FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2073005910> ?p ?o ?g. }

• W2073005910 endingPage "2313" @default.
• W2073005910 startingPage "2302" @default.
• W2073005910 abstract "Neutrophils die rapidly via apoptosis and their survival is contingent upon rescue from constitutive programmed cell death by signals from the microenvironment. In these experiments, we investigated whether prevention of K+ efflux could affect the apoptotic machinery in human neutrophils. Disruption of the natural K+ electrochemical gradient suppressed neutrophil apoptosis (assessed by annexin V binding, nuclear DNA content and nucleosomal DNA fragmentation) and prolonged cell survival within 24–48 h of culture. High extracellular K+ (10–100 mM) did not activate extracellular signal-regulated kinase (ERK) and Akt, nor affected phosphorylation of p38 MAPK associated with constitutive apoptosis. Consistently, pharmacological blockade of ERK kinase or phosphatidylinositol 3-kinase (PI 3-kinase) did not affect the anti-apoptotic action of KCl. Inhibition of K+ efflux effectively reduced, though never completely inhibited, decreases in mitochondrial transmembrane potential (ΔΨm) that preceded development of apoptotic morphology. Changes in ΔΨm resulted in attenuation of cytochrome c release from mitochondria into the cytosol and decreases in caspase-3 activity. Culture of neutrophils in medium containing 80 mM KCl with the pan-caspase inhibitor Z-VAD-FMK resulted in slightly greater suppression of apoptosis than KCl alone. High extracellular KCl also attenuated translocation of apoptosis-inducing factor (AIF) and endonuclease G (EndoG) from mitochondria to nuclei. The DNase inhibitor, aurintricarboxylic acid (ATA) partially inhibited nucleosomal DNA fragmentation, and the effects of ATA and 80 mM KCl were not additive. These results show that prevention of K+ efflux promotes neutrophil survival by suppressing apoptosis through preventing mitochondrial dysfunction and release of the pro-apoptotic proteins cytochrome c, AIF and EndoG independent of ERK, PI 3-kinase and p38 MAPK. Thus, K+ released locally from damaged cells may function as a survival signal for neutrophils." @default.
• W2073005910 created "2016-06-24" @default.
• W2073005910 creator A5038048841 @default.
• W2073005910 creator A5041476676 @default.
• W2073005910 creator A5082807034 @default.
• W2073005910 creator A5086184991 @default.
• W2073005910 date "2006-12-01" @default.
• W2073005910 modified "2023-10-16" @default.
• W2073005910 title "Inhibition of K+ efflux prevents mitochondrial dysfunction, and suppresses caspase-3-, apoptosis-inducing factor-, and endonuclease G-mediated constitutive apoptosis in human neutrophils" @default.
• W2073005910 cites W146301169 @default.
• W2073005910 cites W1480948328 @default.
• W2073005910 cites W1483739722 @default.
• W2073005910 cites W1489532715 @default.
• W2073005910 cites W1550693054 @default.
• W2073005910 cites W1567258255 @default.
• W2073005910 cites W1589670817 @default.
• W2073005910 cites W1621124914 @default.
• W2073005910 cites W1845459216 @default.
• W2073005910 cites W1891774658 @default.
• W2073005910 cites W1965394044 @default.
• W2073005910 cites W1968442371 @default.
• W2073005910 cites W1979039759 @default.
• W2073005910 cites W1979129905 @default.
• W2073005910 cites W1981176905 @default.
• W2073005910 cites W1981886269 @default.
• W2073005910 cites W1987563269 @default.
• W2073005910 cites W1990781055 @default.
• W2073005910 cites W1994583863 @default.
• W2073005910 cites W1994965038 @default.
• W2073005910 cites W2000718683 @default.
• W2073005910 cites W2005417769 @default.
• W2073005910 cites W2008479667 @default.
• W2073005910 cites W2013839735 @default.
• W2073005910 cites W2015717266 @default.
• W2073005910 cites W2024104987 @default.
• W2073005910 cites W2029684134 @default.
• W2073005910 cites W2048692719 @default.
• W2073005910 cites W2049352189 @default.
• W2073005910 cites W2052607700 @default.
• W2073005910 cites W2068848132 @default.
• W2073005910 cites W2070862399 @default.
• W2073005910 cites W2070908828 @default.
• W2073005910 cites W2074148319 @default.
• W2073005910 cites W2077626349 @default.
• W2073005910 cites W2078532650 @default.
• W2073005910 cites W2079472092 @default.
• W2073005910 cites W2080895438 @default.
• W2073005910 cites W2082259697 @default.
• W2073005910 cites W2084814184 @default.
• W2073005910 cites W2084982725 @default.
• W2073005910 cites W2089212253 @default.
• W2073005910 cites W2098712005 @default.
• W2073005910 cites W2107497694 @default.
• W2073005910 cites W2109330502 @default.
• W2073005910 cites W2113990199 @default.
• W2073005910 cites W2123455365 @default.
• W2073005910 cites W2123671636 @default.
• W2073005910 cites W2131726013 @default.
• W2073005910 cites W2133454381 @default.
• W2073005910 cites W2138728269 @default.
• W2073005910 cites W2142332666 @default.
• W2073005910 cites W2159650080 @default.
• W2073005910 cites W2190292329 @default.
• W2073005910 cites W2417660769 @default.
• W2073005910 cites W4244482844 @default.
• W2073005910 cites W99491017 @default.
• W2073005910 doi "https://doi.org/10.1016/j.cellsig.2006.05.013" @default.
• W2073005910 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16806822" @default.
• W2073005910 hasPublicationYear "2006" @default.
• W2073005910 type Work @default.
• W2073005910 sameAs 2073005910 @default.
• W2073005910 citedByCount "28" @default.
• W2073005910 countsByYear W20730059102012 @default.
• W2073005910 countsByYear W20730059102013 @default.
• W2073005910 countsByYear W20730059102014 @default.
• W2073005910 countsByYear W20730059102015 @default.
• W2073005910 countsByYear W20730059102016 @default.
• W2073005910 countsByYear W20730059102017 @default.
• W2073005910 countsByYear W20730059102018 @default.
• W2073005910 countsByYear W20730059102019 @default.
• W2073005910 countsByYear W20730059102020 @default.
• W2073005910 countsByYear W20730059102021 @default.
• W2073005910 countsByYear W20730059102023 @default.
• W2073005910 crossrefType "journal-article" @default.
• W2073005910 hasAuthorship W2073005910A5038048841 @default.
• W2073005910 hasAuthorship W2073005910A5041476676 @default.
• W2073005910 hasAuthorship W2073005910A5082807034 @default.
• W2073005910 hasAuthorship W2073005910A5086184991 @default.
• W2073005910 hasConcept C12519072 @default.
• W2073005910 hasConcept C153911025 @default.
• W2073005910 hasConcept C172043667 @default.
• W2073005910 hasConcept C173358068 @default.
• W2073005910 hasConcept C184235292 @default.
• W2073005910 hasConcept C190283241 @default.
• W2073005910 hasConcept C28406088 @default.
• W2073005910 hasConcept C28859421 @default.
• W2073005910 hasConcept C29311851 @default.
• W2073005910 hasConcept C31573885 @default.

• next