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KCNMA1 activates MYD88. 4 / 4
| 4

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"We found that SLO WT and PFO induced shedding of MyD88, but not Trif (Fig. 5A, Supplementary Fig. S1)."

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"SLO, binding to TLR4, activates the TRIF- and MyD88 dependent signalling pathway, which by inducing p38 MAPK activation, provokes the phosphorylation of cPLA 2, which in turn provides the arachidonic acid to be oxidized by 5-LO, thereby activating the cascade leading to CysLTs production."

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"In conclusion, we hypothesise that GAS sub-acute chronic colonisation of tonsils may contribute to tonsillar hyperplasia via a SLO dependent TLR4 mediated, TRIF and MyD88 dependent p 38MAPK pathway which activates CysLTs production, and that this mechanism, although still requiring evidence of cause-effect relationship, could possibly be associated with paediatric OSAS disease."

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"In conclusion, we hypothesise that GAS sub-acute chronic colonisation of tonsils may contribute to tonsillar hyperplasia via a SLO dependent TLR4 mediated, TRIF and MyD88 dependent p 38MAPK pathway which activates CysLTs production, and that this mechanism could be associated with paediatric OSAS disease."