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@ARTICLE{Taher:893884,
      author       = {Taher, Ali T. and Viprakasit, Vip and Cappellini, Maria
                      Domenica and Kraus, Dominik and Cech, Patrick and Volz,
                      Dietmar and Winter, Erica and Nave, Stephane and Dukart,
                      Juergen and Khwaja, Omar and Koerner, Annette and
                      Hermosilla, Ricardo and Brugnara, Carlo},
      title        = {{H}aematological effects of oral administration of
                      bitopertin, a glycine transport inhibitor, in patients with
                      non‐transfusion‐dependent β‐thalassaemia},
      journal      = {British journal of haematology},
      volume       = {194},
      number       = {2},
      issn         = {1365-2141},
      address      = {Oxford [u.a.]},
      publisher    = {Wiley-Blackwell},
      reportid     = {FZJ-2021-02896},
      pages        = {474–481},
      year         = {2021},
      abstract     = {Bitopertin is a small molecule selective inhibitor of
                      glycine transporter 1 (GlyT1), initially developed to
                      increase brain extracellular levels of glycine in the
                      vicinity of neuronal N-methyl-D-aspartate receptors for the
                      treatment of schizophrenia. GlyT1, the pharmacological
                      target of bitopertin, is also present as a transmembrane
                      transporter in erythroid cells1 and accounts for $50–55\%$
                      of glycine uptake in human red blood cells (RBCs).2, 3
                      Erythroid GlyT1 inhibition by bitopertin leads to reduced
                      intracellular glycine availability, interfering with the
                      first step of haem synthesis, in which 5-aminolevulinate
                      synthase catalyses the condensation reaction between glycine
                      and succinyl-coenzyme A, forming 5-aminolevulinic acid.1},
      cin          = {INM-7},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-7-20090406},
      pnm          = {5252 - Brain Dysfunction and Plasticity (POF4-525)},
      pid          = {G:(DE-HGF)POF4-5252},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33931857},
      UT           = {WOS:000646154400001},
      doi          = {10.1111/bjh.17479},
      url          = {https://juser.fz-juelich.de/record/893884},
}