Tuyển tập các báo cáo nghiên cứu về sinh học được đăng trên tạp chí sinh học Journal of Biology đề tài: Imp-L2, a putative homolog of vertebrate IGF-binding protein 7, counteracts insulin signaling in Drosophila and is essential for starvation resistance. | Journal of Biology BioMed Central Research article Open Access Imp-L2 a putative homolog of vertebrate IGF-binding protein 7 counteracts insulin signaling in Drosophila and is essential for starvation resistance Basil Honegger Milos Galic Katja Kohler1 Franz Wittwer Walter Brogiolo Ernst Hafen1 and Hugo Stocker1 Addresses Zoological Institute University of Zurich Winterthurerstrasse 190 CH-8057 Zurich Switzerland. institute for Molecular Systems Biology IMSB ETH Zurich Wolfgang-Pauli-Strasse 16 CH-8093 Zurich Switzerland. Current address Chemical and Systems Biology 318 Campus Drive Clark Building W200 Stanford University Medical Center Stanford CA 94305-5174 USA. Correspondence Ernst Hafen. Email hafen@ Published 15 April 2008 Received 21 July 2007 Journal of Biology 2008 7 10 doi jbiol72 Revỉsed ruaR 008 J gy v jy Accepted 13 March 2008 The electronic version of this article is the complete one and can be found online at http content 7 3 10 2008 Honegger et al. licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Insulin and insulin-like growth factors IGFs signal through a highly conserved pathway and control growth and metabolism in both vertebrates and invertebrates. In mammals insulin-like growth factor binding proteins IGFBPs bind IGFs with high affinity and modulate their mitogenic anti-apoptotic and metabolic actions but no functional homologs have been identified in invertebrates so far. Results Here we show that the secreted Imaginal morphogenesis protein-Late 2 Imp-L2 binds Drosophila insulin-like peptide 2 Dilp2 and inhibits growth non-autonomously. Whereas overexpressing Imp-L2 strongly reduces size loss of Imp-L2 function results in an increased body size.
