Protective effect of toll-interacting protein overexpression against paraquat-induced lung injury in mice and A549 cells through inhibiting oxidative stress inflammation and NF-kappaB signaling pathway.
our findings reveal that resting-state STING protein level is strictly regulated by a constant tug-of-war between 'stabilizer' TOLLIP and 'degrader' IRE1alpha-lysosome that together maintain tissue immune homeostasis
Tollip protects against neointima formation by negatively regulating vascular smooth muscle cell proliferation dedifferentiation and migration in an Akt-dependent manner.
IL-13-treated Tollip-knockout (KO) mice exihibt increased lung eosinophilic inflammation and eotaxin-2 levels. IL-13- treated Tollip KO macrophages in the absence and particularly in the presence of IL-33 increases expression of IL-33 receptor ST2L and CCL24 which is in part dependent on enhanced activation of interleukin (IL)-1 receptor-associated kinase 1 and signal transducer and activator of transcription 6.
Tollip deficiency selectively leads to enlarged yet stable atherosclerotic plaques increased circulating lipids liver steatosis and reduced inflammation. Compromised lipophagy and reduced expression of inflammatory mediators due to Tollip deficiency may be the underlying causes.
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