PMID- 36865541
OWN - NLM
STAT- MEDLINE
DCOM- 20230306
LR  - 20230328
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 14
DP  - 2023
TI  - Regulation of innate immune signaling by IRAK proteins.
PG  - 1133354
LID - 10.3389/fimmu.2023.1133354 [doi]
LID - 1133354
AB  - The Toll-like receptors (TLRs) and interleukin-1 receptors (IL-1R) families are 
      of paramount importance in coordinating the early immune response to pathogens. 
      Signaling via most TLRs and IL-1Rs is mediated by the protein myeloid 
      differentiation primary-response protein 88 (MyD88). This signaling adaptor forms 
      the scaffold of the myddosome, a molecular platform that employs IL-1R-associated 
      kinase (IRAK) proteins as main players for transducing signals. These kinases are 
      essential in controlling gene transcription by regulating myddosome assembly, 
      stability, activity and disassembly. Additionally, IRAKs play key roles in other 
      biologically relevant responses such as inflammasome formation and 
      immunometabolism. Here, we summarize some of the key aspects of IRAK biology in 
      innate immunity.
CI  - Copyright (c) 2023 Pereira and Gazzinelli.
FAU - Pereira, Milton
AU  - Pereira M
AD  - Division of Infectious Diseases and Immunology, Department of Medicine, 
      University of Massachusetts Chan Medical School, Worcester, MA, United States.
FAU - Gazzinelli, Ricardo T
AU  - Gazzinelli RT
AD  - Division of Infectious Diseases and Immunology, Department of Medicine, 
      University of Massachusetts Chan Medical School, Worcester, MA, United States.
AD  - Centro de Tecnologia de Vacinas, Universidade Federal de Minas Gerais, Belo 
      Horizonte, MG, Brazil.
AD  - Instituto Rene Rachou, Fundacao Oswaldo Cruz, Belo Horizonte, MG, Brazil.
AD  - Plataforma de Medicina Translacional, Fundacao Oswaldo Cruz, Ribeirao Preto, SP, 
      Brazil.
LA  - eng
GR  - R01 NS098747/NS/NINDS NIH HHS/United States
GR  - R01 AI079293/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20230214
PL  - Switzerland
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (Inflammasomes)
RN  - EC 2.7.11.1 (Interleukin-1 Receptor-Associated Kinases)
SB  - IM
MH  - Humans
MH  - *Signal Transduction
MH  - *Adaptor Proteins, Signal Transducing
MH  - Immunity, Innate
MH  - Inflammasomes
MH  - Interleukin-1 Receptor-Associated Kinases
PMC - PMC9972678
OTO - NOTNLM
OT  - IL-1R
OT  - IRAK
OT  - TLR
OT  - cell signaling
OT  - inflammation
OT  - innate immunity
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2023/03/04 06:00
MHDA- 2023/03/07 06:00
PMCR- 2023/01/01
CRDT- 2023/03/03 02:32
PHST- 2022/12/28 00:00 [received]
PHST- 2023/01/30 00:00 [accepted]
PHST- 2023/03/03 02:32 [entrez]
PHST- 2023/03/04 06:00 [pubmed]
PHST- 2023/03/07 06:00 [medline]
PHST- 2023/01/01 00:00 [pmc-release]
AID - 10.3389/fimmu.2023.1133354 [doi]
PST - epublish
SO  - Front Immunol. 2023 Feb 14;14:1133354. doi: 10.3389/fimmu.2023.1133354. 
      eCollection 2023.