4.4 Review

Glycogen synthase kinase 3β in Toll-like receptor signaling

期刊

BMB REPORTS
卷 49, 期 6, 页码 305-310

出版社

KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
DOI: 10.5483/BMBRep.2016.49.6.059

关键词

Glycogen synthase kinase 3 beta (GSK3 beta); Inflammatory cytokines; Toll-like receptor (TLR); Type I interferons (IFNs)

资金

  1. Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Education [2015R1A6A3A0102 0489]
  2. Ministry of Science, ICT and Future Planning [2013R1A2A1A05005153, 2012R1A5A10 48236]
  3. National Research Foundation of Korea [2013R1A2A1A05005153] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

向作者/读者索取更多资源

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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