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Loss of long-chain acyl-CoA synthetase isoform 1 impairs cardiac autophagy and mitochondrial structure through mechanistic target of rapamycin complex 1 activation
Because hearts with a temporally induced knockout of acyl-CoA synthetase 1 (Acsl1(T−/−)) are virtually unable to oxidize fatty acids, glucose use increases 8-fold to compensate. This metabolic switch activates mechanistic target of rapamycin complex 1 (mTORC1), which initiates growth by increasing p...
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| Publicado no: | FASEB J |
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| Main Authors: | , , , , |
| Formato: | Artigo |
| Idioma: | Inglês |
| Publicado em: |
Federation of American Societies for Experimental Biology
2015
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| Assuntos: | |
| Acesso em linha: | https://ncbi.nlm.nih.gov/pmc/articles/PMC4608904/ https://ncbi.nlm.nih.gov/pubmed/26220174 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1096/fj.15-272732 |
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