UMMS Affiliation

Department of Molecular, Cell and Cancer Biology

Publication Date

2018-08-03

Document Type

Editorial

Disciplines

Amino Acids, Peptides, and Proteins | Cell Biology | Cells | Cellular and Molecular Physiology | Enzymes and Coenzymes

Abstract

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].

Keywords

apoptosis-induced proliferation, undead cells, caspase, Myo1D, plasma membrane

Rights and Permissions

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.

DOI of Published Version

10.18632/oncotarget.25796

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

Journal/Book/Conference Title

Oncotarget

Related Resources

Link to Article in PubMed

PubMed ID

30167077

Creative Commons License

Creative Commons Attribution 3.0 License
This work is licensed under a Creative Commons Attribution 3.0 License.

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