Authors
Bergmann, AndreasUMass Chan Affiliations
Department of Molecular, Cell and Cancer BiologyDocument Type
EditorialPublication Date
2018-08-03Keywords
apoptosis-induced proliferationundead cells
caspase
Myo1D
plasma membrane
Amino Acids, Peptides, and Proteins
Cell Biology
Cells
Cellular and Molecular Physiology
Enzymes and Coenzymes
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Show full item recordAbstract
Critical mediators of apoptotic cell death are caspases, a highly specialized class of Cys-proteases that cleave substrates after Asp residues. Under normal conditions, caspases are cytosolic proteins. After their activation, they cleave a large number of cytosolic proteins and execute apoptosis (Figure 1, left). However, in addition to their well-studied role in apoptosis, caspases also have many non-apoptotic functions [1, 2]. It is not very well understood how cells escape the potential harmful action of caspases when they perform nonapoptotic functions. In our recent work, we now show that epithelial cells may prevent apoptosis by sequestration of caspases at the plasma membrane, specifically the basal side of the plasma membrane, for non-apoptotic functions [3].Source
Oncotarget. 2018 Aug 3;9(60):31566-31567. doi: 10.18632/oncotarget.25796. eCollection 2018 Aug 3. Link to article on publisher's site
DOI
10.18632/oncotarget.25796Permanent Link to this Item
http://hdl.handle.net/20.500.14038/40757PubMed ID
30167077Related Resources
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Copyright: Bergmann et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.Distribution License
http://creativecommons.org/licenses/by/3.0/ae974a485f413a2113503eed53cd6c53
10.18632/oncotarget.25796
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Except where otherwise noted, this item's license is described as Copyright: Bergmann et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.