NADK2

Last update 08 May 2025

Basic Info

Synonyms

C5orf33, FLJ30596, Mitochondrial NAD kinase

+ [5]

Introduction

Mitochondrial NAD(+) kinase that phosphorylates NAD(+) to yield NADP(+). Can use both ATP or inorganic polyphosphate as the phosphoryl donor. Also has weak NADH kinase activity in vitro; however NADH kinase activity is much weaker than the NAD(+) kinase activity and may not be relevant in vivo.

100 Clinical Results associated with NADK2

100 Translational Medicine associated with NADK2

0 Patents (Medical) associated with NADK2

Literatures (Medical) associated with NADK2

01 Jun 2025·Experimental Gerontology

Molecular mechanism of melatonin-mediated mitophagy regulating proline production to ameliorate skin aging

Article

Author: Gao, Ting ; Li, Ran ; Quan, Tao

Collagen loss is one of the major contributor to signs of skin aging such as dryness, roughness, and wrinkle formation, which is closely linked to a decline in the amount of proline produced in mitochondria. Melatonin has been shown to improve several clinical signs of skin aging, while the mechanism is unclear. In our study, we found that mitophagy, proline synthesis key enzyme NADK2 and proline and collagen levels were significantly reduced, while oxidative stress levels increased in aging skin, and melatonin supplementation could effectively up-regulate mitophagy level and restore proline synthesis and further improved skin aging. However, proline supplementation could also exert an anti-aging effect, while it had no effect on the mitochondrial dysfunction. Moreover, our study indicated that melatonin enters the cell by binding to the MT1 receptor and then enters the mitochondria via the PEPT1 transporter to exert its mitochondrial protective effects. This study helps to elucidate the mechanism of mitochondrial dysfunction-induced skin aging, and provides new theoretical guidance for revealing the mechanism of skin aging and rationally utilizing endocrine hormones to improve skin aging, which has a broad application prospect.

01 Apr 2025·Aging Cell

Downregulation of NAD Kinase Expression in β‐Cells Contributes to the Aging‐Associated Decline in Glucose‐Stimulated Insulin Secretion

Article

Author: Lin, Gigin ; Chiu, Chih‐Yung ; Lin, Yu‐Ting ; Cheng, Mei‐Ling ; Li, Guan‐Jie ; Ho, Hung‐Yao ; Ho, Yu‐Hsuan

ABSTRACTNicotinamide adenine dinucleotide kinase (NADK) is essential to the generation of nicotinamide adenine dinucleotide phosphate (NADP(H)), an important metabolic coupling factor involved in glucose‐stimulated insulin secretion. In the present study, we showed that the expression of Nadk and Nadk2 transcripts and NADP(H) content were lower in islets of 80‐week‐old (aged) mice than those of 8‐week‐old (young) mice. This was associated with diminished oral glucose tolerance of old mice and the glucose‐stimulated insulin secretion (GSIS) response of islets. Knockdown (KD) of Nadk or Nadk2 gene expression in NIT‐1 cells impaired glucose‐stimulated insulin secretion. Metabolomic analysis revealed that Nadk KD specifically affected purine metabolism in glucose‐stimulated cells. The levels of 5‐aminoimidazole‐4‐carboxamide ribonucleotide (AICAR) were higher in KD cells than in the non‐targeting control (NTC) cells. Phosphorylation of AMP‐activated protein kinase (AMPK) was elevated in glucose‐treated KD cells compared to that of NTC cells. Increased AICAR level and AMPKα phosphorylation were observed in the glucose‐stimulated islets of the aged mice. Genetic and pharmacological inhibition of AMPK promoted glucose‐stimulated insulin release by KD cells and the aged mouse islets. It is likely that NADK is modulatory to AMPK activation in pancreatic β‐cells and to their GSIS response. Enhanced AICAR formation in KD cells was accompanied by significantly increased conversion from inosine monophosphate (IMP) in a tetrahydrofolate (THF)‐dependent manner. Folate supplementation augmented the GSIS response of KD cells and aged mouse islets. Taken together, these findings suggest that the aging‐associated decline in NADK expression may underlie the reduced insulin secretory capacity of pancreatic β‐cells.

01 Nov 2024·iScience

Blood expression of NADK2 as a diagnostic biomarker for sciatica

Article

Author: Wang, Yang ; Liu, Jingmin ; Wang, Xiaobo ; Shi, Jiawei ; Ren, Zhenxiao ; Zheng, Xin ; Wang, Bingyu

Sciatica is characterized by radiating pain along the sciatic nerve, with a lifetime prevalence of up to 43%. This study explored blood biomarkers for sciatica using transcriptomic microarray data (GSE124272 and GSE150408). Differential gene expression analysis identified NADK2 as a potential diagnostic biomarker. A diagnostic model based on NADK2 showed strong validation performance in 200 clinical cases. Gene set enrichment analysis (GSEA) suggested a connection between NADK2 and the aminoacyl-tRNA biosynthesis pathway. In conclusion, NADK2 emerges as promising diagnostic and therapeutic targets for sciatica, significantly advancing our comprehension of potential pathogenic mechanisms and offering perspectives for early diagnosis and treatment.

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NADK2

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