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A., Lee, M.-R., et al

The main progress of our work beyond the CASTOR hypothesis is that that we provide a molecular mechanism in which substrate competition among acyl-CoAs for common enzymes strongly amplifies the depletion of CoASH: levels of CoASH did not decline gradually as a function of palmitoyl-CoA substrate, but declined steeply beyond a threshold value of substrate (Fig

1, 6,11,12 However, mut-MMA cases are more likely to experience more serious clinical manifestations like acute decompensation and metabolic stroke, chronic kidney disease, and the urine MMA (uMMA) level is higher than that of cblC-MMA children, whereas cblC-MMA patients are more susceptible to hydrocephalus and microangiopathy-related manifestations (i.e., atypical hemolytic uremic syndrome), and retinopathy

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