | es |
dc.subject | Skn-1 | es |
dc.subject | Thioredoxin | es |
dc.title | Redox-dependent and redox-independent functions of Caenorhabditis elegans thioredoxin 1 | es |
dc.type | info:eu-repo/semantics/article | es |
dcterms.identifier | https://ror.org/03yxnpp24 | |
dc.type.version | info:eu-repo/semantics/publishedVersion | es |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es |
dc.contributor.affiliation | Instituto de Biomedicina de Sevilla (IBIS) | es |
dc.relation.projectID | P40 OD010440 | es |
dc.relation.projectID | R01AI076406 | es |
dc.relation.projectID | BFU2015- 64408-P | es |
dc.relation.publisherversion | http://doi.org/10.1016/j.redox.2019.101178 | es |
dc.identifier.doi | 10.1016/j.redox.2019.101178 | es |
idus.format.extent | 8 p. | es |
dc.journaltitle | Redox Biology | es |
dc.publication.volumen | 24 | es |
dc.publication.initialPage | 101178-1 | es |
dc.publication.endPage | 101178-8 | es |