FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2110260167> ?p ?o ?g. }

• W2110260167 abstract "Abstract Background During the acute phase of critical illness myopathy (CIM) there is inexcitability of skeletal muscle. In a rat model of CIM, muscle inexcitability is due to inactivation of sodium channels. A major contributor to this sodium channel inactivation is a hyperpolarized shift in the voltage dependence of sodium channel inactivation. The goal of the current study was to find a biochemical correlate of the hyperpolarized shift in sodium channel inactivation. Methods The rat model of CIM was generated by cutting the sciatic nerve and subsequent injections of dexamethasone for 7 days. Skeletal muscle membranes were prepared from gastrocnemius muscles, and purification and biochemical analyses carried out. Immunoprecipitations were performed with a pan-sodium channel antibody, and the resulting complexes probed in Western blots with various antibodies. Results We carried out analyses of sodium channel glycosylation, phosphorylation, and association with other proteins. Although there was some loss of channel glycosylation in the disease, as assessed by size analysis of glycosylated and de-glycosylated protein in control and CIM samples, previous work by other investigators suggest that such loss would most likely shift channel inactivation gating in a depolarizing direction; thus such loss was viewed as compensatory rather than causative of the disease. A phosphorylation site at serine 487 was identified on the Na V 1.4 sodium channel α subunit, but there was no clear evidence of altered phosphorylation in the disease. Co-immunoprecipitation experiments carried out with a pan-sodium channel antibody confirmed that the sodium channel was associated with proteins of the dystrophin associated protein complex (DAPC). This complex differed between control and CIM samples. Syntrophin, dystrophin, and plectin associated strongly with sodium channels in both control and disease conditions, while β-dystroglycan and neuronal nitric oxide synthase (nNOS) associated strongly with the sodium channel only in CIM. Recording of action potentials revealed that denervated muscle in mice lacking nNOS was more excitable than control denervated muscle. Conclusion Taken together, these data suggest that the conformation/protein association of the sodium channel complex differs in control and critical illness myopathy muscle membranes; and suggest that nitric oxide signaling plays a role in development of muscle inexcitability." @default.
• W2110260167 created "2016-06-24" @default.
• W2110260167 creator A5005061089 @default.
• W2110260167 creator A5016382820 @default.
• W2110260167 creator A5028837643 @default.
• W2110260167 creator A5037424395 @default.
• W2110260167 creator A5059981596 @default.
• W2110260167 date "2012-08-30" @default.
• W2110260167 modified "2023-09-25" @default.
• W2110260167 title "Altered sodium channel-protein associations in critical illness myopathy" @default.
• W2110260167 cites W1496192961 @default.
• W2110260167 cites W1570985840 @default.
• W2110260167 cites W1862637346 @default.
• W2110260167 cites W1968130118 @default.
• W2110260167 cites W1978420721 @default.
• W2110260167 cites W1980069082 @default.
• W2110260167 cites W1986698551 @default.
• W2110260167 cites W1987223530 @default.
• W2110260167 cites W2003823325 @default.
• W2110260167 cites W2005373784 @default.
• W2110260167 cites W2005971230 @default.
• W2110260167 cites W2025942837 @default.
• W2110260167 cites W2031119708 @default.
• W2110260167 cites W2035088786 @default.
• W2110260167 cites W2035094622 @default.
• W2110260167 cites W2037903288 @default.
• W2110260167 cites W2039423179 @default.
• W2110260167 cites W2041424015 @default.
• W2110260167 cites W2042868672 @default.
• W2110260167 cites W2043691181 @default.
• W2110260167 cites W2047518846 @default.
• W2110260167 cites W2049407320 @default.
• W2110260167 cites W2051906313 @default.
• W2110260167 cites W2067142070 @default.
• W2110260167 cites W2072514225 @default.
• W2110260167 cites W2081529440 @default.
• W2110260167 cites W2091310730 @default.
• W2110260167 cites W2093693349 @default.
• W2110260167 cites W2095345152 @default.
• W2110260167 cites W2096198350 @default.
• W2110260167 cites W2102982080 @default.
• W2110260167 cites W2106897142 @default.
• W2110260167 cites W2126325231 @default.
• W2110260167 cites W2126664466 @default.
• W2110260167 cites W2129747642 @default.
• W2110260167 cites W2135048812 @default.
• W2110260167 cites W2152709230 @default.
• W2110260167 cites W2153132589 @default.
• W2110260167 cites W2154137950 @default.
• W2110260167 doi "https://doi.org/10.1186/2044-5040-2-17" @default.
• W2110260167 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3441911" @default.
• W2110260167 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22935229" @default.
• W2110260167 hasPublicationYear "2012" @default.
• W2110260167 type Work @default.
• W2110260167 sameAs 2110260167 @default.
• W2110260167 citedByCount "14" @default.
• W2110260167 countsByYear W21102601672014 @default.
• W2110260167 countsByYear W21102601672015 @default.
• W2110260167 countsByYear W21102601672016 @default.
• W2110260167 countsByYear W21102601672018 @default.
• W2110260167 countsByYear W21102601672019 @default.
• W2110260167 countsByYear W21102601672021 @default.
• W2110260167 countsByYear W21102601672022 @default.
• W2110260167 crossrefType "journal-article" @default.
• W2110260167 hasAuthorship W2110260167A5005061089 @default.
• W2110260167 hasAuthorship W2110260167A5016382820 @default.
• W2110260167 hasAuthorship W2110260167A5028837643 @default.
• W2110260167 hasAuthorship W2110260167A5037424395 @default.
• W2110260167 hasAuthorship W2110260167A5059981596 @default.
• W2110260167 hasBestOaLocation W21102601671 @default.
• W2110260167 hasConcept C11960822 @default.
• W2110260167 hasConcept C12554922 @default.
• W2110260167 hasConcept C126322002 @default.
• W2110260167 hasConcept C134018914 @default.
• W2110260167 hasConcept C178790620 @default.
• W2110260167 hasConcept C185592680 @default.
• W2110260167 hasConcept C2776414672 @default.
• W2110260167 hasConcept C2777300911 @default.
• W2110260167 hasConcept C2779959927 @default.
• W2110260167 hasConcept C50952357 @default.
• W2110260167 hasConcept C537181965 @default.
• W2110260167 hasConcept C55493867 @default.
• W2110260167 hasConcept C71924100 @default.
• W2110260167 hasConcept C86803240 @default.
• W2110260167 hasConceptScore W2110260167C11960822 @default.
• W2110260167 hasConceptScore W2110260167C12554922 @default.
• W2110260167 hasConceptScore W2110260167C126322002 @default.
• W2110260167 hasConceptScore W2110260167C134018914 @default.
• W2110260167 hasConceptScore W2110260167C178790620 @default.
• W2110260167 hasConceptScore W2110260167C185592680 @default.
• W2110260167 hasConceptScore W2110260167C2776414672 @default.
• W2110260167 hasConceptScore W2110260167C2777300911 @default.
• W2110260167 hasConceptScore W2110260167C2779959927 @default.
• W2110260167 hasConceptScore W2110260167C50952357 @default.
• W2110260167 hasConceptScore W2110260167C537181965 @default.
• W2110260167 hasConceptScore W2110260167C55493867 @default.
• W2110260167 hasConceptScore W2110260167C71924100 @default.
• W2110260167 hasConceptScore W2110260167C86803240 @default.
• W2110260167 hasIssue "1" @default.
• W2110260167 hasLocation W21102601671 @default.

• next