FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2939969384> ?p ?o ?g. }

• W2939969384 endingPage "283" @default.
• W2939969384 startingPage "205" @default.
• W2939969384 abstract "Two types of anion channels are directly activated by osmotic swelling and are involved in the regulatory volume decrease (RVD) in most types of mammalian cells, and they include the volume-sensitive outwardly rectifying anion channel (VSOR), also called the volume-regulated anion channel (VRAC), and the large-conductance maxi-anion channel (Maxi-Cl). In cardiomyocytes, a splice variant of cystic fibrosis transmembrane conductance regulator anion channel (cardiac CFTR) participates in the RVD mechanism under β-adrenergic stimulation. VSOR and Maxi-Cl are also involved in facilitation of the RVD process by releasing extracellular autocrine/paracrine signals, glutamate and ATP. Apoptotic cell death starts with cell shrinkage, called the apoptotic volume decrease (AVD), which is also caused by activation of VSOR. Since VSOR is implicated not only in the AVD induction but also in the uptake of an anti-cancer drug, cisplatin, downregulation of VSOR activity is causatively involved in acquisition of cisplatin resistance in cancer cells. Necrotic cell death exhibits persistent cell swelling, called the necrotic volume increase (NVI), which is coupled to RVD dysfunction due to impaired VSOR function. Acidotoxic and lactacidosis-induced necrotic cell death is induced both by glutamate release mediated by astroglial VSOR and Maxi-Cl and by exaggerated Cl− influx mediated by neuronal VSOR under prolonged depolarization caused by activation of ionotropic glutamate receptor (iGluR) cation channels. Both VSOR and Maxi-Cl are elaborately involved, in a manner as double-edged swords, in ischemia- and ischemia-reperfusion-induced apoptotic or necrotic cell death in cerebral and myocardial cells by mediating not only Cl− transport but also release of glutamate and/or ATP. Cardiac CFTR exerts a protective action against ischemia(-reperfusion)-induced cardiac injury, called myocardial infarction (MI), which is largely necrotic. Cardiac Maxi-Cl activity may participate in protection against ischemia(-reperfusion) injury by mediating ATP release." @default.
• W2939969384 created "2019-04-25" @default.
• W2939969384 creator A5011306623 @default.
• W2939969384 creator A5014496158 @default.
• W2939969384 creator A5027026994 @default.
• W2939969384 creator A5027563984 @default.
• W2939969384 creator A5028769986 @default.
• W2939969384 creator A5079417201 @default.
• W2939969384 creator A5090563200 @default.
• W2939969384 date "2019-01-01" @default.
• W2939969384 modified "2023-10-04" @default.
• W2939969384 title "Roles of volume-regulatory anion channels, VSOR and Maxi-Cl, in apoptosis, cisplatin resistance, necrosis, ischemic cell death, stroke and myocardial infarction" @default.
• W2939969384 cites W1019748883 @default.
• W2939969384 cites W1497207210 @default.
• W2939969384 cites W1500192109 @default.
• W2939969384 cites W1509313163 @default.
• W2939969384 cites W1513833747 @default.
• W2939969384 cites W1517594284 @default.
• W2939969384 cites W1523845694 @default.
• W2939969384 cites W1525394709 @default.
• W2939969384 cites W1529025484 @default.
• W2939969384 cites W1535725158 @default.
• W2939969384 cites W1550247880 @default.
• W2939969384 cites W1557291445 @default.
• W2939969384 cites W1567321500 @default.
• W2939969384 cites W1581626040 @default.
• W2939969384 cites W1589402586 @default.
• W2939969384 cites W1589415602 @default.
• W2939969384 cites W1593826108 @default.
• W2939969384 cites W1595629690 @default.
• W2939969384 cites W1602049707 @default.
• W2939969384 cites W1674335052 @default.
• W2939969384 cites W1684019827 @default.
• W2939969384 cites W1859174804 @default.
• W2939969384 cites W1864129699 @default.
• W2939969384 cites W1864325817 @default.
• W2939969384 cites W1882905539 @default.
• W2939969384 cites W1897205131 @default.
• W2939969384 cites W1908459925 @default.
• W2939969384 cites W1913353167 @default.
• W2939969384 cites W1913801606 @default.
• W2939969384 cites W1932887968 @default.
• W2939969384 cites W1936849452 @default.
• W2939969384 cites W1961610463 @default.
• W2939969384 cites W1963165149 @default.
• W2939969384 cites W1964260585 @default.
• W2939969384 cites W1964455968 @default.
• W2939969384 cites W1964617786 @default.
• W2939969384 cites W1964842209 @default.
• W2939969384 cites W1965130745 @default.
• W2939969384 cites W1965216782 @default.
• W2939969384 cites W1965480868 @default.
• W2939969384 cites W1965638288 @default.
• W2939969384 cites W1966977448 @default.
• W2939969384 cites W1967211953 @default.
• W2939969384 cites W1967394868 @default.
• W2939969384 cites W1968304355 @default.
• W2939969384 cites W1968561251 @default.
• W2939969384 cites W1969254429 @default.
• W2939969384 cites W1969800959 @default.
• W2939969384 cites W1970083805 @default.
• W2939969384 cites W1970093689 @default.
• W2939969384 cites W1970294642 @default.
• W2939969384 cites W1970573857 @default.
• W2939969384 cites W1970684711 @default.
• W2939969384 cites W1971156162 @default.
• W2939969384 cites W1971512819 @default.
• W2939969384 cites W1971621147 @default.
• W2939969384 cites W1972710532 @default.
• W2939969384 cites W1973792516 @default.
• W2939969384 cites W1974155494 @default.
• W2939969384 cites W1974695854 @default.
• W2939969384 cites W1975150345 @default.
• W2939969384 cites W1975272789 @default.
• W2939969384 cites W1976129366 @default.
• W2939969384 cites W1976824217 @default.
• W2939969384 cites W1977213966 @default.
• W2939969384 cites W1977832455 @default.
• W2939969384 cites W1978656431 @default.
• W2939969384 cites W1979039759 @default.
• W2939969384 cites W1979487594 @default.
• W2939969384 cites W1979572339 @default.
• W2939969384 cites W1979881262 @default.
• W2939969384 cites W1980041137 @default.
• W2939969384 cites W1980098832 @default.
• W2939969384 cites W1980155320 @default.
• W2939969384 cites W1981133890 @default.
• W2939969384 cites W1981146929 @default.
• W2939969384 cites W1982165091 @default.
• W2939969384 cites W1982422779 @default.
• W2939969384 cites W1982892406 @default.
• W2939969384 cites W1983196712 @default.
• W2939969384 cites W1983358372 @default.
• W2939969384 cites W1983602414 @default.
• W2939969384 cites W1983986241 @default.
• W2939969384 cites W1984075560 @default.
• W2939969384 cites W1984241500 @default.
• W2939969384 cites W1984256619 @default.

• next