FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2024754162> ?p ?o ?g. }

• W2024754162 endingPage "6117" @default.
• W2024754162 startingPage "6109" @default.
• W2024754162 abstract "Most animal cell types regulate their cell volume after an osmotic volume change. The regulatory volume increase (RVI) occurs through uptake of NaCl and osmotically obliged water after osmotic shrinkage. However, apoptotic cells undergo persistent cell shrinkage without showing signs of RVI. Persistence of the apoptotic volume decrease is a prerequisite to apoptosis induction. We previously demonstrated that volume regulation is inhibited in human epithelial HeLa cells stimulated with the apoptosis inducer. Here, we studied signaling mechanisms underlying the apoptotic inhibition of RVI in HeLa cells. Hypertonic stimulation was found to induce phosphorylation of a Ser/Thr protein kinase Akt (protein kinase B). Shrinkage-induced Akt activation was essential for RVI induction because RVI was suppressed by an Akt inhibitor, expression of a dominant negative form of Akt, or small interfering RNA-mediated knockdown of Akt1 (but not Akt2). Staurosporine, tumor necrosis factor-α, or a Fas ligand inhibited both RVI and hypertonicity-induced Akt activation in a manner sensitive to a scavenger for reactive oxygen species (ROS). Any of apoptosis inducers also induced phosphorylation of apoptosis signal-regulating kinase 1 (ASK1) in a ROS-dependent manner. Suppression of (ASK1) expression blocked the effects of apoptosis, in hypertonic conditions, on both RVI induction and Akt activation. Thus, it is concluded that in human epithelial cells, shrinkage-induced activation of Akt1 is involved in the RVI process and that apoptotic inhibition of RVI is caused by inhibition of Akt activation, which results from ROS-mediated activation of ASK1. Most animal cell types regulate their cell volume after an osmotic volume change. The regulatory volume increase (RVI) occurs through uptake of NaCl and osmotically obliged water after osmotic shrinkage. However, apoptotic cells undergo persistent cell shrinkage without showing signs of RVI. Persistence of the apoptotic volume decrease is a prerequisite to apoptosis induction. We previously demonstrated that volume regulation is inhibited in human epithelial HeLa cells stimulated with the apoptosis inducer. Here, we studied signaling mechanisms underlying the apoptotic inhibition of RVI in HeLa cells. Hypertonic stimulation was found to induce phosphorylation of a Ser/Thr protein kinase Akt (protein kinase B). Shrinkage-induced Akt activation was essential for RVI induction because RVI was suppressed by an Akt inhibitor, expression of a dominant negative form of Akt, or small interfering RNA-mediated knockdown of Akt1 (but not Akt2). Staurosporine, tumor necrosis factor-α, or a Fas ligand inhibited both RVI and hypertonicity-induced Akt activation in a manner sensitive to a scavenger for reactive oxygen species (ROS). Any of apoptosis inducers also induced phosphorylation of apoptosis signal-regulating kinase 1 (ASK1) in a ROS-dependent manner. Suppression of (ASK1) expression blocked the effects of apoptosis, in hypertonic conditions, on both RVI induction and Akt activation. Thus, it is concluded that in human epithelial cells, shrinkage-induced activation of Akt1 is involved in the RVI process and that apoptotic inhibition of RVI is caused by inhibition of Akt activation, which results from ROS-mediated activation of ASK1." @default.
• W2024754162 created "2016-06-24" @default.
• W2024754162 creator A5018235068 @default.
• W2024754162 creator A5027563984 @default.
• W2024754162 creator A5046262040 @default.
• W2024754162 creator A5054408940 @default.
• W2024754162 creator A5086495272 @default.
• W2024754162 date "2010-02-01" @default.
• W2024754162 modified "2023-10-15" @default.
• W2024754162 title "Inhibition of Protein Kinase Akt1 by Apoptosis Signal-regulating Kinase-1 (ASK1) Is Involved in Apoptotic Inhibition of Regulatory Volume Increase" @default.
• W2024754162 cites W1493574533 @default.
• W2024754162 cites W1969268163 @default.
• W2024754162 cites W1970751001 @default.
• W2024754162 cites W1971289872 @default.
• W2024754162 cites W1977225705 @default.
• W2024754162 cites W1979037935 @default.
• W2024754162 cites W1981243271 @default.
• W2024754162 cites W1982165091 @default.
• W2024754162 cites W1985904396 @default.
• W2024754162 cites W1991865867 @default.
• W2024754162 cites W1991870376 @default.
• W2024754162 cites W1993216157 @default.
• W2024754162 cites W1996979039 @default.
• W2024754162 cites W2004199183 @default.
• W2024754162 cites W2013936743 @default.
• W2024754162 cites W2015717266 @default.
• W2024754162 cites W2019136847 @default.
• W2024754162 cites W2029962300 @default.
• W2024754162 cites W2030542406 @default.
• W2024754162 cites W2033431458 @default.
• W2024754162 cites W2034580062 @default.
• W2024754162 cites W2034718304 @default.
• W2024754162 cites W2037596908 @default.
• W2024754162 cites W2039355845 @default.
• W2024754162 cites W2045882427 @default.
• W2024754162 cites W2046705531 @default.
• W2024754162 cites W2047682144 @default.
• W2024754162 cites W2050498522 @default.
• W2024754162 cites W2055981402 @default.
• W2024754162 cites W2056198198 @default.
• W2024754162 cites W2061908395 @default.
• W2024754162 cites W2065477903 @default.
• W2024754162 cites W2068768903 @default.
• W2024754162 cites W2069075668 @default.
• W2024754162 cites W2069331655 @default.
• W2024754162 cites W2078652183 @default.
• W2024754162 cites W2080933642 @default.
• W2024754162 cites W2084086160 @default.
• W2024754162 cites W2087102350 @default.
• W2024754162 cites W2088947190 @default.
• W2024754162 cites W2090193716 @default.
• W2024754162 cites W2099000660 @default.
• W2024754162 cites W2107813980 @default.
• W2024754162 cites W2108140000 @default.
• W2024754162 cites W2116938728 @default.
• W2024754162 cites W2123619341 @default.
• W2024754162 cites W2124557239 @default.
• W2024754162 cites W2125013655 @default.
• W2024754162 cites W2125588561 @default.
• W2024754162 cites W2136986018 @default.
• W2024754162 cites W2151501496 @default.
• W2024754162 cites W2162690000 @default.
• W2024754162 cites W2169825848 @default.
• W2024754162 cites W2268409423 @default.
• W2024754162 cites W2365266337 @default.
• W2024754162 cites W4361805428 @default.
• W2024754162 cites W2043522529 @default.
• W2024754162 doi "https://doi.org/10.1074/jbc.m109.072785" @default.
• W2024754162 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2825405" @default.
• W2024754162 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20048146" @default.
• W2024754162 hasPublicationYear "2010" @default.
• W2024754162 type Work @default.
• W2024754162 sameAs 2024754162 @default.
• W2024754162 citedByCount "30" @default.
• W2024754162 countsByYear W20247541622012 @default.
• W2024754162 countsByYear W20247541622013 @default.
• W2024754162 countsByYear W20247541622016 @default.
• W2024754162 countsByYear W20247541622017 @default.
• W2024754162 countsByYear W20247541622018 @default.
• W2024754162 countsByYear W20247541622019 @default.
• W2024754162 countsByYear W20247541622021 @default.
• W2024754162 crossrefType "journal-article" @default.
• W2024754162 hasAuthorship W2024754162A5018235068 @default.
• W2024754162 hasAuthorship W2024754162A5027563984 @default.
• W2024754162 hasAuthorship W2024754162A5046262040 @default.
• W2024754162 hasAuthorship W2024754162A5054408940 @default.
• W2024754162 hasAuthorship W2024754162A5086495272 @default.
• W2024754162 hasBestOaLocation W20247541621 @default.
• W2024754162 hasConcept C124160383 @default.
• W2024754162 hasConcept C154137905 @default.
• W2024754162 hasConcept C184235292 @default.
• W2024754162 hasConcept C185592680 @default.
• W2024754162 hasConcept C190283241 @default.
• W2024754162 hasConcept C55493867 @default.
• W2024754162 hasConcept C62478195 @default.
• W2024754162 hasConcept C75217442 @default.
• W2024754162 hasConcept C82495950 @default.
• W2024754162 hasConcept C86803240 @default.

• next