@article{WeingartRailaLuebkeBeckeretal.2018,
  author    = {Weingart, C. and Raila, Jens and L{\"u}bke-Becker, A. and Kershaw, O. and Brunnberg, M. and Kohn, B.},
  title     = {Calcitriol induced hypercalcemia in a hunting dog with a disseminated Paecilomyces variotii infection},
  series = {Schweizer Archiv f{\"u}r Tierheilkunde},
  journal   = {Schweizer Archiv f{\"u}r Tierheilkunde},
  number    = {5},
  edition   = {160},
  publisher = {Gesellschaft Schweizer Tier{\"a}rztinnen und Tier{\"a}rzte},
  address   = {Bern},
  issn      = {0036-7281},
  doi       = {10.17236/sat00161},
  pages     = {313 -- 319},
  year      = {2018},
  abstract  = {A 5-year old hunting dog was presented with reduced appetite, weight loss and polyuria/polydipsia. Hematology and clinical chemistry revealed anemia, leukocytosis, increased liver enzymes, hypoalbuminemia and hypercalcemia. The cytological, pathohistological and microbiological examination identified a disseminated infection with the saprophytic mould fungus Paecilomyces variotii in the biopsies of the spleen and a lymph node. Determination of vitamin D metabolites confirmed a calcitriol induced hypercalcemia.},
  language  = {en}
}
@article{KobelHoellerGleyJochinkeetal.2018,
  author    = {Kobel-H{\"o}ller, Konstanze and Gley, Kevin and Jochinke, Janina and Heider, Kristina and Fritsch, Verena Nadin and Ha Viet Duc Nguyen, and Lischke, Timo and Radek, Renate and Baumgrass, Ria and Mutzel, Rupert and Thewes, Sascha},
  title     = {Calcineurin Silencing in Dictyostelium discoideum Leads to Cellular Alterations Affecting Mitochondria, Gene Expression, and Oxidative Stress Response},
  series = {Protist},
  volume    = {169},
  journal   = {Protist},
  number    = {4},
  publisher = {Elsevier GMBH},
  address   = {M{\"u}nchen},
  issn      = {1434-4610},
  doi       = {10.1016/j.protis.2018.04.004},
  pages     = {584 -- 602},
  year      = {2018},
  abstract  = {Calcineurin is involved in development and cell differentiation of the social amoeba Dictyostelium discoideum. However, since knockouts of the calcineurin-encoding genes are not possible in D. discoideum it is assumed that the phosphatase also plays a crucial role during vegetative growth of the amoebae. Therefore, we investigated the role of calcineurin during vegetative growth in D. discoideum. RNAi-silenced calcineurin mutants showed cellular alterations with an abnormal morphology of mitochondria and had increased content of mitochondrial DNA (mtDNA). In contrast, mitochondria showed no substantial functional impairment. Calcineurin-silencing led to altered expression of calcium-regulated genes as well as mitochondrially-encoded genes. Furthermore, genes related to oxidative stress were higher expressed in the mutants, which correlated to an increased resistance towards reactive oxygen species (ROS). Most of the changes observed during vegetative growth were not seen after starvation of the calcineurin mutants. We show that impairment of calcineurin led to many subtle, but in the sum crucial cellular alterations in vegetative D. discoideum cells. As these alterations were not observed after starvation we propose a dual role for calcineurin during growth and development. Our results imply that calcineurin is one player in the mutual interplay between mitochondria and ROS during vegetative growth.},
  language  = {en}
}
@article{GlosseFegerMutigetal.2018,
  author    = {Glosse, Philipp and Feger, Martina and Mutig, Kerim and Chen, Hong and Hirche, Frank and Hasan, Ahmed Abdallah Abdalrahman Mohamed and Gaballa, Mohamed Mahmoud Salem Ahmed and Hocher, Berthold and Lang, Florian and F{\"o}ller, Michael},
  title     = {AMP-activated kinase is a regulator of fibroblast growth factor 23 production},
  series = {Kidney international : official journal of the International Society of Nephrology},
  volume    = {94},
  journal   = {Kidney international : official journal of the International Society of Nephrology},
  number    = {3},
  publisher = {Elsevier},
  address   = {New York},
  issn      = {0085-2538},
  doi       = {10.1016/j.kint.2018.03.006},
  pages     = {491 -- 501},
  year      = {2018},
  abstract  = {Fibroblast growth factor 23 (FGF23) is a proteohormone regulating renal phosphate transport and vitamin D metabolism as well as inducing left heart hypertrophy. FGF23-deficient mice suffer from severe tissue calcification, accelerated aging and a myriad of aging-associated diseases. Bone cells produce FGF23 upon store-operated calcium ion entry (SOCE) through the calcium selective ion channel Orai1. AMP-activated kinase (AMPK) is a powerful energy sensor helping cells survive states of energy deficiency, and AMPK down-regulates Orai1. Here we investigated the role of AMPK in FGF23 production. Fgf23 gene transcription was analyzed by qRT-PCR and SOCE by fluorescence optics in UMR106 osteoblast-like cells while the serum FGF23 concentration and phosphate metabolism were assessed in AMPKa1-knockout and wild-type mice. The AMPK activator, 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) down-regulated, whereas the AMPK inhibitor, dorsomorphin dihydrochloride (compound C) and AMPK gene silencing induced Fgf23 transcription. AICAR decreased membrane abundance of Orai1 and SOCE. SOCE inhibitors lowered Fgf23 gene expression induced by AMPK inhibition. AMPKa1-knockout mice had a higher serum FGF23 concentration compared to wild-type mice. Thus, AMPK participates in the regulation of FGF23 production in vitro and in vivo. The inhibitory effect of AMPK on FGF23 production is at least in part mediated by Orai1-involving SOCE.},
  language  = {en}
}