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Biological Chemistry

Editor-in-Chief: Brüne, Bernhard

Editorial Board: Buchner, Johannes / Lei, Ming / Ludwig, Stephan / Sies, Helmut / Thomas, Douglas D. / Turk, Boris / Wittinghofer, Alfred

12 Issues per year


IMPACT FACTOR 2017: 3.022

CiteScore 2017: 2.81

SCImago Journal Rank (SJR) 2017: 1.562
Source Normalized Impact per Paper (SNIP) 2017: 0.705

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1437-4315
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Volume 390, Issue 12

Issues

EFEMP1 binds the EGF receptor and activates MAPK and Akt pathways in pancreatic carcinoma cells

Peter Camaj
  • Department of Surgery, Munich University Medical Center, Campus Großhadern, Marchioninistr. 15, D-81377 Munich, Germany
  • These authors contributed equally to this work.
  • Other articles by this author:
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/ Hendrik Seeliger
  • Department of Surgery, Munich University Medical Center, Campus Großhadern, Marchioninistr. 15, D-81377 Munich, Germany
  • These authors contributed equally to this work.
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  • De Gruyter OnlineGoogle Scholar
/ Ivan Ischenko
  • Department of Surgery, Munich University Medical Center, Campus Großhadern, Marchioninistr. 15, D-81377 Munich, Germany
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/ Stefan Krebs
  • Laboratory for Functional Genome Analysis (LAFUGA), Gene Center, Ludwig Maximilians University, D-81377 Munich, Germany
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/ Helmut Blum
  • Laboratory for Functional Genome Analysis (LAFUGA), Gene Center, Ludwig Maximilians University, D-81377 Munich, Germany
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/ Enrico N. De Toni
  • Department of Gastroenterology, Munich University Medical Center, Campus Großhadern, Marchioninistr. 15, D-81377 Munich, Germany
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/ Dagmar Faktorova
  • Department of Measurement and Applied Electrical Engineering, University of Zilina, SK-01026 Zilina, Slovak Republic
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/ Karl-Walter Jauch
  • Department of Surgery, Munich University Medical Center, Campus Großhadern, Marchioninistr. 15, D-81377 Munich, Germany
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/ Christiane J. Bruns
  • Department of Surgery, Munich University Medical Center, Campus Großhadern, Marchioninistr. 15, D-81377 Munich, Germany
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Published Online: 2009-10-06 | DOI: https://doi.org/10.1515/BC.2009.140

Abstract

The EGF-related protein EFEMP1 (EGF-containing fibulin-like extracellular matrix protein 1) has been shown to promote tumor growth in human adenocarcinoma. To understand the mechanism of this action, the signal transduction activated upon treatment with this protein has been investigated. We show that EFEMP1 binds EGF receptor (EGFR) in a competitive manner relative to epidermal growth factor (EGF), implicating that EFEMP1 and EGF share the same or adjacent binding sites on the EGFR. Treatment of pancreatic carcinoma cells with purified EFEMP1 activates autophosphorylation of EGFR at the positions Tyr-992 and Tyr-1068, but not at the position Tyr-1048. This signal is further transduced to phosphorylation of Akt at position Thr-308 and p44/p42 MAPK (mitogen-activated protein kinase) at positions Thr-202 and Tyr-204. These downstream phosphorylation events can be inhibited by treatment with the EGFR kinase inhibitor PD 153035. The observed signal transduction upon treatment with EFEMP1 can contribute to the enhancement of tumor growth shown in pancreatic carcinoma cells overexpressing EFEMP1.

Keywords: downstream signaling; EFEMP1; EGF receptor (EGFR); epidermal growth factor (EGF); phosphorylation

About the article

Corresponding author


Received: 2009-05-08

Accepted: 2009-08-08

Published Online: 2009-10-06

Published in Print: 2009-12-01


Citation Information: Biological Chemistry, Volume 390, Issue 12, Pages 1293–1302, ISSN (Online) 1437-4315, ISSN (Print) 1431-6730, DOI: https://doi.org/10.1515/BC.2009.140.

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