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The suppression of Th1-like cytokines is likely mediated through suppression of IL-12 synthesis.
One important clinical consequence of UVB-induced inflammation is increased pain or hyperalgesia, which is likely mediated by enhanced sensitivity of cutaneous sensory neurons.
This effect is likely mediated through repression of the Myocd promoter.
The induction is likely mediated through the STRE elements, leading to more PrC secreted into medium.
This regulation is likely mediated through an as-yet-unidentified new ligand of GHS-R.
HLH-1 activity is likely mediated through direct binding to E-box sequences (CANNTG) in the promoter of target genes.
These results suggest that SYT-SSX2 colocalization with the Bmi1/Ring1B complex in polycomb bodies is likely mediated by its direct binding to Ring1B.
A rise in cAMP levels also induces Nocturnin expression, suggesting that Nocturnin's induction in eWAT by fasting is likely mediated through the same pathways that activate lipolysis.
These results demonstrated that the inhibition of TNF-activated IP-10 expression by L. casei is likely mediated through a cell surface protein.
The contribution of LeTx to anthrax pathogenesis is complex and is likely mediated through several different mechanisms and cell types [8].
The inhibitorial effect is likely mediated through a diffusible agent.
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