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10.1038/s41467-017-00357-2

http://scihub22266oqcxt.onion/10.1038/s41467-017-00357-2
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suck abstract from ncbi


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pmid28874659
      Nat+Commun 2017 ; 8 (1 ): 443
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  • Internalized TSH receptors en route to the TGN induce local G(s)-protein signaling and gene transcription #MMPMID28874659
  • Godbole A ; Lyga S ; Lohse MJ ; Calebiro D
  • Nat Commun 2017[Sep]; 8 (1 ): 443 PMID28874659 show ga
  • A new paradigm of G-protein-coupled receptor (GPCR) signaling at intracellular sites has recently emerged, but the underlying mechanisms and functional consequences are insufficiently understood. Here, we show that upon internalization in thyroid cells, endogenous TSH receptors traffic retrogradely to the trans-Golgi network (TGN) and activate endogenous G(s)-proteins in the retromer-coated compartment that brings them to the TGN. Receptor internalization is associated with a late cAMP/protein kinase A (PKA) response at the Golgi/TGN. Blocking receptor internalization, inhibiting PKA II/interfering with its Golgi/TGN localization, silencing retromer or disrupting Golgi/TGN organization all impair efficient TSH-dependent cAMP response element binding protein (CREB) phosphorylation. These results suggest that retrograde trafficking to the TGN induces local G(s)-protein activation and cAMP/PKA signaling at a critical position near the nucleus, which appears required for efficient CREB phosphorylation and gene transcription. This provides a new mechanism to explain the functional consequences of GPCR signaling at intracellular sites and reveals a critical role for the TGN in GPCR signaling.Recent investigations suggest that G-protein-coupled receptors (GPCRs) can signal during intracellular trafficking. Here the authors use fluorescence microscopy approaches to directly visualize and investigate functional consequences of GPCR-mediated signaling at the Golgi/trans-Golgi network.
  • |*Signal Transduction [MESH]
  • |*Transcription, Genetic [MESH]
  • |Animals [MESH]
  • |Cells, Cultured [MESH]
  • |Cyclic AMP-Dependent Protein Kinases/metabolism [MESH]
  • |Endosomes/metabolism [MESH]
  • |GTP-Binding Protein alpha Subunits, Gs/*metabolism [MESH]
  • |Gene Expression Regulation [MESH]
  • |Gene Silencing [MESH]
  • |Golgi Apparatus/metabolism [MESH]
  • |HEK293 Cells [MESH]
  • |Humans [MESH]
  • |Mice [MESH]
  • |Mice, Transgenic [MESH]
  • |Phosphorylation [MESH]
  • |Protein Transport [MESH]
  • |RNA, Small Interfering [MESH]
  • |Receptors, G-Protein-Coupled/metabolism [MESH]
  • |Receptors, Thyrotropin/*metabolism [MESH]
  • |Thyroid Gland/metabolism [MESH]


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