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Description

Although the mechanism of pathogenesis is unclear, it is thought that the clinical phenotypes of SSMD patients involve complete loss of GPX4 enzymatic function

4,031.72 g/mol Purity 98% CAS No

Proglucagon would thus be processed in a tissue-specific, differential manner, giving rise to glucagon in the pancreas and to glicentin and oxyntomodulin in the so-called L-cells in the gut, the cells that harbored the glucagon immunoreactivity