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@ARTICLE{Paiva:140217,
      author       = {Paiva, Isabel and Jain, Gaurav and Lázaro, Diana F and
                      Jerčić, Kristina Gotovac and Hentrich, Thomas and
                      Kerimoglu, Cemil and Pinho, Raquel and Szegő, Èva M and
                      Burkhardt, Susanne and Capece, Vincenzo and Halder, Rashi
                      and Islam, Rezaul and Xylaki, Mary and Caldi Gomes, Lucas A
                      and Roser, Anna-Elisa and Lingor, Paul and Schulze-Hentrich,
                      Julia M and Borovečki, Fran and Fischer, André and
                      Outeiro, Tiago F},
      title        = {{A}lpha-synuclein deregulates the expression of {COL}4{A}2
                      and impairs {ER}-{G}olgi function.},
      journal      = {Neurobiology of disease},
      volume       = {119},
      issn         = {0969-9961},
      address      = {Orlando, Fla.},
      publisher    = {Academic Press},
      reportid     = {DZNE-2020-06539},
      pages        = {121-135},
      year         = {2018},
      abstract     = {Alpha-synuclein (aSyn) is the major protein component of
                      Lewy bodies and Lewy neurites, the typical pathological
                      hallmarks in Parkinson's disease (PD) and Dementia with Lewy
                      bodies. aSyn is capable of inducing transcriptional
                      deregulation, but the precise effect of specific aSyn
                      mutants associated with familial forms of PD, remains
                      unclear. Here, we used transgenic mice overexpressing human
                      wild-type (WT) or A30P aSyn to compare the transcriptional
                      profiles of the two animal models. We found that A30P aSyn
                      promotes strong transcriptional deregulation and increases
                      DNA binding. Interestingly, COL4A2, a major component of
                      basement membranes, was found to be upregulated in both A30P
                      aSyn transgenic mice and in dopaminergic neurons expressing
                      A30P aSyn, suggesting a crucial role for collagen related
                      genes in aSyn-induced toxicity. Finally, we observed that
                      A30P aSyn alters Golgi morphology and increases the
                      susceptibility to endoplasmic reticulum (ER) stress in
                      dopaminergic cells. In total, our findings provide novel
                      insight into the putative role of aSyn on transcription and
                      on the molecular mechanisms involved, thereby opening novel
                      avenues for future therapeutic interventions in PD and other
                      synucleinopathies.},
      keywords     = {Animals / Cells, Cultured / Collagen Type IV: biosynthesis
                      / Collagen Type IV: genetics / Endoplasmic Reticulum:
                      physiology / Gene Expression / Golgi Apparatus: physiology /
                      Humans / Mice / Mice, Inbred C57BL / Mice, Transgenic /
                      Peptide Fragments: biosynthesis / Peptide Fragments:
                      genetics / alpha-Synuclein: biosynthesis / alpha-Synuclein:
                      genetics / Col4a2 protein, mouse (NLM Chemicals) / Collagen
                      Type IV (NLM Chemicals) / Peptide Fragments (NLM Chemicals)
                      / Snca protein, mouse (NLM Chemicals) / alpha-Synuclein (NLM
                      Chemicals)},
      cin          = {AG Fischer / AG Bonn 2},
      ddc          = {570},
      cid          = {I:(DE-2719)1410002 / I:(DE-2719)1440012},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30092270},
      doi          = {10.1016/j.nbd.2018.08.001},
      url          = {https://pub.dzne.de/record/140217},
}