| Home > Publications Database > Assembly and regulation of ASC specks. |
| Journal Article (Review Article) | DZNE-2020-05473 |
; ;
2017
Springer International Publishing AG
Cham (ZG)
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Please use a persistent id in citations: doi:10.1007/s00018-016-2396-6
Abstract: The inflammasome adapter ASC links activated inflammasome sensors to the effector molecule pro-caspase-1. Recruitment of pro-caspase-1 to ASC promotes the autocatalytic activation of caspase-1, which leads to the release of pro-inflammatory cytokines, such as IL-1β. Upon triggering of inflammasome sensors, ASC assembles into large helical fibrils that interact with each other serving as a supramolecular signaling platform termed the ASC speck. Alternative splicing, post-translational modifications of ASC, as well as interaction with other proteins can perturb ASC function. In several inflammatory diseases, ASC specks can be found in the extracellular space and its presence correlates with poor prognosis. Here, we review the role of ASC in inflammation, and focus on the structural mechanisms that lead to ASC speck formation, the regulation of ASC function during inflammasome assembly, and the importance of ASC specks in disease.
Keyword(s): Apoptosis Regulatory Proteins: chemistry (MeSH) ; Apoptosis Regulatory Proteins: genetics (MeSH) ; Apoptosis Regulatory Proteins: metabolism (MeSH) ; Carrier Proteins: metabolism (MeSH) ; Extracellular Matrix: metabolism (MeSH) ; Humans (MeSH) ; Inflammasomes: metabolism (MeSH) ; Inflammation: metabolism (MeSH) ; Inflammation: pathology (MeSH) ; Protein Isoforms: chemistry (MeSH) ; Protein Isoforms: genetics (MeSH) ; Protein Isoforms: metabolism (MeSH) ; Protein Multimerization (MeSH) ; Protein Processing, Post-Translational (MeSH) ; RNA Splicing (MeSH) ; Apoptosis Regulatory Proteins ; Carrier Proteins ; Inflammasomes ; LLID-114769 protein, human ; Protein Isoforms
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