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Upon ligand binding, TR II phosphorylates and activates TR I, forming a heteromeric receptor complex that initiates downstream signaling through both SMAD-dependent and SMAD-independent pathways, such as ERK, p38, JNK, and PI3K-Akt cascades [33, 36, 39]

Now a growing number of researchers, payers and providers are exploring deliberate "deprescription," which aims to taper some patients off their medication after they have taken it for a certain amount of time or lost a certain amount of weight

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