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@ARTICLE{Pirona:1024274,
      author       = {Pirona, Lorenza and Ballabio, Federico and Alfonso-Prieto,
                      Mercedes and Capelli, Riccardo},
      title        = {{C}alcium-{D}riven {I}n {S}ilico {I}nactivation of a
                      {H}uman {O}lfactory {R}eceptor},
      journal      = {Journal of chemical information and modeling},
      volume       = {64},
      number       = {8},
      issn         = {1549-9596},
      address      = {Washington, DC},
      publisher    = {American Chemical Society},
      reportid     = {FZJ-2024-02081},
      pages        = {2971–2978},
      year         = {2024},
      note         = {Preprint available at bioRxiv:
                      https://doi.org/10.1101/2024.01.31.578070. Enclosed you can
                      find the author's version of the main text and SI submitted
                      right before acceptance by the journal.},
      abstract     = {Conformational changes as well as molecular determinants
                      related to the activation and inactivation of olfactory
                      receptors are still poorly understood due to the intrinsic
                      difficulties in the structural determination of this GPCR
                      family. Here, we perform, for the first time, the in silico
                      inactivation of human olfactory receptor OR51E2,
                      highlighting the possible role of calcium in this receptor
                      state transition. Using molecular dynamics simulations, we
                      show that a divalent ion in the ion binding site,
                      coordinated by two acidic residues at positions 2.50 and
                      3.39 conserved across most ORs, stabilizes the receptor in
                      its inactive state. In contrast, protonation of the same two
                      acidic residues is not sufficient to drive inactivation
                      within the microsecond timescale of our simulations. Our
                      findings suggest a novel molecular mechanism for OR
                      inactivation, potentially guiding experimental validation
                      and offering insights into the possible broader role of
                      divalent ions in GPCR signaling.},
      cin          = {IAS-5 / INM-9},
      ddc          = {540},
      cid          = {I:(DE-Juel1)IAS-5-20120330 / I:(DE-Juel1)INM-9-20140121},
      pnm          = {5241 - Molecular Information Processing in Cellular Systems
                      (POF4-524) / DFG project 291198853 - FOR 2518: Funktionale
                      Dynamik von Ionenkanälen und Transportern - DynIon -
                      (291198853) / DFG project 329460521 - Protonentransfer und
                      Substraterkennung in SLC17-Transportern (329460521)},
      pid          = {G:(DE-HGF)POF4-5241 / G:(GEPRIS)291198853 /
                      G:(GEPRIS)329460521},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {38523266},
      UT           = {WOS:001190706500001},
      doi          = {10.1021/acs.jcim.4c00249},
      url          = {https://juser.fz-juelich.de/record/1024274},
}