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Transcriptional regulation of Annexin A2 promotes starvation-induced autophagy

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dc.contributor.authorMoreau, Kevin
dc.contributor.authorHochfeld, Warren
dc.contributor.authorRenna, Maurizio
dc.contributor.authorZavodszky, Eszter
dc.contributor.authorRunwal, Gautam
dc.contributor.authorPuri, Claudia
dc.contributor.authorLee, Shirley
dc.contributor.authorSiddiqi, Farah
dc.contributor.authorMenzies, Fiona
dc.contributor.authorRavikumar, Brinda
dc.contributor.authorRubinsztein, David
dc.contributor.otherBiomolecular & Analytical Mass Spectrometry (BAMS)
dc.contributor.otherAntwerp X-ray Analysis, Electrochemistry and Speciation (AXES)
dc.date.accessioned2019-04-26T08:57:24Z
dc.date.available2019-04-26T08:57:24Z
dc.date.issued20/08/15
dc.descriptionAutophagy is an important degradation pathway, which is induced after starvation, where it buffers nutrient deprivation by recycling macromolecules in organisms from yeast to man. While the classical pathway mediating this response is via mTOR inhibition, there are likely to be additional pathways that support the process. Here, we identify Annexin A2 as an autophagy modulator that regulates autophagosome formation by enabling appropriate ATG9A trafficking from endosomes to autophagosomes via actin. This process is dependent on the Annexin A2 effectors ARP2 and Spire1. Annexin A2 expression increases after starvation in cells in an mTOR-independent fashion. This is mediated via Jun N-terminal kinase activation of c-Jun, which, in turn, enhances the trans-activation of the Annexin A2 promoter. Annexin A2 knockdown abrogates starvation-induced autophagy, while its overexpression induces autophagy. Hence, c-Jun-mediated transcriptional responses support starvation-induced autophagy by regulating Annexin A2 expression levels.
dc.identifier.urihttps://demo7.dspace.org/handle/123456789/470
dc.languageen
dc.publisherNature Publishing Group
dc.titleTranscriptional regulation of Annexin A2 promotes starvation-induced autophagy
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