@article{ScharawIskarOrietal.2016,
  author    = {Scharaw, Sandra and Iskar, Murat and Ori, Alessandro and Boncompain, Gaelle and Laketa, Vibor and Poser, Ina and Lundberg, Emma and Perez, Franck and Beck, Martin and Bork, Peer and Pepperkok, Rainer},
  title     = {The endosomal transcriptional regulator RNF11 integrates degradation and transport of EGFR},
  series = {Journal of Cell Biology},
  volume    = {215},
  journal   = {Journal of Cell Biology},
  number    = {4},
  doi       = {10.1083/jcb.201601090},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-186731},
  pages     = {543-558},
  year      = {2016},
  abstract  = {Stimulation of cells with epidermal growth factor (EGF) induces internalization and partial degradation of the EGF receptor (EGFR) by the endo-lysosomal pathway. For continuous cell functioning, EGFR plasma membrane levels are maintained by transporting newly synthesized EGFRs to the cell surface. The regulation of this process is largely unknown. In this study, we find that EGF stimulation specifically increases the transport efficiency of newly synthesized EGFRs from the endoplasmic reticulum to the plasma membrane. This coincides with an up-regulation of the inner coat protein complex II (COP II) components SEC23B, SEC24B, and SEC24D, which we show to be specifically required for EGFR transport. Up-regulation of these COP II components requires the transcriptional regulator RNF11, which localizes to early endosomes and appears additionally in the cell nucleus upon continuous EGF stimulation. Collectively, our work identifies a new regulatory mechanism that integrates the degradation and transport of EGFR in order to maintain its physiological levels at the plasma membrane.},
  language  = {en}
}
@article{JohnFranckAlAouaetal.2022,
  author    = {John, Katharina and Franck, Martin and Al Aoua, Sherin and Rau, Monika and Huber, Yvonne and Schattenberg, Joern M. and Geier, Andreas and Bahr, Matthias J. and Wedemeyer, Heiner and Schulze-Osthoff, Klaus and Bantel, Heike},
  title     = {Non-invasive detection of fibrotic NASH in NAFLD patients with low or intermediate FIB-4},
  series = {Journal of Clinical Medicine},
  volume    = {11},
  journal   = {Journal of Clinical Medicine},
  number    = {15},
  issn      = {2077-0383},
  doi       = {10.3390/jcm11154394},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-281824},
  year      = {2022},
  abstract  = {Background: Non-alcoholic steatohepatitis (NASH) and fibrosis are the main prognostic factors in non-alcoholic fatty liver disease (NAFLD). The FIB-4 score has been suggested as an initial test for the exclusion of progressed fibrosis. However, increasing evidence suggests that also NASH patients with earlier fibrosis stages are at risk of disease progression, emphasizing the need for improved non-invasive risk stratification. Methods: We evaluated whether the apoptosis biomarker M30 can identify patients with fibrotic NASH despite low or intermediate FIB-4 values. Serum M30 levels were assessed by ELISA, and FIB-4 was calculated in an exploration (n = 103) and validation (n = 100) cohort of patients with histologically confirmed NAFLD. Results: The majority of patients with low FIB-4 (cut-off value < 1.3) in the exploration cohort revealed increased M30 levels (>200 U/L) and more than 80\% of them had NASH, mostly with fibrosis. NASH was also detected in all patients with intermediate FIB-4 (1.3 to 2.67) and elevated M30, from which ~80\% showed fibrosis. Importantly, in the absence of elevated M30, most patients with FIB-4 < 1.3 and NASH showed also no fibrosis. Similar results were obtained in the validation cohort. Conclusions: The combination of FIB-4 with M30 enables a more reliable identification of patients at risk for progressed NAFLD and might, therefore, improve patient stratification.},
  language  = {en}
}