Chemical inhibition of p38 and MK2, and siRNA knockdown of MK2 relieved dsRNA-triggered prolongation of IFN-β mRNA half-life. Taken together, these results suggest that TLR3 induces signaling mechanisms involving TRIF, p38 MAPK and MK2 to enhance stabilization of IFN-β mRNA contributing to enhanced IFN-β levels during pathogen infections.

Phosphoinositide 3-kinase (PI3K), p38-mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK) are also activated by TLR3 signaling (Schröder and Bowie, 2005).

2024年11月1日 · Pharmacologically targeting the TLR3/MAPK pathway to inhibit mast cell activation normalizes the proinflammatory microenvironment and alleviates lung inflammation and injury in the preclinical TRALI mouse model.

2004年12月15日 · In accordance with the expression of Toll-like receptor-3 (TLR3) and of TRIF/TICAM-1 adaptor, poly I:C stimulation induces the activation of interferon regulatory factor-3 (IRF-3) transcription factor and of p38 mitogen-activated …

TAK1，转化生长因子激酶1，是MAP3K家族的成员，它可以激活经典IκB激酶（IKK）复合物和促分裂原活化蛋白激酶的激酶（MKK），MKK激活p38 MAP激酶和c-Jun氨基末端激酶1和2（JNK1和JNK2）。 TLRs：Toll样受体，是PRRs（pathogen recognition receptors）的关键成员，可以识别PAMPs（pathogen-associated molecular patterns），是参与天然免疫的一类重要的跨膜非催化性蛋白质分子。 Toll样受体胞膜外区主…

2012年3月1日 · We wanted to determine if p38 MAPK and MK2 were activated downstream of TLR3/TRIF and contributed to stabilization of IFN-β mRNA. TLR3-HEK293 cells were treated with PIC for various time-points and analyzed by immunoblotting using antibodies specific to phosphorylated p38 MAPK and MK2.

2024年12月25日 · TLR3 (Toll Like Receptor 3) is a Protein Coding gene. Diseases associated with TLR3 include Immunodeficiency 83 Viral Infections and Human Immunodeficiency Virus Type 1. Among its related pathways are Toll Like Receptor 7/8 (TLR7/8) Cascade and Toll-Like receptor Signaling Pathways.

2013年2月6日 · Data demonstrated a consistent role for elements of the MAPK pathway (p38, MEK and JNK) in agonist-dependent regulation of cognate TLR mRNA levels. LPS consistently and significantly affected levels of mRNA encoding several different TLR (Figure 3). Thus, the effect of MAPK inhibition on LPS-induced TLR cross-regulation was assessed (Figure 5 ...

MyD88是TIR家族中第一个被发现的成员，除TLR3外，所有的TLR都普遍使用MyD88，它能激活转录因子NF-κB和丝裂原激活的蛋白激酶 (MAPK)来诱导炎性细胞因子。 相反，TRIF被TLR3和TLR4使用，并诱导不同的途径，导致转录因子IRF3和NF-κB的激活，从而诱导I型干扰素和炎性细胞因子的产生。 TRAM和TIRAP分别作为分选适配器将TRIF招募到TLR4，将MyD88招募到TLR2和TLR4。 因此，TLR信号通路可以很大程度上分为MyD88依赖的通路和TRIF依赖的通路，前者 …

Toll-like receptor 3 (TLR3) and TLR4 utilize adaptor proteins to activate mitogen‑activated protein kinase (MAPK), resulting in the acute but transient inflammatory response aimed at the clearance of pathogens. In the present study, it was demonstrated that macrophage activation by lipopolysaccharid …