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@ARTICLE{Fleck:136519,
      author       = {Fleck, Daniel and Garratt, Alistair N and Haass, Christian
                      and Willem, Michael},
      title        = {{BACE}1 dependent neuregulin processing: review.},
      journal      = {Current Alzheimer research},
      volume       = {9},
      number       = {2},
      issn         = {1567-2050},
      address      = {Hilversum},
      publisher    = {Bentham Science Publ. Ltd.},
      reportid     = {DZNE-2020-02841},
      pages        = {178-183},
      year         = {2012},
      abstract     = {Neuregulin-1 (NRG1), known also as heregulin, acetylcholine
                      receptor inducing activity (ARIA), glial growth factor
                      (GGF), or sensory and motor neuron derived factor (SMDF),
                      plays essential roles in several developmental processes,
                      and is required also later in life. Many variants of NRG1
                      are produced via alternative splicing and usage of distinct
                      promoters. All contain an epidermal growth factor (EGF)-like
                      domain, which alone is sufficient to bind and activate the
                      cognate receptors, members of the ErbB family. NRG1 mediated
                      signaling is crucial for cardiogenesis and the development
                      of the mammary gland and ErbB2 (HER2), an orphan co-receptor
                      for NRG1 is the target of the drug Herceptin�
                      (trastuzumab) used for treatment of metastatic breast
                      cancer. In the nervous system, NRG1 controls the early
                      development of subpopulations of neural crest cells. In
                      particular, NRG1 acts as an essential paracrine signaling
                      molecule expressed on the axonal surface, where it signals
                      to Schwann cells throughout development and regulates the
                      thickness of the myelin sheath. NRG1 is required also by
                      other cell types in the nervous system, for instance as an
                      axonal signal released by proprioceptive afferents to induce
                      development of the muscle spindle, and it controls aspects
                      of cortical interneuron development as well as the formation
                      of thalamocortical projections. Work from several
                      laboratories implicates dysregulation of NRG1/ErbB4
                      signaling in the etiology of schizophrenia. Biochemical
                      studies have shown that the precursor proteins of NRG1 can
                      be released from the membrane through limited proteolysis.
                      In addition, most NRG1 isoforms contain a transmembrane
                      domain, which is processed by γ-secretase after shedding.
                      Thereby the intracellular domain is released into the
                      cytoplasm. Despite this, the importance of NRG1 cleavage for
                      its functions in vivo remained unclear until recently. β-
                      Secretase (β-site amyloid precursor protein cleaving enzyme
                      1, BACE1) was first identified through its function as the
                      rate limiting enzyme of amyloid-β-peptide (Aβ) production.
                      Aβ is the major component of amyloid plaques in Alzheimer's
                      disease (AD). More recently it was shown that Neuregulin-1
                      is a major physiological substrate of BACE1 during early
                      postnatal development. Mutant mice lacking BACE1 display
                      severe hypomyelination of peripheral nerves similar to that
                      seen in mice lacking NRG1/ErbB signaling in Schwann cells,
                      and a BACE1-dependent activation of NRG1 in the process of
                      peripheral myelination was proposed. Here we summarize the
                      current knowledge about the role of NRG1 proteolysis for
                      ErbB receptor mediated signaling during development and in
                      Alzheimer's disease.},
      subtyp        = {Review Article},
      keywords     = {Amyloid Precursor Protein Secretases: metabolism / Animals
                      / Aspartic Acid Endopeptidases: metabolism / ErbB Receptors:
                      metabolism / Humans / Mice / Models, Biological /
                      Neuregulins: genetics / Neuregulins: metabolism / Signal
                      Transduction: physiology / Neuregulins (NLM Chemicals) /
                      EGFR protein, human (NLM Chemicals) / ErbB Receptors (NLM
                      Chemicals) / Amyloid Precursor Protein Secretases (NLM
                      Chemicals) / Aspartic Acid Endopeptidases (NLM Chemicals) /
                      BACE1 protein, human (NLM Chemicals)},
      cin          = {AG Haass old / Ext LMU},
      ddc          = {610},
      cid          = {I:(DE-2719)1110007 / I:(DE-2719)5000048},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:22455478},
      doi          = {10.2174/156720512799361637},
      url          = {https://pub.dzne.de/record/136519},
}