PMID- 9918122
OWN - NLM
STAT- MEDLINE
DCOM- 19990614
LR  - 20191102
IS  - 1359-6101 (Print)
IS  - 1359-6101 (Linking)
VI  - 9
IP  - 3-4
DP  - 1998 Sep-Dec
TI  - The interleukin 1 receptor: ligand interactions and signal transduction.
PG  - 221-37
AB  - The interleukin 1 (IL-1) receptor is a critical component in mediating the 
      inflammatory responses of IL-1, which affect nearly every cell type. Recently, 
      major inroads have been made toward understanding the mechanism by which IL-1 
      interacts with its receptor and activates signal transduction. The 
      receptor-ligand association has been visualized by X-ray crystal structure 
      analysis, revealing intimate details that distinguish IL-1beta from the 
      naturally-occuring receptor antagonist. Signaling studies have focused primarily 
      on the ability of IL-1 to transduce the activation of the transcription factor, 
      NF-kappaB, which is of central importance to inflammatory and immune responses. 
      Virtually all of the effort has targeted the activation of a kinase which results 
      in the phosphorylation of the inhibitory IkappaB molecule at two serines that 
      precedes the proteolytic degradation of this inhibitor and the release of active 
      NF-kappaB. The recent characterization of an IL-1 receptor associated kinase 
      (IRAK) and a continuous molecular path between this kinase and that which 
      directly phosphorylates IkappaB would seem to all but close the basic 
      understanding of IL-1 receptor signal transduction. However, at least half of the 
      IL-1-dependent NF-kappaB activation is independent of IRAK and uses a novel 
      pathway involving the recruitment of phosphatidylinositol 3-kinase (PI3K) to a 
      distinct site within the cytoplasmic domain of the IL-1 receptor. This novel 
      pathway for NF-kappaB activation and the fact that other important transcription 
      factors are also activated by an IL-1 receptor-dependent signal event, clearly 
      defines additional mechanisms that influence inflammation.
FAU - Auron, P E
AU  - Auron PE
AD  - Department of Pathology, Harvard Medical School, Harvard Institutes of Medicine, 
      Boston, MA 02115, USA. auron@cbrsgi.med.harvard.edu
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Cytokine Growth Factor Rev
JT  - Cytokine & growth factor reviews
JID - 9612306
RN  - 0 (Ligands)
RN  - 0 (Receptors, Interleukin-1)
SB  - IM
MH  - Animals
MH  - Humans
MH  - Ligands
MH  - Models, Molecular
MH  - Protein Binding/immunology
MH  - Receptors, Interleukin-1/metabolism/*physiology
MH  - Signal Transduction/*immunology
RF  - 91
EDAT- 1999/01/26 00:00
MHDA- 1999/01/26 00:01
CRDT- 1999/01/26 00:00
PHST- 1999/01/26 00:00 [pubmed]
PHST- 1999/01/26 00:01 [medline]
PHST- 1999/01/26 00:00 [entrez]
AID - S1359-6101(98)00018-5 [pii]
AID - 10.1016/s1359-6101(98)00018-5 [doi]
PST - ppublish
SO  - Cytokine Growth Factor Rev. 1998 Sep-Dec;9(3-4):221-37. doi: 
      10.1016/s1359-6101(98)00018-5.