FGF2 and IL-1β - explorers of unconventional secretory pathways at a glance

Skip to Next Section - Fibroblast growth factor 2 (FGF2) and interleukin 1β (IL-1β) were among the earliest examples of a subclass of proteins with extracellular functions that were found to lack N-terminal secretory signal peptides and were shown to be secreted in an ER- and Golgi-independent manne...

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Bibliographic Details
Main Authors: Pallotta, Maria Teresa (Author) , Nickel, Walter (Author)
Format: Article (Journal)
Language:English
Published: November 5, 2020
In: Journal of cell science
Year: 2020, Volume: 133, Issue: 21, Pages: 1-7
ISSN:1477-9137
DOI:10.1242/jcs.250449
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1242/jcs.250449
Verlag, lizenzpflichtig, Volltext: https://jcs.biologists.org/content/133/21/jcs250449
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Author Notes:Maria Teresa Pallotta and Walter Nickel
Description
Summary:Skip to Next Section - Fibroblast growth factor 2 (FGF2) and interleukin 1β (IL-1β) were among the earliest examples of a subclass of proteins with extracellular functions that were found to lack N-terminal secretory signal peptides and were shown to be secreted in an ER- and Golgi-independent manner. Many years later, a number of alternative secretory pathways have been discovered, processes collectively termed unconventional protein secretion (UPS). In the course of these studies, unconventional secretion of FGF2 and IL-1β were found to be based upon distinct pathways, mechanisms and molecular machineries. Following a concise introduction into various pathways mediating unconventional secretion and transcellular spreading of proteins, this Cell Science at a Glance poster article aims at a focused analysis of recent key discoveries providing unprecedented detail about the molecular mechanisms and machineries driving FGF2 and IL-1β secretion. These findings are also highly relevant for other unconventionally secreted cargoes that, like FGF2 and IL1β, exert fundamental biological functions in biomedically relevant processes, such as tumor-induced angiogenesis and inflammation.
Item Description:Gesehen am 27.01.2021
Physical Description:Online Resource
ISSN:1477-9137
DOI:10.1242/jcs.250449