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JAMA Netw

Apr 15 2004;19(8):861-70

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Interestingly, increased STAT3 signaling exerts a negative feedback response to the function of the JAK-STAT3 signaling pathways, i.e., STAT3 factor induces the expression of SOCS proteins which can interact with and inhibit the function of cytokine receptors and insulin/IGF-1 receptors (Figs

This conversion process is remarkably efficient when selenium status is optimal, with approximately 80% of circulating T3 produced through peripheral deiodination rather than direct thyroid secretion

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