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@ARTICLE{Conrad:851427,
      author       = {Conrad, Rachel and Stölting, Gabriel and Hendriks, Johnny
                      and Ruello, Giovanna and Kortzak, Daniel and Jordan, Nadine
                      and Gensch, Thomas and Hidalgo, Patricia},
      title        = {{R}apid {T}urnover of the {C}ardiac {L}-{T}ype {C}a{V}1.2
                      {C}hannel by {E}ndocytic {R}ecycling {R}egulates {I}ts
                      {C}ell {S}urface {A}vailability},
      journal      = {iScience},
      volume       = {7},
      issn         = {2589-0042},
      address      = {Amsterdam},
      publisher    = {Elsevier},
      reportid     = {FZJ-2018-05074},
      pages        = {1 - 15},
      year         = {2018},
      abstract     = {Calcium entry through CaV1.2 L-type calcium channels
                      regulates cardiac contractility. Here, we study the impact
                      of exocytic and post-endocytic trafficking on cell surface
                      channel abundance in cardiomyocytes. Single-molecule
                      localization and confocal microscopy reveal an intracellular
                      CaV1.2 pool tightly associated with microtubules from the
                      perinuclear region to the cell periphery, and with actin
                      filaments at the cell cortex. Channels newly inserted into
                      the plasma membrane become internalized with an average time
                      constant of 7.5 min and are sorted out to the
                      Rab11a-recycling compartment. CaV1.2 recycling suffices for
                      maintaining stable L-type current amplitudes over 20 hr
                      independent of de novo channel transport along microtubules.
                      Disruption of the actin cytoskeleton re-routes CaV1.2 from
                      recycling toward lysosomal degradation. We identify
                      endocytic recycling as essential for the homeostatic
                      regulation of voltage-dependent calcium influx into
                      cardiomyocytes. This mechanism provides the basis for a
                      dynamic adjustment of the channel's surface availability and
                      thus, of heart's contraction.},
      cin          = {ICS-4},
      ddc          = {050},
      cid          = {I:(DE-Juel1)ICS-4-20110106},
      pnm          = {552 - Engineering Cell Function (POF3-552)},
      pid          = {G:(DE-HGF)POF3-552},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30267672},
      UT           = {WOS:000449735000001},
      doi          = {10.1016/j.isci.2018.08.012},
      url          = {https://juser.fz-juelich.de/record/851427},
}