Product Details

ALDH1A2 antibody product
ALDH1A2 (retinaldehyde dehydrogenase 1, also known as RALDH1) is a cytosolic homotetramer consisting of catalytic domain, cofactor (NAD) binding domain and oligomerization domain. It is a key member of the Nrf2 and Keap1-like epichlorohydrin-associated protein-1 (Keap1) signaling pathways that promote the detoxification of endogenous oxidized aldehyde polymers such as acrylonitrile (ACH) [1,2]. It has been shown that the expression level of ALDH1A2 is down-regulated in patients with hepatocellular carcinoma (HCC).

It has been reported that ALDH1A2 antibody product supports energy production by facilitating glycolysis and the tricarboxylic acid cycle and by affecting multiple metabolic enzymes to increase ATP production. In addition, metabolomic profiling revealed that ALDH1A2 metabolizes ACH to reduce the expression of BTEB and prevents cellular stress by inhibiting the generation of ROS [3].

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Genetic depletion of ALDH1A2 by shRNA or sgRNA resulted in increased levels of ROS in cells and primary leukemia cell lines from a patient-derived xenograft model. In contrast, N-acetyl cysteine treatment significantly reduced the ROS level in cells after ALDH1A2 depletion. This indicates that while ALDH1A2 supports energy production and the tricarboxylic acid cycles, its main role is to protect against oxidative stress by decreasing the accumulation of oxidized aldehydes such as ACH.

In vivo studies have also demonstrated that ALDH1A2 regulates the synthesis of fatty acids and cholesterol in hepatocytes to alleviate hepatic fibrosis by metabolizing fatty acid amides and inhibiting glycerolipid synthesis [4,7]. Moreover, a liposome-formulated miR-34a mimic (MRX34) can induce the expression of ALDH1A2 to reduce hepatocellular oxidative stress in mice and prevent liver disease [8,9]. Considering these results, we hypothesized that the expression of ALDH1A2 can be manipulated by RNA-targeted drugs to treat various liver diseases.