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- W2914838081 abstract "TRAFs [tumor necrosis factor (TNF) receptor associated factors] are a family of signaling molecules that function downstream of multiple receptor signaling pathways and play a pivotal role in the biology of innate, and adaptive immune cells. Following receptor ligation, TRAFs generally function as adapter proteins to mediate the activation of intracellular signaling cascades. With the exception of TRAF1 that lacks a Ring domain, TRAFs have an E3 ubiquitin ligase activity which also contributes to their ability to activate downstream signaling pathways. TRAF-mediated signaling pathways culminate in the activation of several transcription factors, including nuclear factor-κB (NF-κB), mitogen-activated protein kinases (MAPKs; e.g., ERK-1 and ERK-2, JNK, and p38), and interferon-regulatory factors (IRF; e.g., IRF3 and IRF7). The biological role of TRAFs is largely due to their ability to positively or negatively regulate canonical and non-canonical NF-κB signaling. While TRAF-mediated signaling regulates various immune cell functions, this review is focused on the recent advances in our knowledge regarding the molecular mechanisms through which TRAF proteins regulate, positively and negatively, inflammatory signaling pathways, including Toll-IL-1 receptors, RIG-I like receptors, and Nod-like receptors. The review also offers a perspective on the unanswered questions that need to be addressed to fully understand how TRAFs regulate inflammation." @default.
- W2914838081 created "2019-02-21" @default.
- W2914838081 creator A5003059628 @default.
- W2914838081 creator A5028764160 @default.
- W2914838081 creator A5056485484 @default.
- W2914838081 creator A5079277179 @default.
- W2914838081 date "2019-02-04" @default.
- W2914838081 modified "2023-10-17" @default.
- W2914838081 title "The Evolving Role of TRAFs in Mediating Inflammatory Responses" @default.
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- W2914838081 doi "https://doi.org/10.3389/fimmu.2019.00104" @default.
- W2914838081 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6369152" @default.
- W2914838081 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30778351" @default.
- W2914838081 hasPublicationYear "2019" @default.
- W2914838081 type Work @default.