Volker Ellenrieder

Summary

Affiliation: University of Ulm
Country: Germany

Publications

  1. ncbi request reprint The tumor suppressor KLF11 mediates a novel mechanism in transforming growth factor beta-induced growth inhibition that is inactivated in pancreatic cancer
    Anita Buck
    Department of Internal Medicine I, University of Ulm, Germany
    Mol Cancer Res 4:861-72. 2006
  2. ncbi request reprint TGFbeta-regulated transcriptional mechanisms in cancer
    Volker Ellenrieder
    Department of Internal Medicine I, University of Ulm, Ulm, Germany
    Int J Gastrointest Cancer 31:61-9. 2002
  3. ncbi request reprint KLF11 mediates a critical mechanism in TGF-beta signaling that is inactivated by Erk-MAPK in pancreatic cancer cells
    Volker Ellenrieder
    Department of Internal Medicine, University of Ulm, Germany
    Gastroenterology 127:607-20. 2004
  4. ncbi request reprint Sp1 is required for transforming growth factor-beta-induced mesenchymal transition and migration in pancreatic cancer cells
    Kerstin Jungert
    Department of Gastroenterology, University of Ulm, 35043 Ulm, Germany
    Cancer Res 67:1563-70. 2007
  5. ncbi request reprint Smad-Sp1 complexes mediate TGFbeta-induced early transcription of oncogenic Smad7 in pancreatic cancer cells
    Kerstin Jungert
    Department of Gastroenterology, University of Ulm, 89081 Ulm, Germany
    Carcinogenesis 27:2392-401. 2006
  6. ncbi request reprint Expression profiling of the influence of RAS mutants on the TGFB1-induced phenotype of the pancreatic cancer cell line PANC-1
    Heiko Fensterer
    Department of Internal Medicine I, University of Ulm, Germany
    Genes Chromosomes Cancer 39:224-35. 2004
  7. doi request reprint Inflammation, regeneration, and transformation in the pancreas: results of the Collaborative Research Center 518 (SFB 518) at the University of Ulm
    Klaudia Giehl
    Department of Internal Medicine I, Center for Internal Medicine, University of Ulm, Germany
    Pancreas 40:489-502. 2011
  8. ncbi request reprint Transcriptome analysis of human hepatic and pancreatic stellate cells: organ-specific variations of a common transcriptional phenotype
    Malte Buchholz
    Department of Internal Medicine I, University Hospital of Ulm, Germany
    J Mol Med (Berl) 83:795-805. 2005
  9. doi request reprint Lef-1 isoforms regulate different target genes and reduce cellular adhesion
    Sarah Jesse
    Department of Internal Medicine I, University of Ulm, D 89081 Ulm, Germany
    Int J Cancer 126:1109-20. 2010
  10. pmc Overexpression of c-myc in pancreatic cancer caused by ectopic activation of NFATc1 and the Ca2+/calcineurin signaling pathway
    Malte Buchholz
    Translational Genome Research Group, Department of Internal Medicine I, University of Ulm, Ulm, Germany
    EMBO J 25:3714-24. 2006

Collaborators

Detail Information

Publications15

  1. ncbi request reprint The tumor suppressor KLF11 mediates a novel mechanism in transforming growth factor beta-induced growth inhibition that is inactivated in pancreatic cancer
    Anita Buck
    Department of Internal Medicine I, University of Ulm, Germany
    Mol Cancer Res 4:861-72. 2006
    ....
  2. ncbi request reprint TGFbeta-regulated transcriptional mechanisms in cancer
    Volker Ellenrieder
    Department of Internal Medicine I, University of Ulm, Ulm, Germany
    Int J Gastrointest Cancer 31:61-9. 2002
    ..New insights into transcriptional mechanisms activated by TGFbeta are providing a better understanding of the cellular changes involved in the switch of TGFbeta from a tumor suppressor to a tumor promotor...
  3. ncbi request reprint KLF11 mediates a critical mechanism in TGF-beta signaling that is inactivated by Erk-MAPK in pancreatic cancer cells
    Volker Ellenrieder
    Department of Internal Medicine, University of Ulm, Germany
    Gastroenterology 127:607-20. 2004
    ..Here, we investigated the functional implications of KLF11 in TGF-beta signaling and transcription in normal epithelial as well as pancreatic cancer cells...
  4. ncbi request reprint Sp1 is required for transforming growth factor-beta-induced mesenchymal transition and migration in pancreatic cancer cells
    Kerstin Jungert
    Department of Gastroenterology, University of Ulm, 35043 Ulm, Germany
    Cancer Res 67:1563-70. 2007
    ..It suggests that Sp1, via transcriptional induction of vimentin, cooperates with activated Smad complexes in mesenchymal transition and migration of pancreatic cancer cells upon TGF-beta stimulation...
  5. ncbi request reprint Smad-Sp1 complexes mediate TGFbeta-induced early transcription of oncogenic Smad7 in pancreatic cancer cells
    Kerstin Jungert
    Department of Gastroenterology, University of Ulm, 89081 Ulm, Germany
    Carcinogenesis 27:2392-401. 2006
    ..We thus conclude that Sp1 strongly contributes to the aberrant transcriptional response of transformed epithelial cells to TGFbeta stimulation...
  6. ncbi request reprint Expression profiling of the influence of RAS mutants on the TGFB1-induced phenotype of the pancreatic cancer cell line PANC-1
    Heiko Fensterer
    Department of Internal Medicine I, University of Ulm, Germany
    Genes Chromosomes Cancer 39:224-35. 2004
    ....
  7. doi request reprint Inflammation, regeneration, and transformation in the pancreas: results of the Collaborative Research Center 518 (SFB 518) at the University of Ulm
    Klaudia Giehl
    Department of Internal Medicine I, Center for Internal Medicine, University of Ulm, Germany
    Pancreas 40:489-502. 2011
    ....
  8. ncbi request reprint Transcriptome analysis of human hepatic and pancreatic stellate cells: organ-specific variations of a common transcriptional phenotype
    Malte Buchholz
    Department of Internal Medicine I, University Hospital of Ulm, Germany
    J Mol Med (Berl) 83:795-805. 2005
    ..Despite this high degree of similarity, distinct differences in expression patterns were observed between HSCs and PSCs, reflecting organ-specific variations of the common stellate cell-specific phenotype...
  9. doi request reprint Lef-1 isoforms regulate different target genes and reduce cellular adhesion
    Sarah Jesse
    Department of Internal Medicine I, University of Ulm, D 89081 Ulm, Germany
    Int J Cancer 126:1109-20. 2010
    ..Our findings indicate that expression of alternatively spliced Lef-1 isoforms is involved in the determination of proliferative or migratory characteristics of pancreatic carcinoma cells...
  10. pmc Overexpression of c-myc in pancreatic cancer caused by ectopic activation of NFATc1 and the Ca2+/calcineurin signaling pathway
    Malte Buchholz
    Translational Genome Research Group, Department of Internal Medicine I, University of Ulm, Ulm, Germany
    EMBO J 25:3714-24. 2006
    ..Together, these results demonstrate that ectopic activation of NFATc1 and the Ca2+/calcineurin signaling pathway is an important mechanism of oncogenic c-myc activation in pancreatic cancer...
  11. ncbi request reprint Pancreatic stellate cells potentiate proinvasive effects of SERPINE2 expression in pancreatic cancer xenograft tumors
    Albrecht Neesse
    Department of Internal Medicine I, University Hospital of Ulm, Ulm, Germany
    Pancreatology 7:380-5. 2007
    ..Our data thus suggest that SERPINE2 is an important modulator of tumor cell/host interactions in pancreatic cancer...
  12. ncbi request reprint TGFbeta regulated gene expression by Smads and Sp1/KLF-like transcription factors in cancer
    Volker Ellenrieder
    Signal Transduction Laboratory, Internal Medicine, Department of Gastroenterology and Endocrinology, University of Marburg, Marburg, Germany
    Anticancer Res 28:1531-9. 2008
    ..In this article, the current knowledge on the peculiar roles of Sp1/KLF-like proteins in Smad dependent and -independent gene regulation initiated by TGFbeta, are summarized...
  13. pmc An mSin3A interaction domain links the transcriptional activity of KLF11 with its role in growth regulation
    Martin E Fernandez-Zapico
    Gastroenterology Research Unit, Saint Mary s Hospital, Mayo Clinic, Rochester, MN 55905, USA
    EMBO J 22:4748-58. 2003
    ..These results demonstrate that SID-containing KLF repressor proteins can inhibit cell growth and neoplastic transformation, and outline for the first time cellular and molecular mechanisms by which these functions may be achieved...
  14. pmc Signaling disrupts mSin3A binding to the Mad1-like Sin3-interacting domain of TIEG2, an Sp1-like repressor
    Volker Ellenrieder
    Gastroenterology Research Unit, Mayo Clinic, Rochester, MN 55905, USA
    EMBO J 21:2451-60. 2002
    ....
  15. ncbi request reprint An emerging role for Ca2+/calcineurin/NFAT signaling in cancerogenesis
    Malte Buchholz
    Department of Gastroenterology, University of Marburg, Marburg, Hessen, Germany
    Cell Cycle 6:16-9. 2007
    ....