<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Fregno, Ilaria</dc:creator>
  <dc:creator>Molinari, Maurizio</dc:creator>
  <dc:date>2018-04-13</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">The endoplasmic reticulum (ER) is a highly dynamic organelle in eukaryotic cells. It is  deputed to lipid and protein biosynthesis, calcium storage, and the detoxification of various  exogenous and endogenous harmful compounds. ER activity and size must be adapted  rapidly to environmental and developmental conditions or biosynthetic demand. This is  achieved on induction of thoroughly studied transcriptional/translational programs defined as  “unfolded protein responses” that increase the ER volume and the expression of ER- resident proteins regulating the numerous ER functions. Less understood are the lysosomal  catabolic processes that maintain ER size at steady state, that prevent excessive ER  expansion during ER stresses, or that ensure return to physiologic ER size during recovery  from ER stresses. These catabolic processes may also be activated to remove ER  subdomains where proteasome-resistant misfolded proteins or damaged lipids have been  segregated. Insights into these catabolic mechanisms have only recently emerged with the  identification of so-called ER-phagy receptors, which label specific ER subdomains for  selective lysosomal delivery for clearance. Here, in eight chapters and one addendum, we  comment on recent advances in ER turnover pathways induced by ER stress, nutrient  deprivation, misfolded proteins, and live bacteria. We highlight the role of yeast (Atg39 and  Atg40) and mammalian (FAM134B, SEC62, RTN3, and CCPG1) ER-phagy receptors and of  autophagy genes in selective and non-selective catabolic processes that regulate cellular  proteostasis by controlling ER size, turnover, and function.</dc:description>
  <dc:format>application/pdf</dc:format>
  <dc:identifier>https://n2t.net/ark:/12658/srd1318937</dc:identifier>
  <dc:identifier>https://susi.usi.ch/global/documents/318937</dc:identifier>
  <dc:identifier>https://susi.usi.ch/documents/318937/files/Fregno_F1000R_2018.pdf</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.12688/f1000research.13968.1</dc:relation>
  <dc:relation>info:eu-repo/semantics/altIdentifier/ark/12658/srd1318937</dc:relation>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>CC BY</dc:rights>
  <dc:source>F1000Research. - 2018, vol. 7, p. 454</dc:source>
  <dc:subject xmlns:ns1="xml" ns1:lang="en">Autophagy and macroautophagy</dc:subject>
  <dc:subject xmlns:ns2="xml" ns2:lang="en">ER turnover</dc:subject>
  <dc:subject xmlns:ns3="xml" ns3:lang="en">ER-phagy and recovER-phagy receptors</dc:subject>
  <dc:subject xmlns:ns4="xml" ns4:lang="en">ER stress</dc:subject>
  <dc:subject xmlns:ns5="xml" ns5:lang="en">LC3-interacting region (LIR)</dc:subject>
  <dc:subject xmlns:ns6="xml" ns6:lang="en">Live bacteria</dc:subject>
  <dc:subject xmlns:ns7="xml" ns7:lang="en">Nutrient deprivation</dc:subject>
  <dc:subject xmlns:ns8="xml" ns8:lang="en">Proteostasis</dc:subject>
  <dc:subject>info:eu-repo/classification/udc/61</dc:subject>
  <dc:title xmlns:ns9="xml" ns9:lang="en">Endoplasmic reticulum turnover : ER-phagy and other flavors in selective and non-selective ER clearance</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>
