FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2741474168> ?p ?o ?g. }

• W2741474168 endingPage "239" @default.
• W2741474168 startingPage "229" @default.
• W2741474168 abstract "Purpose: Supplemental oxygen (hyperoxia) used to treat individuals in respiratory distress causes cell injury by enhancing the production of toxic reactive oxygen species (ROS) and inhibiting mitochondrial respiration. The suppressor of morphogenesis of genitalia (SMG-1) kinase is activated during hyperoxia and promotes cell survival by phosphorylating the tumor suppressor p53 on serine 15. Here, we investigate whether SMG-1 and p53 blunt this vicious cycle of progressive ROS production and decline in mitochondrial respiration seen during hyperoxia. Materials and Methods: Human lung adenocarcinoma A549 and H1299 or colon carcinoma HCT116 cells were depleted of SMG-1, UPF-1, or p53 using RNA interference, and then exposed to room air (21% oxygen) or hyperoxia (95% oxygen). Immunoblotting was used to evaluate protein expression; a Seahorse Bioanalyzer was used to assess cellular respiration; and flow cytometry was used to evaluate fluorescence intensity of cells stained with mitochondrial or redox sensitive dyes. Results: Hyperoxia increased mitochondrial and cytoplasmic ROS and suppressed mitochondrial respiration without changing mitochondrial mass or membrane potential. Depletion of SMG-1 or its cofactor, UPF1, significantly enhanced hyperoxia-induced mitochondrial but not cytosolic ROS abundance. They did not affect mitochondrial mass, membrane potential, or hyperoxia-induced deficits in mitochondrial respiration. Genetic depletion of p53 in A549 cells and ablation of the p53 gene in H1299 or HCT116 cells revealed that SMG-1 influences mitochondrial ROS through activation of p53. Conclusions: Our findings show that hyperoxia does not promote a vicious cycle of progressive mitochondrial ROS and dysfunction because SMG-1-p53 signaling attenuates production of mitochondrial ROS without preserving respiration. This suggests antioxidant therapies that blunt ROS production during hyperoxia may not suffice to restore cellular respiration." @default.
• W2741474168 created "2017-08-08" @default.
• W2741474168 creator A5034996780 @default.
• W2741474168 creator A5055508411 @default.
• W2741474168 creator A5060599255 @default.
• W2741474168 date "2017-07-27" @default.
• W2741474168 modified "2023-10-10" @default.
• W2741474168 title "SMG-1 kinase attenuates mitochondrial ROS production but not cell respiration deficits during hyperoxia" @default.
• W2741474168 cites W1566624716 @default.
• W2741474168 cites W1916773004 @default.
• W2741474168 cites W1973593141 @default.
• W2741474168 cites W1979881414 @default.
• W2741474168 cites W1984356380 @default.
• W2741474168 cites W1986104995 @default.
• W2741474168 cites W1986216062 @default.
• W2741474168 cites W1992352189 @default.
• W2741474168 cites W1997980793 @default.
• W2741474168 cites W1999348374 @default.
• W2741474168 cites W2003230246 @default.
• W2741474168 cites W2007735570 @default.
• W2741474168 cites W2009902514 @default.
• W2741474168 cites W2010077871 @default.
• W2741474168 cites W2013830376 @default.
• W2741474168 cites W2015372769 @default.
• W2741474168 cites W2019332869 @default.
• W2741474168 cites W2028717822 @default.
• W2741474168 cites W2039093830 @default.
• W2741474168 cites W2039698012 @default.
• W2741474168 cites W2050426823 @default.
• W2741474168 cites W2062857017 @default.
• W2741474168 cites W2063057532 @default.
• W2741474168 cites W2071457560 @default.
• W2741474168 cites W2073204556 @default.
• W2741474168 cites W2082520656 @default.
• W2741474168 cites W2085496347 @default.
• W2741474168 cites W2085896125 @default.
• W2741474168 cites W2087770023 @default.
• W2741474168 cites W2089993659 @default.
• W2741474168 cites W2094000643 @default.
• W2741474168 cites W2131077173 @default.
• W2741474168 cites W2133959309 @default.
• W2741474168 cites W2135535670 @default.
• W2741474168 cites W2136965788 @default.
• W2741474168 cites W2142812553 @default.
• W2741474168 cites W2151334606 @default.
• W2741474168 cites W2166213130 @default.
• W2741474168 cites W2170576927 @default.
• W2741474168 doi "https://doi.org/10.1080/01902148.2017.1339143" @default.
• W2741474168 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5956894" @default.
• W2741474168 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28749708" @default.
• W2741474168 hasPublicationYear "2017" @default.
• W2741474168 type Work @default.
• W2741474168 sameAs 2741474168 @default.
• W2741474168 citedByCount "2" @default.
• W2741474168 countsByYear W27414741682020 @default.
• W2741474168 countsByYear W27414741682023 @default.
• W2741474168 crossrefType "journal-article" @default.
• W2741474168 hasAuthorship W2741474168A5034996780 @default.
• W2741474168 hasAuthorship W2741474168A5055508411 @default.
• W2741474168 hasAuthorship W2741474168A5060599255 @default.
• W2741474168 hasBestOaLocation W27414741682 @default.
• W2741474168 hasConcept C153911025 @default.
• W2741474168 hasConcept C178790620 @default.
• W2741474168 hasConcept C185592680 @default.
• W2741474168 hasConcept C2778175917 @default.
• W2741474168 hasConcept C2780672939 @default.
• W2741474168 hasConcept C28859421 @default.
• W2741474168 hasConcept C48349386 @default.
• W2741474168 hasConcept C540031477 @default.
• W2741474168 hasConcept C86803240 @default.
• W2741474168 hasConcept C95444343 @default.
• W2741474168 hasConceptScore W2741474168C153911025 @default.
• W2741474168 hasConceptScore W2741474168C178790620 @default.
• W2741474168 hasConceptScore W2741474168C185592680 @default.
• W2741474168 hasConceptScore W2741474168C2778175917 @default.
• W2741474168 hasConceptScore W2741474168C2780672939 @default.
• W2741474168 hasConceptScore W2741474168C28859421 @default.
• W2741474168 hasConceptScore W2741474168C48349386 @default.
• W2741474168 hasConceptScore W2741474168C540031477 @default.
• W2741474168 hasConceptScore W2741474168C86803240 @default.
• W2741474168 hasConceptScore W2741474168C95444343 @default.
• W2741474168 hasIssue "6-7" @default.
• W2741474168 hasLocation W27414741681 @default.
• W2741474168 hasLocation W27414741682 @default.
• W2741474168 hasLocation W27414741683 @default.
• W2741474168 hasLocation W27414741684 @default.
• W2741474168 hasOpenAccess W2741474168 @default.
• W2741474168 hasPrimaryLocation W27414741681 @default.
• W2741474168 hasRelatedWork W1993332233 @default.
• W2741474168 hasRelatedWork W2047509150 @default.
• W2741474168 hasRelatedWork W2053022803 @default.
• W2741474168 hasRelatedWork W2111757377 @default.
• W2741474168 hasRelatedWork W2117929483 @default.
• W2741474168 hasRelatedWork W2170729914 @default.
• W2741474168 hasRelatedWork W2547134376 @default.
• W2741474168 hasRelatedWork W2700688926 @default.
• W2741474168 hasRelatedWork W3176674250 @default.
• W2741474168 hasRelatedWork W3213309159 @default.

• next