FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1993850699> ?p ?o ?g. }

• W1993850699 endingPage "25532" @default.
• W1993850699 startingPage "25524" @default.
• W1993850699 abstract "Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) activity is increased in heart failure (HF), a syndrome characterized by markedly increased risk of arrhythmia. Activation of CaMKII increases peak L-type Ca(2+) current (I(Ca)) and slows I(Ca) inactivation. Whether these events are linked mechanistically is unknown. I(Ca) was recorded in acutely dissociated subepicardial and subendocardial murine left ventricular (LV) myocytes using the whole cell patch clamp method. Pressure overload heart failure was induced by surgical constriction of the thoracic aorta. I(Ca) density was significantly larger in subepicardial myocytes than in subendocardial/myocytes. Similar patterns were observed in the cell surface expression of alpha1c, the channel pore-forming subunit. In failing LV, I(Ca) density was increased proportionately in both cell types, and the time course of I(Ca) inactivation was slowed. This typical pattern of changes suggested a role of CaMKII. Consistent with this, measurements of CaMKII activity revealed a 2-3-fold increase (p < 0.05) in failing LV. To test for a causal link, we measured frequency-dependent I(Ca) facilitation. In HF myocytes, this CaMKII-dependent process could not be induced, suggesting already maximal activation. Internal application of active CaMKII in failing myocytes did not elicit changes in I(Ca). Finally, CaMKII inhibition by internal diffusion of a specific peptide inhibitor reduced I(Ca) density and inactivation time course to similar levels in control and HF myocytes. I(Ca) density manifests a significant transmural gradient, and this gradient is preserved in heart failure. Activation of CaMKII, a known pro-arrhythmic molecule, is a major contributor to I(Ca) remodeling in load-induced heart failure." @default.
• W1993850699 created "2016-06-24" @default.
• W1993850699 creator A5001982715 @default.
• W1993850699 creator A5025483680 @default.
• W1993850699 creator A5034662690 @default.
• W1993850699 creator A5036678006 @default.
• W1993850699 creator A5037342073 @default.
• W1993850699 creator A5061252249 @default.
• W1993850699 creator A5062734766 @default.
• W1993850699 creator A5066748216 @default.
• W1993850699 creator A5081821816 @default.
• W1993850699 date "2008-09-01" @default.
• W1993850699 modified "2023-10-18" @default.
• W1993850699 title "Ca2+/Calmodulin-dependent Protein Kinase II-dependent Remodeling of Ca2+ Current in Pressure Overload Heart Failure" @default.
• W1993850699 cites W1602116268 @default.
• W1993850699 cites W1972276841 @default.
• W1993850699 cites W1975570280 @default.
• W1993850699 cites W1977643020 @default.
• W1993850699 cites W1985538999 @default.
• W1993850699 cites W1989745031 @default.
• W1993850699 cites W1992290425 @default.
• W1993850699 cites W1998489509 @default.
• W1993850699 cites W2001261561 @default.
• W1993850699 cites W2005766827 @default.
• W1993850699 cites W2012879884 @default.
• W1993850699 cites W2014441557 @default.
• W1993850699 cites W2016448886 @default.
• W1993850699 cites W2017583361 @default.
• W1993850699 cites W2032555893 @default.
• W1993850699 cites W2033844584 @default.
• W1993850699 cites W2036272929 @default.
• W1993850699 cites W2039087156 @default.
• W1993850699 cites W2040337560 @default.
• W1993850699 cites W2056481979 @default.
• W1993850699 cites W2063972551 @default.
• W1993850699 cites W2079417512 @default.
• W1993850699 cites W2080358319 @default.
• W1993850699 cites W2088236700 @default.
• W1993850699 cites W2090619430 @default.
• W1993850699 cites W2097875771 @default.
• W1993850699 cites W2100078256 @default.
• W1993850699 cites W2103879623 @default.
• W1993850699 cites W2112798012 @default.
• W1993850699 cites W2117156482 @default.
• W1993850699 cites W2117668393 @default.
• W1993850699 cites W2131098465 @default.
• W1993850699 cites W2132321965 @default.
• W1993850699 cites W2133851654 @default.
• W1993850699 cites W2139060480 @default.
• W1993850699 cites W2150921421 @default.
• W1993850699 cites W2151912878 @default.
• W1993850699 cites W2154537902 @default.
• W1993850699 cites W2155253298 @default.
• W1993850699 cites W2155745071 @default.
• W1993850699 cites W2159774610 @default.
• W1993850699 cites W2165620104 @default.
• W1993850699 cites W2168269637 @default.
• W1993850699 cites W2168556429 @default.
• W1993850699 cites W2169542774 @default.
• W1993850699 cites W2170341039 @default.
• W1993850699 cites W2171323879 @default.
• W1993850699 cites W267585157 @default.
• W1993850699 cites W318071722 @default.
• W1993850699 cites W4232767515 @default.
• W1993850699 cites W4246665087 @default.
• W1993850699 cites W565127267 @default.
• W1993850699 doi "https://doi.org/10.1074/jbc.m803043200" @default.
• W1993850699 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2533065" @default.
• W1993850699 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18622016" @default.
• W1993850699 hasPublicationYear "2008" @default.
• W1993850699 type Work @default.
• W1993850699 sameAs 1993850699 @default.
• W1993850699 citedByCount "55" @default.
• W1993850699 countsByYear W19938506992012 @default.
• W1993850699 countsByYear W19938506992013 @default.
• W1993850699 countsByYear W19938506992014 @default.
• W1993850699 countsByYear W19938506992015 @default.
• W1993850699 countsByYear W19938506992016 @default.
• W1993850699 countsByYear W19938506992017 @default.
• W1993850699 countsByYear W19938506992018 @default.
• W1993850699 countsByYear W19938506992019 @default.
• W1993850699 countsByYear W19938506992020 @default.
• W1993850699 countsByYear W19938506992021 @default.
• W1993850699 countsByYear W19938506992022 @default.
• W1993850699 crossrefType "journal-article" @default.
• W1993850699 hasAuthorship W1993850699A5001982715 @default.
• W1993850699 hasAuthorship W1993850699A5025483680 @default.
• W1993850699 hasAuthorship W1993850699A5034662690 @default.
• W1993850699 hasAuthorship W1993850699A5036678006 @default.
• W1993850699 hasAuthorship W1993850699A5037342073 @default.
• W1993850699 hasAuthorship W1993850699A5061252249 @default.
• W1993850699 hasAuthorship W1993850699A5062734766 @default.
• W1993850699 hasAuthorship W1993850699A5066748216 @default.
• W1993850699 hasAuthorship W1993850699A5081821816 @default.
• W1993850699 hasBestOaLocation W19938506991 @default.
• W1993850699 hasConcept C12554922 @default.
• W1993850699 hasConcept C126322002 @default.
• W1993850699 hasConcept C134018914 @default.

• next