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Intracellular Signaling from the Secretory Pathway

Call for Papers

Proteins that are destined to the extracellular space or to secretory pathway organelles are synthetized on endoplasmic reticulum (ER) associated ribosomes. ER resident chaperones, oxidoreductases, and modifying enzymes assist newly synthetized proteins in attaining their native structure. A strict quality control system ensures that only proteins that are correctly folded can leave the ER and proceed along the secretory pathway to reach their destination.

The secretory pathway has a key role in intercellular signaling, ensuring that functional receptors are displayed on the plasma membrane and active signaling molecules are timely secreted. Recently, however, several compartments of the endomembrane system have emerged as signaling hubs for intracellular communication, too. For example, the secretory pathway itself can gauge the load of cargo proteins to be folded/secreted and, via specific signaling cascades, adapt its capacity to this task. Moreover, the ER is the site of Ca2+ storage, and the ER-resident process of oxidative protein folding generates H2O2, a key signaling molecule in the cell. Post-ER organelles are also important signaling platforms: for example, lysosomes orchestrate the cellular response to nutrient conditions and regulate their own biogenesis. The ensemble of all of these interconnected reactions is central to cellular homeostasis, and alterations can result in severe pathologies.

We are thus interested in manuscripts (both original research papers and reviews), investigating the signaling pathways emanating from the endomembrane system. The implications of these signaling networks in the pathology and physiology of mammalian cells and organisms will be of particular interest for our readers.

Potential topics include, but are not limited to:

  • Unfolded protein response
  • Ca2+ signaling from the ER
  • KDEL-receptor signaling and golgi signaling
  • Secretory pathway redox homeostasis and H2O2 signaling
  • Signaling from endosomes
  • Lysosome biogenesis and mTORC1 activation

Authors can submit their manuscripts via the Manuscript Tracking System at http://mts.hindawi.com/submit/journals/bmri/physiology/ssp/.

Manuscript DueFriday, 27 February 2015
First Round of ReviewsFriday, 22 May 2015
Publication DateFriday, 17 July 2015

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