FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2912123613> ?p ?o ?g. }

• W2912123613 endingPage "2014" @default.
• W2912123613 startingPage "1998" @default.
• W2912123613 abstract "Ataxia telangiectasia (AT) is a genetic disease caused by mutations in the ATM gene but the mechanisms underlying AT are not completely understood. Key functions of the ATM protein are to sense and regulate cellular redox status and to transduce DNA double-strand break signals to downstream effectors. ATM-deficient cells show increased ROS accumulation, activation of p38 protein kinase, and increased levels of DNA damage. GSE24.2 peptide and a short derivative GSE4 peptide corresponding to an internal domain of Dyskerin have proved to induce telomerase activity, decrease oxidative stress, and protect from DNA damage in dyskeratosis congenita (DC) cells. We have found that expression of GSE24.2 and GSE4 in human AT fibroblast is able to decrease DNA damage, detected by γ-H2A.X and 53BP1 foci. However, GSE24.2/GSE4 expression does not improve double-strand break signaling and repair caused by the lack of ATM activity. In contrast, they cause a decrease in 8-oxoguanine and OGG1-derived lesions, particularly at telomeres and mitochondrial DNA, as well as in reactive oxygen species, in parallel with increased expression of SOD1. These cells also showed lower levels of IL6 and decreased p38 phosphorylation, decreased senescence and increased ability to divide for longer times. Additionally, these cells are more resistant to treatment with H202 and the radiomimetic-drug bleomycin. Finally, we found shorter telomere length (TL) in AT cells, lower levels of TERT expression, and telomerase activity that were also partially reverted by GSE4. These observations suggest that GSE4 may be considered as a new therapy for the treatment of AT that counteracts the cellular effects of high ROS levels generated in AT cells and in addition increases telomerase activity contributing to increased cell proliferation." @default.
• W2912123613 created "2019-02-21" @default.
• W2912123613 creator A5003429159 @default.
• W2912123613 creator A5021455621 @default.
• W2912123613 creator A5026350375 @default.
• W2912123613 creator A5028089976 @default.
• W2912123613 creator A5036307012 @default.
• W2912123613 creator A5039323932 @default.
• W2912123613 creator A5042720583 @default.
• W2912123613 creator A5048489410 @default.
• W2912123613 creator A5062090815 @default.
• W2912123613 creator A5066115254 @default.
• W2912123613 creator A5071512795 @default.
• W2912123613 creator A5071808636 @default.
• W2912123613 creator A5074467963 @default.
• W2912123613 creator A5082989863 @default.
• W2912123613 creator A5083075419 @default.
• W2912123613 creator A5089899406 @default.
• W2912123613 date "2019-01-22" @default.
• W2912123613 modified "2023-10-18" @default.
• W2912123613 title "GSE4 peptide suppresses oxidative and telomere deficiencies in ataxia telangiectasia patient cells" @default.
• W2912123613 cites W1571145613 @default.
• W2912123613 cites W1576964011 @default.
• W2912123613 cites W1631957153 @default.
• W2912123613 cites W1972936481 @default.
• W2912123613 cites W1980695429 @default.
• W2912123613 cites W1985031521 @default.
• W2912123613 cites W1989061028 @default.
• W2912123613 cites W1999872096 @default.
• W2912123613 cites W1999963842 @default.
• W2912123613 cites W2000081173 @default.
• W2912123613 cites W2000083752 @default.
• W2912123613 cites W2005459546 @default.
• W2912123613 cites W2012520931 @default.
• W2912123613 cites W2019276374 @default.
• W2912123613 cites W2019362208 @default.
• W2912123613 cites W2021061167 @default.
• W2912123613 cites W2022811243 @default.
• W2912123613 cites W2024209230 @default.
• W2912123613 cites W2030093453 @default.
• W2912123613 cites W2041051519 @default.
• W2912123613 cites W2044593924 @default.
• W2912123613 cites W2045175039 @default.
• W2912123613 cites W2045629535 @default.
• W2912123613 cites W2052730253 @default.
• W2912123613 cites W2064956702 @default.
• W2912123613 cites W2067847016 @default.
• W2912123613 cites W2071457560 @default.
• W2912123613 cites W2075554815 @default.
• W2912123613 cites W2076538377 @default.
• W2912123613 cites W2076586707 @default.
• W2912123613 cites W2079771477 @default.
• W2912123613 cites W2105406871 @default.
• W2912123613 cites W2112451788 @default.
• W2912123613 cites W2113320982 @default.
• W2912123613 cites W2115852450 @default.
• W2912123613 cites W2116054786 @default.
• W2912123613 cites W2130658521 @default.
• W2912123613 cites W2139777089 @default.
• W2912123613 cites W2140126848 @default.
• W2912123613 cites W2149489809 @default.
• W2912123613 cites W2152859536 @default.
• W2912123613 cites W2156430848 @default.
• W2912123613 cites W2158762934 @default.
• W2912123613 cites W2160621707 @default.
• W2912123613 cites W2177413804 @default.
• W2912123613 cites W2239541667 @default.
• W2912123613 cites W2324510469 @default.
• W2912123613 cites W2327617960 @default.
• W2912123613 cites W2394983080 @default.
• W2912123613 cites W2407975629 @default.
• W2912123613 cites W2553312780 @default.
• W2912123613 cites W4249104425 @default.
• W2912123613 doi "https://doi.org/10.1038/s41418-018-0272-7" @default.
• W2912123613 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6748109" @default.
• W2912123613 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30670828" @default.
• W2912123613 hasPublicationYear "2019" @default.
• W2912123613 type Work @default.
• W2912123613 sameAs 2912123613 @default.
• W2912123613 citedByCount "17" @default.
• W2912123613 countsByYear W29121236132019 @default.
• W2912123613 countsByYear W29121236132020 @default.
• W2912123613 countsByYear W29121236132021 @default.
• W2912123613 countsByYear W29121236132022 @default.
• W2912123613 countsByYear W29121236132023 @default.
• W2912123613 crossrefType "journal-article" @default.
• W2912123613 hasAuthorship W2912123613A5003429159 @default.
• W2912123613 hasAuthorship W2912123613A5021455621 @default.
• W2912123613 hasAuthorship W2912123613A5026350375 @default.
• W2912123613 hasAuthorship W2912123613A5028089976 @default.
• W2912123613 hasAuthorship W2912123613A5036307012 @default.
• W2912123613 hasAuthorship W2912123613A5039323932 @default.
• W2912123613 hasAuthorship W2912123613A5042720583 @default.
• W2912123613 hasAuthorship W2912123613A5048489410 @default.
• W2912123613 hasAuthorship W2912123613A5062090815 @default.
• W2912123613 hasAuthorship W2912123613A5066115254 @default.
• W2912123613 hasAuthorship W2912123613A5071512795 @default.
• W2912123613 hasAuthorship W2912123613A5071808636 @default.

• next