Inquiry Basket
Loading ......
Filter By Product Search for
ADH6
ADH6 Full Name
alcohol dehydrogenase 6 (class V)
ADH6 Introduction
Alcohol dehydrogenase 6 (ADH6), also classified as class V alcohol dehydrogenase, is a specialized metabolic enzyme belonging to the highly conserved ADH superfamily. While the ADH family is classically recognized for metabolizing dietary ethanol, ADH6 distinguishes itself through its unique substrate specificity. Predominantly expressed in the liver and the gastrointestinal tract, ADH6 exhibits relatively low catalytic efficiency for ethanol but demonstrates a remarkably high affinity for complex, long-chain alcohols and xenobiotics. Structurally functioning as a zinc-dependent oxidoreductase, one of the most critical physiological roles of ADH6 lies in its direct contribution to systemic retinol (Vitamin A) metabolism. It actively functions as an all-trans-retinol dehydrogenase, facilitating the oxidative conversion of retinol into retinal. This rate-limiting step is indispensable for the subsequent synthesis of retinoic acid, a powerful endogenous signaling molecule that strictly dictates cellular differentiation, immune responses, and epithelial barrier maintenance. Furthermore, ADH6 contributes to the hepatic detoxification of lipid peroxidation products and other reactive metabolic byproducts, thereby protecting vital barrier tissues from severe oxidative stress.
Figure 1. Schematic diagram showing the metabolic pathways of vitamin A metabolism. (Source: Kam RK, et al. 2012)
Clinically, the dysregulation of ADH6 is robustly associated with the pathogenesis and progression of several major human malignancies, particularly gastrointestinal and hepatic cancers. Because cancer cells must undergo profound metabolic reprogramming to survive, the expression of critical metabolic enzymes is frequently altered to benefit tumor growth. In hepatocellular carcinoma (HCC) and gastric cancer, ADH6 is consistently and significantly downregulated compared to healthy surrounding tissues. The loss of ADH6 in the liver is particularly detrimental; it not only impairs the critical detoxification of xenobiotics but also severely disrupts local retinoic acid synthesis. A deficiency in retinoic acid signaling often traps cells in an undifferentiated, highly proliferative state, thereby promoting tumor aggressiveness and chemoresistance. Consequently, extensive bioinformatic and clinical analyses have identified ADH6 as a potent protective prognostic biomarker. Patients with HCC who retain higher levels of ADH6 expression generally experience significantly longer overall survival and a lower risk of postoperative recurrence. As research into metabolic oncology deepens, restoring ADH6 activity or bypassing its metabolic blockade presents a highly promising avenue for targeted cancer therapies.
Alternate Names for ADH6
ADH6; alcohol dehydrogenase 6 (class V); alcohol dehydrogenase 6; ADH 5; ADH 5; ADH 6; Alcohol dehydrogenase 6 (class V); Alcohol dehydrogenase 6; Aldehyde reductase; Class V alcohol dehydrogenase 6; UDP GLUCURONOSYLTRANSFERASE 2B10 PRECURSOR, MICROSOMAL;
Loading ......
