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Inhibition of glutaminolysis by Gln depletion, by chemical inhibition of the critical regulators of Gln metabolism such as GLS and MYC, or genetic knockdown of these genes and Gln transporters resulted in the inhibition of the essential CSC-driving signaling mechanisms (e.g., WNT/-catenin

Instead, they are cofactors for antioxidant enzymes

In vitro assays show increased glycerol release from adipose tissue following exposure to AOD 9604, a widely used biochemical marker of active lipolysis [1]

S-adenosylmethionine in a feline acetominophen model of oxidative injury