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@ARTICLE{Spreen:282562,
      author       = {Spreen, Anika and Sadanandan, Nidish Ponath and Schneider,
                      Martin Winfried and Kuehn, Enrico and Leemisa, Andries Napo
                      and De Zio, Roberta and Meyer, Niklas and Busse, Wayne and
                      Erlinghagen, Bela and Adenauer, Lea and Opitz, Thoralf and
                      Bönigk, Wolfgang and Schiewer, Enrico and Heer, Jonas and
                      Schmitz, Dietmar and Vierock, Johannes and Beck, Heinz and
                      Hegemann, Peter and Baier, Herwig and Schneider-Warme,
                      Franziska and Sierra, Yinth Andrea Bernal and Seifert,
                      Reinhard},
      title        = {{O}ptogenetic silencing by combining a rhodopsin cyclase
                      with an engineered c{GMP}-gated potassium channel.},
      journal      = {Science advances},
      volume       = {11},
      number       = {48},
      issn         = {2375-2548},
      address      = {Washington, DC [u.a.]},
      publisher    = {Assoc.},
      reportid     = {DZNE-2025-01325},
      pages        = {eadx1195},
      year         = {2025},
      abstract     = {Since the advent of optogenetics, great progress has been
                      made in developing tools to modulate and detect cellular
                      activity using light. We present a two-component optogenetic
                      silencing tool, RoCK (rhodopsin cyclase/K+ channel), which
                      pairs the rhodopsin-guanylyl cyclase CaRhGC with customized
                      SthK K+ channels that are engineered to open selectively
                      upon guanosine 3',5'-monophosphate (cGMP) binding. By
                      enhancing the cGMP sensitivity and open probability of SthK
                      mutants, we obtained four channel variants suited for
                      different levels of cGMP concentration. CaRhGC's
                      membrane-bound nature enables localized cGMP production, and
                      the lack of dark activity reduces the risk for off-target
                      effects. Optimized RoCK effectively modulated cellular
                      activity in mouse hippocampal neurons, in acute hippocampal
                      slices, and in rabbit cardiomyocytes. In zebrafish, RoCK
                      silenced motor neurons in vivo, suppressing the
                      characteristic coiling behavior of embryos, thus
                      highlighting its potential for behavioral studies. In
                      summary, RoCK expands our optogenetic toolkit threefold for
                      fast cGMP production, fast cGMP sensing, and K+-based cell
                      silencing.},
      keywords     = {Optogenetics: methods / Animals / Cyclic GMP: metabolism /
                      Mice / Rhodopsin: metabolism / Rhodopsin: genetics / Humans
                      / Hippocampus: metabolism / Hippocampus: cytology /
                      Guanylate Cyclase: metabolism / Guanylate Cyclase: genetics
                      / Zebrafish / Potassium Channels: metabolism / Potassium
                      Channels: genetics / Protein Engineering / Myocytes,
                      Cardiac: metabolism / Neurons: metabolism / HEK293 Cells /
                      Cyclic GMP (NLM Chemicals) / Rhodopsin (NLM Chemicals) /
                      Guanylate Cyclase (NLM Chemicals) / Potassium Channels (NLM
                      Chemicals)},
      cin          = {AG Schmitz / Bonn common},
      ddc          = {500},
      cid          = {I:(DE-2719)1810004 / I:(DE-2719)6000011},
      pnm          = {351 - Brain Function (POF4-351) / 899 - ohne Topic
                      (POF4-899)},
      pid          = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41313760},
      pmc          = {pmc:PMC12662207},
      doi          = {10.1126/sciadv.adx1195},
      url          = {https://pub.dzne.de/record/282562},
}