IndraLab

Statements

SCN5A binds DMD. 13 / 13
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"Ankyrins, fibroblast growth factor homologous factor 1B, calmodulin, caveolin-3, Nedd4-like ubiquitin-protein ligases, dystrophin, syntrophin, glycerol 3-phosphate dehydrogenase 1-like protein (GPD1L), and RAN guanine nucleotide release factor (MOG1) can directly bind to Nav1.5 and regulate Na channel transport, expression, and gating [75,76,77]."
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"Furthermore, we observed less co-localization and weaker binding between Nav1.5 and ankyrin-G or dystrophin after the long-term treatments with amitriptyline, indicating the disrupted Nav1.5-ankyrin-G interaction and Nav1.5-dystrophin interaction induced by amitriptyline."
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"These results suggested that the interaction between Nav1.5 and ankyrin-G or dystrophin could be weakened by the long-term effect of amitriptyline."
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"Although there is a long distance between these two binding sites on the primary sequence, the spatial proximity may exist to provide the necessary conditions for amitriptyline to impair the interaction between Nav1.5 and ankyrin-G. On the other hand, we discovered that the long-term effect of amitriptyline could destroy the Nav1.5-dystrophin interaction."
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"Impaired Nav1.5 trafficking, regulated by Nav1.5-ankyrin-G and Nav1.5-dystrophin interaction, was suggested to be the mechanism related to such a long-term effect."
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"As deduced from these findings, the novel mechanism responsible for the long-term blockade effect of amitriptyline on Nav1.5 was the impairment of Nav1.5 trafficking.Furthermore, we observed less co-localization and weaker binding between Nav1.5 and ankyrin-G or dystrophin after the long-term treatments with amitriptyline, indicating the disrupted Nav1.5-ankyrin-G interaction and Nav1.5-dystrophin interaction induced by amitriptyline."
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"Disruption of Nav1.5 dystrophin complex have also been shown to impair Nav1.5 function [ 25 , 59 , 61 ]."
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"Co-immunoprecipitation experiments were used to test the Nav1.5-ankyrin-G interaction and Nav1.5-dystrophin interaction."
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"Cav3, SNTA1, and SCN5A also bind to dystrophin, the protein that causes Duchenne and Becker muscular dystrophy with DCM or LVNC, as does SAP97."
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"Co-immunoprecipitation experiments further testified that the combination of Nav1.5 and ankyrin-G or dystrophin was severely weakened after long-term treatments to amitriptyline, implying the failed interaction between Nav1.5 and ankyrin-G or dystrophin."
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"The mechanisms of BrS induced by amitriptyline were related to Nav1.5 trafficking and could be explained by the disrupted interaction of ankyrin-G, dystrophin and Nav1.5."
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"The underlying mechanisms involved the impairment of Nav1.5 trafficking, which could be regulated by the Nav1.5-ankyrin-G interaction and Nav1.5-dystrophin interaction."
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"The latter appears to be a more plausible explanation because a similar mechanism has been shown to occur for Nav1.5 channel lateral membrane pool in mdx mice, in which utrophin a homolog of dystrophi[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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