| http://purl.uniprot.org/citations/27941154 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/27941154 | http://www.w3.org/2000/01/rdf-schema#comment | "The obligatory role of carnitine palmitoyltransferase-I (CPT-I) in mediating mitochondrial lipid transport is well established, a process attenuated by malonyl-CoA (M-CoA). However, the necessity of reducing M-CoA concentrations to promote lipid oxidation has recently been challenged, suggesting external regulation on CPT-I. Since previous work in hepatocytes suggests the involvement of the intermediate filament fraction of the cytoskeleton in regulating CPT-I, we investigated in skeletal muscle if CPT-I sensitivity for M-CoA inhibition could be regulated by the intermediate filaments, and whether AMP-activated protein kinase (AMPK) could be involved in this process. Chemical disruption (3,3'-iminodipropionitrile, IDPN) of the intermediate filaments did not alter mitochondrial respiration or sensitivity for numerous substrates (palmitoyl-CoA, ADP, palmitoyl carnitine and pyruvate). In contrast, IDPN reduced CPT-I sensitivity for M-CoA inhibition in permeabilized muscle fibers, identifying M-CoA kinetics as a specific target for intermediate filament regulation. Importantly, exercise mimicked the effect of IDPN on M-CoA sensitivity, suggesting that intermediate filament disruption in vivo is physiologically important for CPT-I regulation. To ascertain a potential mechanism, since AMPK is activated during exercise, AMPK β1β2-KO mice were utilized in an attempt to ablate the observed exercise response. Unexpectedly, these mice displayed drastic attenuation in resting M-CoA sensitivity, such that exercise and IDPN could not further alter M-CoA sensitivity. These data suggest that AMPK is not required for the regulation of the intermediate filament interaction with CPT-I. Altogether, these data highlight that M-CoA sensitivity is important for regulating mitochondrial lipid transport. Moreover, M-CoA sensitivity appears to be regulated by intermediate filament interaction with CPT-I, a process that is important when metabolic homeostasis is challenged."xsd:string |
| http://purl.uniprot.org/citations/27941154 | http://purl.org/dc/terms/identifier | "doi:10.1042/bcj20160913"xsd:string |
| http://purl.uniprot.org/citations/27941154 | http://purl.uniprot.org/core/author | "Steinberg G.R."xsd:string |
| http://purl.uniprot.org/citations/27941154 | http://purl.uniprot.org/core/author | "Holloway G.P."xsd:string |
| http://purl.uniprot.org/citations/27941154 | http://purl.uniprot.org/core/author | "Miotto P.M."xsd:string |
| http://purl.uniprot.org/citations/27941154 | http://purl.uniprot.org/core/date | "2017"xsd:gYear |
| http://purl.uniprot.org/citations/27941154 | http://purl.uniprot.org/core/name | "Biochem J"xsd:string |
| http://purl.uniprot.org/citations/27941154 | http://purl.uniprot.org/core/pages | "557-569"xsd:string |
| http://purl.uniprot.org/citations/27941154 | http://purl.uniprot.org/core/title | "Controlling skeletal muscle CPT-I malonyl-CoA sensitivity: the importance of AMPK-independent regulation of intermediate filaments during exercise."xsd:string |
| http://purl.uniprot.org/citations/27941154 | http://purl.uniprot.org/core/volume | "474"xsd:string |
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