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Two major Ca 2+ entry pathways are important for NO production: store-operated Ca 2+ entry (SOCE), the main agonist-induced Ca 2+ entry mechanism in ECs (Tran, 2020), and mechanosensitive Ca 2+ entry, stimulated by blood shear stress
Directly activating GIPR in hepatocytes is an unlikely explanation for the decrease in apoC-III levels with tirzepatide [91, 92]
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Glucagon-Like Peptide 1 Modulates Calcium Responses to Glutamate and Membrane Depolarization in Hippocampal Neurons
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