In this work, we investigate the molecular mechanisms by which GLP-1, oxyntomodulin, exendin-4, and exendin-P5 bind and activate the GLP-1R using a combination of structural biology, molecular dynamics simulations, and pharmacological studies combined with extensive receptor mutagenesis
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Treatment consists of replacement of kidney tubular losses, symptomatic management of systemic complications, and specific therapy directed at the basic defect, i.e., lysosomal cystine accumulation
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