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@ARTICLE{Castillo:917482,
      author       = {Castillo, Stuart R. and Rickeard, Brett W. and DiPasquale,
                      Mitchell and Nguyen, Michael H. L. and Lewis-Laurent, Aislyn
                      and Doktorova, Milka and Kav, Batuhan and Miettinen, Markus
                      S. and Nagao, Michihiro and Kelley, Elizabeth G. and
                      Marquardt, Drew},
      title        = {{P}robing the {L}ink between {P}ancratistatin and
                      {M}itochondrial {A}poptosis through {C}hanges in the
                      {M}embrane {D}ynamics on the {N}anoscale},
      journal      = {Molecular pharmaceutics},
      volume       = {19},
      number       = {6},
      issn         = {1543-8384},
      address      = {Washington, DC},
      publisher    = {American Chemical Society},
      reportid     = {FZJ-2023-00695},
      pages        = {1839 - 1852},
      year         = {2022},
      abstract     = {Pancratistatin (PST) is a natural antiviral alkaloid that
                      has demonstrated specificity toward cancerous cells and
                      explicitly targets the mitochondria. PST initiates apoptosis
                      while leaving healthy, noncancerous cells unscathed.
                      However, the manner by which PST induces apoptosis remains
                      elusive and impedes the advancement of PST as a natural
                      anticancer therapeutic agent. Herein, we use neutron
                      spin-echo (NSE) spectroscopy, molecular dynamics (MD)
                      simulations, and supporting small angle scattering
                      techniques to study PST's effect on membrane dynamics using
                      biologically representative model membranes. Our data
                      suggests that PST stiffens the inner mitochondrial membrane
                      (IMM) by being preferentially associated with cardiolipin,
                      which would lead to the relocation and release of cytochrome
                      c. Second, PST has an ordering effect on the lipids and
                      disrupts their distribution within the IMM, which would
                      interfere with the maintenance and functionality of the
                      active forms of proteins in the electron transport chain.
                      These previously unreported findings implicate PST's effect
                      on mitochondrial apoptosis.},
      cin          = {IBI-7},
      ddc          = {610},
      cid          = {I:(DE-Juel1)IBI-7-20200312},
      pnm          = {5244 - Information Processing in Neuronal Networks
                      (POF4-524)},
      pid          = {G:(DE-HGF)POF4-5244},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {35559658},
      UT           = {WOS:000810650800016},
      doi          = {10.1021/acs.molpharmaceut.1c00926},
      url          = {https://juser.fz-juelich.de/record/917482},
}