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We now demonstrate that GIPR agonist administration critically relies on Gipr expression in the hindbrain, while GIPR antagonism relies on hypothalamic Gipr expressionboth are probably neuronal populations, given that we used hSyn-driven Cre-expression for the region-specific knockout studies

Reslizumab for poorly controlled, eosinophilic asthma: a randomized, placebo-controlled study

Amino acids license kinase mTORC1 activity and treg cell function via small G proteins rag and rheb

4 mL chloroform:methanol (1:1, v/v) was added to each sample and the lipid extraction was performed as described 20,21

Different mechanisms, overlapping tissue endpoints hence the frequent combination in research protocols