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@ARTICLE{Tutas:1039733,
      author       = {Tutas, Janine and Tolve, Marianna and Özer-Yildiz, Ebru
                      and Ickert, Lotte and Klein, Ines and Silverman, Quinn and
                      Liebsch, Filip and Dethloff, Frederik and Giavalisco,
                      Patrick and Endepols, Heike and Georgomanolis, Theodoros and
                      Neumaier, Bernd and Drzezga, Alexander and Schwarz, Guenter
                      and Thorens, Bernard and Gatto, Graziana and Frezza,
                      Christian and Kononenko, Natalia L.},
      title        = {{A}utophagy regulator {ATG}5 preserves cerebellar function
                      by safeguarding its glycolytic activity},
      journal      = {Nature metabolism},
      volume       = {7},
      issn         = {2522-5812},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {FZJ-2025-01777},
      pages        = {297–320},
      year         = {2025},
      abstract     = {Dysfunctions in autophagy, a cellular mechanism for
                      breaking downcomponents within lysosomes, often lead to
                      neurodegeneration. Thespecific mechanisms underlying
                      neuronal vulnerability due to autophagydysfunction remain
                      elusive. Here we show that autophagy contributesto
                      cerebellar Purkinje cell (PC) survival by safeguarding their
                      glycolyticactivity. Outside the conventional housekeeping
                      role, autophagy is alsoinvolved in the ATG5-mediated
                      regulation of glucose transporter 2 (GLUT2)levels during
                      cerebellar maturation. Autophagy-deficient PCs exhibitGLUT2
                      accumulation on the plasma membrane, along with
                      increasedglucose uptake and alterations in glycolysis. We i
                      de nt ify l ys op hosp ha-tidic acid and serine as
                      glycolytic intermediates that trigger PC death
                      anddemonstrate that the deletion of GLUT2 in ATG5-deficient
                      mice mitigates PCne urod egen e ration and rescues their
                      ataxic gait. Taken together, this workreveals a mechanism
                      for regulating GLUT2 levels in neurons and providesinsights
                      into the neuroprotective role of autophagy by controlling
                      glucosehomeostasis in the brain.},
      cin          = {INM-5 / INM-2},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-5-20090406 / I:(DE-Juel1)INM-2-20090406},
      pnm          = {5253 - Neuroimaging (POF4-525)},
      pid          = {G:(DE-HGF)POF4-5253},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {39815080},
      UT           = {WOS:001396167500001},
      doi          = {10.1038/s42255-024-01196-4},
      url          = {https://juser.fz-juelich.de/record/1039733},
}