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Agreeably, we could only detect a non-significant tendency for reduced -arrestin 2 recruitment in our triple AA phospho-null mutant receptor despite significantly reduced internalisation in response to GLP-1 stimulation, with this effect more likely ascribed to the observed reduction in GRK2 recruitment, in agreement with a previous report highlighting GRK expression as required for GLP-1R internalisation (4)
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These medications undergo rigorous clinical trials demonstrating efficacy and safety before receiving MHRA approval
It promotes neuron survival by activating anti-apoptotic pathways through its TrkB receptor
