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Wherein, the phosphorylation of the C-terminus by ERK1/2 recruits -arrestins to sterically hinder interactions with GPCR kinases, initiating endocytosis likely via the assembly of clathrin-coated pits [24, 33]

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In consequence, the virus-hijacked host cellular factors undergo HMRD, with altered or compromised function, which ultimately contributes to a plethora of organ/system impairments with detrimental effects on human metabolism

Persistent lipolytic effect of exogenous growth hormone during caloric restriction