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@ARTICLE{Delling:270868,
      author       = {Delling, Jan Philipp and Bauer, Helen Friedericke and
                      Gerlach-Arbeiter, Susanne and Schön, Michael and Jacob,
                      Christian and Wagner, Jan and Pedro, Maria Teresa and
                      Knöll, Bernd and Boeckers, Tobias M},
      title        = {{C}ombined expansion and {STED} microscopy reveals altered
                      fingerprints of postsynaptic nanostructure across brain
                      regions in {ASD}-related {SHANK}3-deficiency.},
      journal      = {Molecular psychiatry},
      volume       = {29},
      number       = {10},
      issn         = {1359-4184},
      address      = {London},
      publisher    = {Macmillan},
      reportid     = {DZNE-2024-00907},
      pages        = {2997 - 3009},
      year         = {2024},
      abstract     = {Synaptic dysfunction is a key feature of SHANK-associated
                      disorders such as autism spectrum disorder, schizophrenia,
                      and Phelan-McDermid syndrome. Since detailed knowledge of
                      their effect on synaptic nanostructure remains limited, we
                      aimed to investigate such alterations in ex11|SH3 SHANK3-KO
                      mice combining expansion and STED microscopy. This enabled
                      high-resolution imaging of mosaic-like arrangements formed
                      by synaptic proteins in both human and murine brain tissue.
                      We found distinct shape-profiles as fingerprints of the
                      murine postsynaptic scaffold across brain regions and
                      genotypes, as well as alterations in the spatial and
                      molecular organization of subsynaptic domains under
                      SHANK3-deficient conditions. These results provide insights
                      into synaptic nanostructure in situ and advance our
                      understanding of molecular mechanisms underlying synaptic
                      dysfunction in neuropsychiatric disorders.},
      keywords     = {Animals / Female / Humans / Mice / Autism Spectrum
                      Disorder: genetics / Autism Spectrum Disorder: metabolism /
                      Brain: metabolism / Brain: pathology / Chromosome Deletion /
                      Chromosome Disorders / Chromosomes, Human, Pair 22 / Mice,
                      Inbred C57BL / Mice, Knockout / Microfilament Proteins:
                      metabolism / Microfilament Proteins: genetics / Microscopy:
                      methods / Nerve Tissue Proteins: metabolism / Nerve Tissue
                      Proteins: genetics / Synapses: metabolism / Young Adult},
      cin          = {AG Böckers},
      ddc          = {610},
      cid          = {I:(DE-2719)1910002},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC11449788},
      pubmed       = {pmid:38649753},
      doi          = {10.1038/s41380-024-02559-9},
      url          = {https://pub.dzne.de/record/270868},
}