Adenosine receptor ant its downstream targets, Mod(mdg4) and Hsp70, work as a signaling pathway modulating cytotoxic damage in Drosophila

Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60077344%3A_____%2F21%3A00541060" target="_blank" >RIV/60077344:_____/21:00541060 - isvavai.cz</a>
Result on the web
<a href="https://www.frontiersin.org/articles/10.3389/fcell.2021.651367/pdf" target="_blank" >https://www.frontiersin.org/articles/10.3389/fcell.2021.651367/pdf</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.3389/fcell.2021.651367" target="_blank" >10.3389/fcell.2021.651367</a>

Result language
angličtina
Original language name
Adenosine receptor ant its downstream targets, Mod(mdg4) and Hsp70, work as a signaling pathway modulating cytotoxic damage in Drosophila
Original language description
Adenosine (Ado) is an important signaling molecule involved in stress responses. Studies in mammalian models have shown that Ado regulates signaling mechanisms involved in ‘danger-sensing’ and tissue-protection. Yet, little is known about the role of Ado signaling in Drosophila. In the present study, we observed lower extracellular Ado concentration and suppressed expression of Ado transporters in flies expressing mutant huntingtin protein (mHTT). We altered Ado signaling using genetic tools and found that the overexpression of Ado metabolic enzymes, as well as the suppression of Ado receptor (AdoR) and transporters (ENTs), were able to minimize mHTT-induced mortality. We also identified the downstream targets of the AdoR pathway, the modifier of mdg4 (Mod(mdg4)) and heat-shock protein 70 (Hsp70), which carry out its function. Finally, we showed that a decrease in Ado signaling affect other Drosophila stress reactions, including paraquat and heat-shock treatments. Our study provides important insights into how Ado regulates stress responses in Drosophila.
Czech name
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Czech description
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Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
10608 - Biochemistry and molecular biology

Project
<a href="/en/project/GJ19-13784Y" target="_blank" >GJ19-13784Y: Unveiling the mechanism underlying the innate immune response mediated by chitinase-like proteins</a><br>
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Publication year
2021
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

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