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First, though, the part Im not willing to leave out
There appears to be an anomalous storage of mitochondrial ATP synthase subunit c that is neither the result of mutation nor enhanced expression of the protein but rather a slower degradation of the mitochondrial ATP synthase in comparison with normal cells [116]
Knockdown of NNMT in adipocytes was associated with increased NAD+ levels and altered expression of genes involved in energy expenditure, providing the rationale for pharmacological NNMT inhibition [2]
Razi Inst
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