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                  <mods:namePart>Palomo-Guerrero, Marta</mods:namePart>
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                  <mods:namePart>Fadó Andrés, Rut</mods:namePart>
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                  <mods:namePart>Casas, Maria</mods:namePart>
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                  <mods:namePart>Pérez-Montero, Marta</mods:namePart>
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                  <mods:namePart>Baena Muñoz, Miguel</mods:namePart>
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                  <mods:namePart>Helmer, Patrick O</mods:namePart>
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                  <mods:namePart>Domínguez, José Luis</mods:namePart>
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                  <mods:namePart>Roig, Aina</mods:namePart>
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                  <mods:namePart>Serra i Cucurull, Dolors</mods:namePart>
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                  <mods:namePart>Hayen, Heiko</mods:namePart>
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               <mods:name>
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                  <mods:namePart>Stenmark, Harald</mods:namePart>
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               <mods:name>
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                  <mods:namePart>Raiborg, Camilla</mods:namePart>
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               <mods:name>
                  <mods:role>
                     <mods:roleTerm type="text">author</mods:roleTerm>
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                  <mods:namePart>Casals, Núria</mods:namePart>
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               <mods:originInfo>
                  <mods:dateIssued encoding="iso8601">2020-03-13T12:01:36Z2020-03-13T12:01:36Z2019-12-232020-03-13T12:01:37Z</mods:dateIssued>
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               <mods:abstract>Anterograde transport of late endosomes or lysosomes (LE/Lys) is crucial for proper axon growth. However, the role of energetic nutrients has been poorly explored. Malonyl-CoA is a precursor of fatty acids, and its intracellular levels highly fluctuate depending on glucose availability or the energy sensor AMP-activated protein kinase (AMPK). We demonstrate in HeLa cells that carnitine palmitoyltransferase 1C (CPT1C) senses malonyl-CoA and enhances LE/Lys anterograde transport by interacting with the endoplasmic reticulum protein protrudin and facilitating the transfer of Kinesin-1 from protrudin to LE/Lys. In cultured mouse cortical neurons, glucose deprivation, pharmacological activation of AMPK or inhibition of malonyl-CoA synthesis decreases LE/Lys abundance at the axon terminal, and shortens axon length in a CPT1C-dependent manner. These results identify CPT1C as a new regulator of anterograde LE/Lys transport in response to malonyl-CoA changes, and give insight into how axon growth is controlled by nutrients.</mods:abstract>
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               <mods:accessCondition type="useAndReproduction">cc-by (c) Palomo-Guerrero, Marta et al., 2019 http://creativecommons.org/licenses/by/3.0/es info:eu-repo/semantics/openAccess</mods:accessCondition>
               <mods:subject>
                  <mods:topic>Carnitina palmitoïl-transferasa 1</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Axons</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Lisosomes</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Carnitine palmitoyltransferase I</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Axons</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Lysosomes</mods:topic>
               </mods:subject>
               <mods:titleInfo>
                  <mods:title>Sensing of nutrients by CPT1C regulates late endosome/lysosome anterograde transport and axon growth</mods:title>
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