FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2089849293> ?p ?o ?g. }

• W2089849293 endingPage "H1751" @default.
• W2089849293 startingPage "H1736" @default.
• W2089849293 abstract "Ca(+) influx to mitochondria is an important trigger for both mitochondrial dynamics and ATP generation in various cell types, including cardiac cells. Mitochondrial Ca(2+) influx is mainly mediated by the mitochondrial Ca(2+) uniporter (MCU). Growing evidence also indicates that mitochondrial Ca(2+) influx mechanisms are regulated not solely by MCU but also by multiple channels/transporters. We have previously reported that skeletal muscle-type ryanodine receptor (RyR) type 1 (RyR1), which expressed at the mitochondrial inner membrane, serves as an additional Ca(2+) uptake pathway in cardiomyocytes. However, it is still unclear which mitochondrial Ca(2+) influx mechanism is the dominant regulator of mitochondrial morphology/dynamics and energetics in cardiomyocytes. To investigate the role of mitochondrial RyR1 in the regulation of mitochondrial morphology/function in cardiac cells, RyR1 was transiently or stably overexpressed in cardiac H9c2 myoblasts. We found that overexpressed RyR1 was partially localized in mitochondria as observed using both immunoblots of mitochondrial fractionation and confocal microscopy, whereas RyR2, the main RyR isoform in the cardiac sarcoplasmic reticulum, did not show any expression at mitochondria. Interestingly, overexpression of RyR1 but not MCU or RyR2 resulted in mitochondrial fragmentation. These fragmented mitochondria showed bigger and sustained mitochondrial Ca(2+) transients compared with basal tubular mitochondria. In addition, RyR1-overexpressing cells had a higher mitochondrial ATP concentration under basal conditions and showed more ATP production in response to cytosolic Ca(2+) elevation compared with nontransfected cells as observed by a matrix-targeted ATP biosensor. These results indicate that RyR1 possesses a mitochondrial targeting/retention signal and modulates mitochondrial morphology and Ca(2+)-induced ATP production in cardiac H9c2 myoblasts." @default.
• W2089849293 created "2016-06-24" @default.
• W2089849293 creator A5004102489 @default.
• W2089849293 creator A5018770733 @default.
• W2089849293 creator A5019068197 @default.
• W2089849293 creator A5019491267 @default.
• W2089849293 creator A5019673569 @default.
• W2089849293 creator A5043737419 @default.
• W2089849293 creator A5045005778 @default.
• W2089849293 creator A5048262927 @default.
• W2089849293 creator A5065482772 @default.
• W2089849293 creator A5068329388 @default.
• W2089849293 creator A5090451875 @default.
• W2089849293 creator A5091149562 @default.
• W2089849293 date "2013-12-15" @default.
• W2089849293 modified "2023-10-14" @default.
• W2089849293 title "Overexpression of ryanodine receptor type 1 enhances mitochondrial fragmentation and Ca²⁺-induced ATP production in cardiac H9c2 myoblasts" @default.
• W2089849293 cites W1522450427 @default.
• W2089849293 cites W1541024168 @default.
• W2089849293 cites W1550748049 @default.
• W2089849293 cites W1559795048 @default.
• W2089849293 cites W1963643075 @default.
• W2089849293 cites W1965117795 @default.
• W2089849293 cites W1970610775 @default.
• W2089849293 cites W1973281235 @default.
• W2089849293 cites W1976668265 @default.
• W2089849293 cites W1978504047 @default.
• W2089849293 cites W1986213783 @default.
• W2089849293 cites W1987035640 @default.
• W2089849293 cites W1991055482 @default.
• W2089849293 cites W1992865901 @default.
• W2089849293 cites W1995398070 @default.
• W2089849293 cites W1996439971 @default.
• W2089849293 cites W2002791298 @default.
• W2089849293 cites W2007552109 @default.
• W2089849293 cites W2010572143 @default.
• W2089849293 cites W2012335235 @default.
• W2089849293 cites W2012493524 @default.
• W2089849293 cites W2015536770 @default.
• W2089849293 cites W2016936426 @default.
• W2089849293 cites W2024559273 @default.
• W2089849293 cites W2026648000 @default.
• W2089849293 cites W2027525042 @default.
• W2089849293 cites W2033107215 @default.
• W2089849293 cites W2034767282 @default.
• W2089849293 cites W2035885166 @default.
• W2089849293 cites W2038468721 @default.
• W2089849293 cites W2040209343 @default.
• W2089849293 cites W2044539742 @default.
• W2089849293 cites W2044915997 @default.
• W2089849293 cites W2045870786 @default.
• W2089849293 cites W2046353863 @default.
• W2089849293 cites W2048575345 @default.
• W2089849293 cites W2052168634 @default.
• W2089849293 cites W2054792922 @default.
• W2089849293 cites W2054895660 @default.
• W2089849293 cites W2058516202 @default.
• W2089849293 cites W2059065327 @default.
• W2089849293 cites W2060302805 @default.
• W2089849293 cites W2063088638 @default.
• W2089849293 cites W2065383397 @default.
• W2089849293 cites W2065453809 @default.
• W2089849293 cites W2067841051 @default.
• W2089849293 cites W2068048197 @default.
• W2089849293 cites W2074695893 @default.
• W2089849293 cites W2076056262 @default.
• W2089849293 cites W2080150505 @default.
• W2089849293 cites W2080355869 @default.
• W2089849293 cites W2082973248 @default.
• W2089849293 cites W2083502135 @default.
• W2089849293 cites W2092047540 @default.
• W2089849293 cites W2092479957 @default.
• W2089849293 cites W2094154511 @default.
• W2089849293 cites W2094272082 @default.
• W2089849293 cites W2097989216 @default.
• W2089849293 cites W2099551120 @default.
• W2089849293 cites W2099869024 @default.
• W2089849293 cites W2101037339 @default.
• W2089849293 cites W2109692759 @default.
• W2089849293 cites W2110931950 @default.
• W2089849293 cites W2112870272 @default.
• W2089849293 cites W2114228694 @default.
• W2089849293 cites W2115448092 @default.
• W2089849293 cites W2116635624 @default.
• W2089849293 cites W2120379299 @default.
• W2089849293 cites W2123343796 @default.
• W2089849293 cites W2129137736 @default.
• W2089849293 cites W2131666074 @default.
• W2089849293 cites W2132284408 @default.
• W2089849293 cites W2136996563 @default.
• W2089849293 cites W2137341154 @default.
• W2089849293 cites W2137424160 @default.
• W2089849293 cites W2141836995 @default.
• W2089849293 cites W2142756718 @default.
• W2089849293 cites W2144174954 @default.
• W2089849293 cites W2147497718 @default.
• W2089849293 cites W2151947597 @default.
• W2089849293 cites W2155480494 @default.

• next