BioAcyl Corp

WIKINDX Resources

Kimura, T., Jain, A., & Choi, S. W. (2015). TRIM-mediated precision autophagy targets cytoplasmic regulators of innate immunity. Journal of Cell Biology, 210(6), 973–989. 
Added by: Dr. Enrique Feoli (01/07/2023, 15:17)   Last edited by: Dr. Enrique Feoli (01/07/2023, 15:18)
Resource type: Journal Article
DOI: 10.1083/jcb.201503023
ID no. (ISBN etc.): 0021-9525
BibTeX citation key: Kimura2015
View all bibliographic details
Categories: BioAcyl Corp
Subcategories: Inflammasones
Creators: Choi, Jain, Kimura
Collection: Journal of Cell Biology
Views: 3/94
Abstract
{The present paradigms of selective autophagy in mammalian cells cannot fully explain the specificity and selectivity of autophagic degradation. In this paper, we report that a subset of tripartite motif (TRIM) proteins act as specialized receptors for highly specific autophagy (precision autophagy) of key components of the inflammasome and type I interferon response systems. TRIM20 targets the inflammasome components, including NLRP3, NLRP1, and pro–caspase 1, for autophagic degradation, whereas TRIM21 targets IRF3. TRIM20 and TRIM21 directly bind their respective cargo and recruit autophagic machinery to execute degradation. The autophagic function of TRIM20 is affected by mutations associated with familial Mediterranean fever. These findings broaden the concept of TRIMs acting as autophagic receptor regulators executing precision autophagy of specific cytoplasmic targets. In the case of TRIM20 and TRIM21, precision autophagy controls the hub signaling machineries and key factors, inflammasome and type I interferon, directing cardinal innate immunity response systems in humans.}
  
WIKINDX 6.12.1 | Total resources: 1703 | Username: -- | Bibliography: WIKINDX Master Bibliography | Style: American Psychological Association (APA) | Time Zone: America/Costa_Rica (-06:00)