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@ARTICLE{Sharma:130550,
      author       = {K. R. Sharma and K. Heckler and S. J. Stoll$^*$ and J.-L.
                      Hillebrands and K. Kynast and E. Herpel and S. Porubsky and
                      M. Elger and B. Hadaschik and K. Bieback and H.-P. Hammes
                      and P. P. Nawroth and J. Kroll$^*$},
      title        = {{ELMO}1 protects renal structure and ultrafiltration in
                      kidney development and under diabetic conditions.},
      journal      = {Scientific reports},
      volume       = {6},
      number       = {1},
      issn         = {2045-2322},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2017-05629},
      pages        = {37172},
      year         = {2016},
      abstract     = {Engulfment and cell motility 1 (ELMO1) functions as a
                      guanine exchange factor for Rac1 and was recently found to
                      protect endothelial cells from apoptosis. Genome wide
                      association studies suggest that polymorphisms within human
                      elmo1 act as a potential contributing factor for the
                      development of diabetic nephropathy. Yet, the function of
                      ELMO1 with respect to the glomerulus and how this protein
                      contributes to renal pathology was unknown. Thus, this study
                      aimed to identify the role played by ELMO1 in renal
                      development in zebrafish, under hyperglycaemic conditions,
                      and in diabetic nephropathy patients. In zebrafish,
                      hyperglycaemia did not alter renal ELMO1 expression.
                      However, hyperglycaemia leads to pathophysiological and
                      functional alterations within the pronephros, which could be
                      rescued via ELMO1 overexpression. Zebrafish ELMO1 crispants
                      exhibited a renal pathophysiology due to increased apoptosis
                      which could be rescued by the inhibition of apoptosis. In
                      human samples, immunohistochemical staining of ELMO1 in
                      nondiabetic, diabetic and polycystic kidneys localized ELMO1
                      in glomerular podocytes and in the tubules. However, ELMO1
                      was not specifically or distinctly regulated under either
                      one of the disease conditions. Collectively, these results
                      highlight ELMO1 as an important factor for glomerular
                      protection and renal cell survival via decreasing apoptosis,
                      especially under diabetic conditions.},
      cin          = {A190},
      ddc          = {000},
      cid          = {I:(DE-He78)A190-20160331},
      pnm          = {321 - Basic Concepts (POF3-321)},
      pid          = {G:(DE-HGF)POF3-321},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27849017},
      pmc          = {pmc:PMC5111104},
      doi          = {10.1038/srep37172},
      url          = {https://inrepo02.dkfz.de/record/130550},
}