Glycogen synthase kinase 3 beta in Toll-like receptor signaling
- 주제(키워드) Glycogen synthase kinase 3 beta (GSK3 beta) , Inflammatory cytokines , Toll-like receptor (TLR) , Type I interferons (IFNs)
- 등재 SCIE, SCOPUS, KCI등재
- 발행기관 KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
- 발행년도 2016
- 총서유형 Journal
- URI http://www.dcollection.net/handler/ewha/000000140181
- 본문언어 영어
- Published As http://dx.doi.org/10.5483/BMBRep.2016.49.6.059
- 저작권 이화여자대학교 논문은 저작권에 의해 보호받습니다.
초록/요약
Toll-like receptors (TLRs) play a critical role in the innate immune response against pathogens. Each TLR recognizes specific pathogen-associated molecular patterns, after which they activate the adaptor protein MyD88 or TRIF-assembled signaling complex to produce immune mediators, including inflammatory cytokines and type I IFNs. Although the activation of TLR is important for host defense, its uncontrolled activation can damage the host. During the past decade, numerous studies have demonstrated that GSK3 beta is a key regulator of inflammatory cytokine production in MyD88-mediated TLR signaling via TLR2 and TLR4. Recently, GSK3 beta has also been implicated in the TRIF-dependent signaling pathway via TLR3. In this review, we describe current advances on the regulatory role of GSK3 beta in immune responses associated with various TLRs. A better understanding of the role of GSK3 beta. in TLR signaling might lead to more effective anti-inflammatory interventions.
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