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The aforementioned results indicated that in the ovaries, CXCL10 could bind to IL18R1 to activate downstream p-P65 IFN signaling, which subsequently promoted the transformation of macrophages into pro-inflammatory type I macrophages (Fig

It binds and activates GHRH receptors on pituitary somatotrophs, directly stimulating growth hormone synthesis and pulsatile release the same signaling axis as endogenous GHRH, but massively extended

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