English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/143789
logo share SHARE   Add this article to your Mendeley library MendeleyBASE
Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar a otros formatos:


TRX-1 as a potential redox regulator of the major C. elegans oxidative stress transcription factor, SKN-1

AuthorsMcCallum, Katie C.; Liu, Bin; Fierro-González, Juan Carlos; Swoboda, Peter; Arur, Swathi; Miranda-Vizuete, Antonio ; Garsin, Danielle A.
Issue DateJun-2015
Citation20th International Meeting C. elegans (2015)
AbstractThe ability of an organism to maintain oxidative homeostasis is critical for its survival. At the cellular level, exposure to oxidative insult can irreversibly damage DNA, proteins, and lipids, all of which can lead to cell apoptosis or necrosis. At the organismal level, unresolved oxidative stress can lead to several life-threatening diseases, including Alzheimer’s, Parkinson’s disease, and atherosclerosis. Our lab uses the model organism C. elegans to study the regulation of the major oxidative stress transcription factor, SKN -1, which is a functional homolog of the major mammalian oxidative stress transcription factor, Nrf2. Recently, we identified a thioredoxin as a novel regulator of SKN -1. Thioredoxins are small redox reactive proteins that have been shown to play a prominent role in redox signaling. In light of this, we hypothesized that thioredoxins are the ‘first responders’ to oxidative stress and may serve as the link between stress sensing and stress signaling that has yet to be fully elucidated in many organisms. In support of this hypothesis, we have shown that the loss of trx-1 promotes intestinal nuclear localization of SKN-1, even in the absence of stress, indicating that TRX-1 regulates SKN-1 localization. Interestingly, TRX -1-dependent regulation of intestinal SKN-1 nuclear localization is specific, occurs cell non-autonomously, and is dependent on the p38 MAPK pathway. However, while TRX -1 is able to regulate SKN-1 localization, we do not see increased activation of this transcription factor. Interestingly, loss of trx-1 elicited a general, organismal down-regulation of several classes of genes, with collagens and lipid transport and localization proteins being most prevalent.However, one prominent lipase-related gene, lips-6, was highly up regulated upon loss of trx-1. Furthermore, this up regulation was dependent on skn-1.
DescriptionPóster presentado en la 20th International Meeting C. elegans, celebrada en Los Ángeles del 24 al 28 de junio de 2015.
Appears in Collections:(IBIS) Comunicaciones congresos
Files in This Item:
File Description SizeFormat 
accesoRestringido.pdf15,38 kBAdobe PDFThumbnail
Show full item record
Review this work

WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.