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Mziaut, H.* ; Trajkovski, M.* ; Kersting, S.* ; Ehninger, A.* ; Altkrüger, A.* ; Lemaitre, R.P.* ; Schmidt, D.* ; Saeger, H.-D.* ; Lee, M.S.* ; Drechsel, D.N.* ; Müller, S.* ; Solimena, M.*

Synergy of glucose and growth hormone signalling in islet cells through ICA512 and STAT5.

Nat. Cell Biol. 8, 435-445 (2006)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Nutrients and growth hormones promote insulin production and the proliferation of pancreatic beta-cells. An imbalance between ever-increasing metabolic demands and insulin output causes diabetes. Recent evidence indicates that beta-cells enhance insulin gene expression depending on their secretory activity. This signalling pathway involves a catalytically inactive receptor tyrosine phosphatase, ICA512, whose cytoplasmic tail is cleaved on glucose-stimulated exocytosis of insulin secretory granules and then moves into the nucleus, where it upregulates insulin transcription. Here, we show that the cleaved cytosolic fragment of ICA512 enhances the transcription of secretory granule genes (including its own gene) by binding to tyrosine phosphorylated signal transducers and activators of transcription (STAT) 5 and preventing its dephosphorylation. Sumoylation of ICA512 by the E3 SUMO ligase PIASy, in turn, may reverse this process by decreasing the binding of ICA512 to STAT5. These findings illustrate how the exocytosis of secretory granules, through a retrograde pathway that sustains STAT activity, converges with growth hormone signalling to induce adaptive changes in beta-cells in response to metabolic demands.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Sprache englisch
Veröffentlichungsjahr 2006
HGF-Berichtsjahr 0
ISSN (print) / ISBN 1465-7392
e-ISSN 1476-4679
Zeitschrift Nature Cell Biology
Quellenangaben Band: 8, Heft: 5, Seiten: 435-445 Artikelnummer: , Supplement: ,
Verlag Nature Publishing Group
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Pancreatic Islet Research (IPI)
PubMed ID 16622421
DOI 10.1038/ncb1395
Erfassungsdatum 2006-12-31
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