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@ARTICLE{Arora:151645,
      author       = {Arora, Amandeep Singh and Zafar, Saima and Latif, Umair and
                      Llorens, Franc and Sabine, Mihm and Kumar, Prateek and
                      Tahir, Waqas and Thüne, Katrin and Shafiq, Mohsin and
                      Schmitz, Matthias and Zerr, Inga},
      title        = {{T}he role of cellular prion protein in lipid metabolism in
                      the liver.},
      journal      = {Prion},
      volume       = {14},
      number       = {1},
      issn         = {1933-690X},
      address      = {London [u.a.]},
      publisher    = {Taylor $\&$ Francis},
      reportid     = {DZNE-2020-01224},
      pages        = {95 - 108},
      year         = {2020},
      abstract     = {Cellular prion protein (PrPC) is a plasma membrane
                      glycophosphatidylinositol-anchored protein and it is
                      involved in multiple functions, including neuroprotection
                      and oxidative stress. So far, most of the PrPC functional
                      research is done in neuronal tissue or cell lines; the role
                      of PrPC in non-neuronal tissues such as liver is only poorly
                      understood. To characterize the role of PrPC in the liver, a
                      proteomics approach was applied in the liver tissue of PrPC
                      knockout mice. The proteome analysis and biochemical
                      validations showed an excessive fat accumulation in the
                      liver of PrPC knockout mice with a change in mRNA expression
                      of genes linked to lipid metabolism. In addition, the higher
                      Bax to Bcl2 ratio, up-regulation of tgfb1 mRNA expression in
                      PrPC knockout mice liver, further showed the evidences of
                      metabolic disease. Over-expression of PrPC in fatty
                      acid-treated AML12 hepatic cell line caused a reduction in
                      excessive intracellular fat accumulation; shows association
                      of PrPC levels and lipid metabolism. Therefore, based on
                      observation of excessive fat globules in the liver of ageing
                      PrPC knockout mice and the reduction of fat accumulation in
                      AML12 cell line with PrPC over-expression, the role of PrPC
                      in lipid metabolism is described.},
      keywords     = {Acetyl-CoA Carboxylase: genetics / Acetyl-CoA Carboxylase:
                      metabolism / Adiposity / Animals / Cell Line /
                      Electrophoresis, Gel, Two-Dimensional / Fatty Acid
                      Synthases: genetics / Fatty Acid Synthases: metabolism /
                      Female / Gene Expression Regulation / Lipid Metabolism:
                      genetics / Liver: metabolism / Male / Metabolic Diseases:
                      metabolism / Mice, Inbred C57BL / Mice, Knockout / PPAR
                      alpha: metabolism / Prion Proteins: metabolism / Proteome:
                      metabolism / Proteomics / RNA, Messenger: genetics / RNA,
                      Messenger: metabolism / Transforming Growth Factor beta1:
                      genetics / Transforming Growth Factor beta1: metabolism /
                      Triglycerides: metabolism},
      cin          = {Göttingen common / Ext UMG Zerr / AG Zerr},
      ddc          = {570},
      cid          = {I:(DE-2719)6000014 / I:(DE-2719)5000037 /
                      I:(DE-2719)1440011-1},
      pnm          = {344 - Clinical and Health Care Research (POF3-344)},
      pid          = {G:(DE-HGF)POF3-344},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32138593},
      pmc          = {pmc:PMC7153832},
      doi          = {10.1080/19336896.2020.1729074},
      url          = {https://pub.dzne.de/record/151645},
}