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In this study, as amino acid precursors could be fed to improve concentrations of intracellular free l-cysteine, we resorted to overexpression of GK instead of loss-of-function mutations in GPR for accumulation of -glutamyl phosphate to strengthen the redirection of -glutamyl phosphate to GSH synthesis

and (4) exercise intolerance appearing from 6 to 33 years of age, with muscular weakness and high serum creatine kinase

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BPC-157 in this model compensated for that deficit

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