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Glycogen synthase kinase 3ß in Toll-like receptor signaling.
Ko, Ryeojin; Lee, Soo Young.
Afiliação
  • Ko R; Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 03760, Korea.
  • Lee SY; Department of Life Science and the Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 03760, Korea.
BMB Rep ; 49(6): 305-10, 2016 Jun.
Article em En | MEDLINE | ID: mdl-26996345
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 GSK3ß is a key regulator of inflammatory cytokine production in MyD88-mediated TLR signaling via TLR2 and TLR4. Recently, GSK3ß has also been implicated in the TRIF-dependent signaling pathway via TLR3. In this review, we describe current advances on the regulatory role of GSK3ß in immune responses associated with various TLRs. A better understanding of the role of GSK3ß in TLR signaling might lead to more effective anti-inflammatory interventions. [BMB Reports 2016; 49(6): 305-310].
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Transdução de Sinais / Receptores Toll-Like / Glicogênio Sintase Quinase 3 beta Limite: Animals / Humans Idioma: En Revista: BMB Rep Assunto da revista: BIOLOGIA MOLECULAR / BIOQUIMICA Ano de publicação: 2016 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Transdução de Sinais / Receptores Toll-Like / Glicogênio Sintase Quinase 3 beta Limite: Animals / Humans Idioma: En Revista: BMB Rep Assunto da revista: BIOLOGIA MOLECULAR / BIOQUIMICA Ano de publicação: 2016 Tipo de documento: Article