Last update 01 Nov 2024

NADK

Last update 01 Nov 2024

Basic Info

Synonyms

FLJ13052, NAD kinase, NADK

+ [1]

Introduction-

Drugs associated with NADK

NKI-1

Target

NADK

Mechanism

NADK inhibitors

Active Org.

Universite de Montpellier II [+2]

Originator Org.

Institut Pasteur

Active Indication

Staphylococcal Infections

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with NADK

100 Translational Medicine associated with NADK

0 Patents (Medical) associated with NADK

416

Literatures (Medical) associated with NADK

01 Nov 2024·Food Chemistry

Tert-Butylhydroquinone retards longan fruit deterioration by regulating membrane lipid and energy metabolisms

Article

Author: Jiang, Yueming ; Yang, Jiali ; Yu, Zhiqian ; Tang, Dingtao ; Pan, Yonggui ; Zhang, Zhengke

Longan fruit deteriorates rapidly after harvest, which limits its storability. This study aimed to investigate the effect of tert-butylhydroquinone (TBHQ) on quality maintenance, membrane lipid metabolism, and energy status of longan fruit during 25 °C storage. Compared with control fruit, TBHQ treatment maintained better marketable fruit rate and suppressed activities of phospholipase D (PLD), lipase, and lipoxygenase (LOX), and downregulated expressions of DlPLD, DlLOX, and Dllipase. TBHQ also increased the ratio of unsaturated fatty acids to saturated fatty acids (U/S) and the index of unsaturated fatty acids (IUFA). In addition, higher levels of ATP, ADP, energy charge, NADP⁺/ NADPH as well as higher activities of H⁺-ATPase, Ca²⁺-ATPase and NADK were also observed in TBHQ-treated fruit. These results suggested that TBHQ may maintain postharvest quality of longan fruit by regulating membrane lipid and energy metabolisms.

01 Nov 2024·Free Radical Biology and Medicine

Acute and prolonged effects of Bacillus amyloliquefaciens GF424-derived SOD on antioxidant defense in healthy individuals challenged with intense aerobic exercise

Article

Author: Kim, Hye Jin ; Kwon, Oran ; Nam, Yea-Eun ; Nam, Yea-eun

Reactive oxygen species (ROS) play a vital role in cellular functions but can lead to oxidative stress and contribute to degenerative diseases when produced in excess. Maintaining redox balance is essential and can be achieved through innate defense mechanisms or external antioxidants. Superoxide dismutase (SOD) is a key enzyme that mitigates intracellular oxidative stress by converting harmful free radicals into hydrogen peroxide, which is subsequently neutralized by catalase and glutathione peroxidase. Previous studies have demonstrated the antioxidant capabilities of SOD derived from Bacillus amyloquefaciens GF424 (BA-SOD) in murine models exposed to either irradiation or SOD1 gene deletion. In this study, a randomized clinical trial was conducted to evaluate the antioxidative benefits of BA-SOD in healthy individuals undergoing acute aerobic exercise (AAE). Eighty participants were randomly assigned to receive either BA-SOD or a placebo for 8 weeks. Antioxidant enzyme activities and glutathione levels were measured before, immediately after, and 30 min post-exercise. A single dose of BA-SOD significantly reduced ROS levels induced by AAE, primarily by enhancing SOD activity in erythrocytes and activating glutathione peroxidase. Continuous BA-SOD administration was associated with a sustained increase in catalase activity and elevated levels of reduced glutathione (GSH). Transcriptomic and metabolomic analyses revealed that a single BA-SOD dose facilitated GSH oxidation, as evidenced by decreased levels of serine, glutamine, and glycine, and increased pyroglutamate levels. Additionally, repeated dosing led to increased expression of genes encoding isocitrate dehydrogenase and malic enzyme, which are involved in NADPH synthesis, as well as nicotinamide phosphoribosyl transferase and NAD kinase, which are essential for NADP availability-critical for converting oxidized glutathione (GSSG) back to GSH. These molecular insights align with clinical observations, suggesting that both acute and long-term BA-SOD supplementation may effectively enhance antioxidant defenses and maintain redox balance under oxidative stress conditions.

01 Oct 2024·Redox Biology

Transcriptional Isoforms of NAD+ kinase regulate oxidative stress resistance and melanoma metastasis

Article

Author: Aguirre, Kelsey N. ; Davis, Hannah J ; Cascio, Graciela ; Church, Kellsey P ; Delclaux, Ines ; Church, Kellsey P. ; Aguirre, Kelsey N ; Nease, Leona A ; Nease, Leona A. ; Piskounova, Elena ; Hughes, Riley O. ; Davis, Hannah J. ; Hughes, Riley O

Metastasizing cancer cells encounter a multitude of stresses throughout the metastatic cascade. Oxidative stress is known to be a major barrier for metastatic colonization, such that metastasizing cancer cells must rewire their metabolic pathways to increase their antioxidant capacity. NADPH is essential for regeneration of cellular antioxidants and several NADPH-regenerating pathways have been shown to play a role in metastasis. We have found that metastatic melanoma cells have increased levels of both NADPH and NADP⁺ suggesting increased de novo biosynthesis of NADP⁺. De novo biosynthesis of NADP⁺ occurs through a single enzymatic reaction catalyzed by NAD⁺ kinase (NADK). Here we show that different NADK isoforms are differentially expressed in metastatic melanoma cells, with Isoform 3 being specifically upregulated in metastasis. We find that Isoform 3 is more potent in expanding the NADP(H) pools, increasing oxidative stress resistance and promoting metastatic colonization compared to Isoform 1. We have found that Isoform 3 is transcriptionally upregulated by oxidative stress through the action of NRF2. Together, our work presents a previously uncharacterized role of NADK isoforms in oxidative stress resistance and metastasis and suggests that NADK Isoform 3 is a potential therapeutic target in metastatic disease.

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NADK

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