Show simple item record

dc.contributor.authorSharma, Rohit B.
dc.contributor.authorSnyder, Jarin T.
dc.contributor.authorAlonso, Laura C.
dc.date2022-08-11T08:09:54.000
dc.date.accessioned2022-08-23T16:48:06Z
dc.date.available2022-08-23T16:48:06Z
dc.date.issued2019-09-01
dc.date.submitted2019-10-27
dc.identifier.citation<p>Mol Metab. 2019 Sep;27S:S69-S80. doi: 10.1016/j.molmet.2019.06.005. <a href="https://doi.org/10.1016/j.molmet.2019.06.005">Link to article on publisher's site</a></p>
dc.identifier.issn2212-8778 (Linking)
dc.identifier.doi10.1016/j.molmet.2019.06.005
dc.identifier.pmid31500833
dc.identifier.urihttp://hdl.handle.net/20.500.14038/41207
dc.description.abstractBACKGROUND: A growing body of literature suggests the cell-intrinsic activity of Atf6alpha during ER stress responses has implications for tissue cell number during growth and development, as well as in adult biology and tumorigenesis [1]. This concept is important, linking the cellular processes of secretory protein synthesis and endoplasmic reticulum stress response with functional tissue capacity and organ size. However, the field contains conflicting observations, especially notable in secretory cell types like the pancreatic beta cell. SCOPE OF REVIEW: Here we summarize current knowledge of the basic biology of Atf6alpha, along with the pleiotropic roles Atf6alpha plays in cell life and death decisions and possible explanations for conflicting observations. We include studies investigating the roles of Atf6alpha in cell survival, death and proliferation using well-controlled methodology and specific validated outcome measures, with a focus on endocrine and metabolic tissues when information was available. MAJOR CONCLUSIONS: The net outcome of Atf6alpha on cell survival and cell death depends on cell type and growth conditions, the presence and degree of ER stress, and the duration and intensity of Atf6alpha activation. It is unquestioned that Atf6alpha activity influences the cell fate decision between survival and death, although opposite directions of this outcome are reported in different contexts. Atf6alpha can also trigger cell cycle activity to expand tissue cell number through proliferation. Much work remains to be done to clarify the many gaps in understanding in this important emerging field.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=31500833&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsCopyright 2019 Published by Elsevier GmbH. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectActivating transcription factor 6
dc.subjectApoptosis
dc.subjectCell survival
dc.subjectPancreatic beta cell
dc.subjectReplication
dc.subjectAmino Acids, Peptides, and Proteins
dc.subjectBiological Phenomena, Cell Phenomena, and Immunity
dc.subjectCell Biology
dc.subjectCells
dc.subjectCellular and Molecular Physiology
dc.subjectMolecular Biology
dc.titleAtf6alpha impacts cell number by influencing survival, death and proliferation
dc.typeJournal Article
dc.source.journaltitleMolecular metabolism
dc.source.volume27S
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=5011&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/3994
dc.identifier.contextkey15631393
refterms.dateFOA2022-08-23T16:48:06Z
html.description.abstract<p>BACKGROUND: A growing body of literature suggests the cell-intrinsic activity of Atf6alpha during ER stress responses has implications for tissue cell number during growth and development, as well as in adult biology and tumorigenesis [1]. This concept is important, linking the cellular processes of secretory protein synthesis and endoplasmic reticulum stress response with functional tissue capacity and organ size. However, the field contains conflicting observations, especially notable in secretory cell types like the pancreatic beta cell.</p> <p>SCOPE OF REVIEW: Here we summarize current knowledge of the basic biology of Atf6alpha, along with the pleiotropic roles Atf6alpha plays in cell life and death decisions and possible explanations for conflicting observations. We include studies investigating the roles of Atf6alpha in cell survival, death and proliferation using well-controlled methodology and specific validated outcome measures, with a focus on endocrine and metabolic tissues when information was available.</p> <p>MAJOR CONCLUSIONS: The net outcome of Atf6alpha on cell survival and cell death depends on cell type and growth conditions, the presence and degree of ER stress, and the duration and intensity of Atf6alpha activation. It is unquestioned that Atf6alpha activity influences the cell fate decision between survival and death, although opposite directions of this outcome are reported in different contexts. Atf6alpha can also trigger cell cycle activity to expand tissue cell number through proliferation. Much work remains to be done to clarify the many gaps in understanding in this important emerging field.</p>
dc.identifier.submissionpathoapubs/3994
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.contributor.departmentDiabetes Center of Excellence, Department of Medicine
dc.source.pagesS69-S80


Files in this item

Thumbnail
Name:
Publisher version
Thumbnail
Name:
1_s2.0_S2212877819305666_main.pdf
Size:
1.102Mb
Format:
PDF

This item appears in the following Collection(s)

Show simple item record

Copyright 2019 Published by Elsevier GmbH. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Except where otherwise noted, this item's license is described as Copyright 2019 Published by Elsevier GmbH. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).