NAXE

Last update 08 May 2025

Basic Info

Synonyms

AI-BP, AIBP, APOA1BP

+ [10]

Introduction

Catalyzes the epimerization of the S- and R-forms of NAD(P)HX, a damaged form of NAD(P)H that is a result of enzymatic or heat-dependent hydration (By similarity) (PubMed:27616477). This is a prerequisite for the S-specific NAD(P)H-hydrate dehydratase to allow the repair of both epimers of NAD(P)HX (By similarity). Accelerates cholesterol efflux from endothelial cells to high-density lipoprotein (HDL) and thereby regulates angiogenesis (PubMed:23719382).

100 Clinical Results associated with NAXE

100 Translational Medicine associated with NAXE

0 Patents (Medical) associated with NAXE

Literatures (Medical) associated with NAXE

01 Mar 2025·Pediatric Dermatology

Cutaneous Manifestations of NAXD or NAXE Deficiency: A Literature Review for the Dermatologist

Review

Author: Davis, Dawn Marie ; Vahidnezhad, Hassan ; Mohandesi, Nessa Aghazadeh ; Camilleri, Michael J. ; Mittal, Setu ; Abdulkarim, Boraan

ABSTRACTNicotinamide adenine dinucleotide phosphate hydrate dehydratase (NAXD) and nicotinamide adenine dinucleotide phosphate hydrate epimerase (NAXE) deficiencies are rare autosomal recessive metabolic disorders characterized by severe neurological manifestations during infancy. In affected individuals, febrile illnesses can trigger progressive encephalopathy often accompanied by distinctive skin eruptions, resulting in high mortality rates. This study reviews the literature on NAXD/NAXE deficiencies, focusing on dermatological manifestations and their correlation with genotypic variations and treatment responses. A comprehensive literature search identified 45 patients with 31 pathogenic/likely pathogenic mutations, and a median age of onset at 1.16 years. Patients with NAXE deficiency exhibited a broader range of age of symptom onset compared to those affected with NAXD deficiency. Fever or infections were identified as the most common triggers for decompensation episodes. Skin manifestations were observed in 31% of patients with whole cell NAXD and NAXE deficiencies. The characteristic skin eruption comprises well‐demarcated erythematous and erosive plaques progressing to blistering and necrosis, predominantly affecting flexural surfaces. The mortality rate was 78%, with survivors experiencing varying degrees of neurological sequelae. Niacin/nicotinamide supplementation resulted in improvements in skin lesions and survival rates. The review underscores the critical role of dermatologists in early diagnosis and intervention of NAXE and NAXD deficiencies. Recognizing characteristic skin manifestations is essential, particularly in patients with acute neurological decline following infections or vaccinations. Early intervention with specific supplements shows promise; however, further research is needed to establish standardized treatment protocols and enhance patient outcomes.

01 Jan 2025·Brain, Behavior, and Immunity

ApoA-I binding protein (AIBP) regulates transient receptor potential vanilloid 1 (TRPV1) activity in rat dorsal root ganglion neurons by selective disruption of toll-like receptor 4 (TLR4)-lipid rafts

Article

Author: Yaksh, Tony L. ; Dougherty, Patrick M ; Li, Yan ; Fan, Dwight H. ; Sheffield, Katherine N ; Miller, Yury I. ; Uhelski, Megan L. ; Dougherty, Patrick M. ; Yaksh, Tony L ; Uhelski, Megan L ; Roland, Gavin H. ; Bankston, Christopher B. ; Kosten, Therese A. ; Farson, Luke B. ; Farson, Luke B ; Bankston, Christopher B ; Orlando, Dana ; Kosten, Therese A ; North, Robert Y. ; Heles, Mario ; Jia, Amy ; North, Robert Y ; Sheffield, Katherine N. ; Miller, Yury I ; Fan, Dwight H ; Roland, Gavin H

Toll-like receptor 4 (TLR4) and the transient receptor potential vanilloid subtype 1 (TRPV1) are both upregulated and play key roles in the induction and expression of paclitaxel-related chemotherapy-induced peripheral neuropathy (CIPN). Using Apolipoprotein A-I binding protein, non-specific cholesterol depletion, TLR4 mis-sense rats and a TLR4 inhibitor, we demonstrate that co-localization of TRPV1 with TLR4 to cholesterol-rich lipid membrane rafts in nociceptors is essential for its normal activation as well as for its exaggerated activation that underlies the development and expression of CIPN. The findings suggest that TLR4-lipid rafts may have an essential role in numerous neuroinflammatory and neuropathic pain conditions. This mechanism is also generalized to female rats for the first time.

01 Oct 2024·Journal of Dental Research

Acceleration of HDL-Mediated Cholesterol Efflux Alleviates Periodontitis

Article

Author: Kook, M.-S. ; Lim, H.-P. ; Chung, K.-H. ; Ryu, J. ; Lee, G. ; Huh, Y.H. ; Lee, S.Y. ; Tran, T.-T. ; Kim, O.-S. ; Ryu, J.-H. ; Koh, J.-T. ; Park, K.H. ; Kim, J.-H.

Periodontitis (PD) is a common inflammatory disease known to be closely associated with metabolic disorders, particularly hyperlipidemia. In the current study, we demonstrated that hypercholesterolemia is a predisposing factor in the development of PD. Logistic regression analysis revealed a strong positive correlation between PD and dyslipidemia. Data from in vivo (PD mouse model subjected to a high cholesterol diet) and in vitro (cholesterol treatment of gingival fibroblasts [GFs]) experiments showed that excess cholesterol influx into GFs potentially contributes to periodontal inflammation and, subsequently, alveolar bone erosion. Additionally, we compared the protective efficacies of cholesterol-lowering drugs with their different modes of action against PD pathogenesis in mice. Among the cholesterol-lowering drugs we tested, fenofibrate exerted the most protective effect against PD pathogenesis due to an increased level of high-density lipoprotein cholesterol, a lipoprotein involved in cholesterol efflux from cells and reverse cholesterol transport. Indeed, cholesterol efflux was suppressed during PD progression by downregulation of the apoA-I binding protein (APOA1BP) expression in inflamed GFs. We also demonstrated that the overexpression of APOA1BP efficiently regulated periodontal inflammation and the subsequent alveolar bone loss by inducing cholesterol efflux. Our collective findings highlight the potential utility of currently available cholesterol-lowering medications for the mitigation of PD pathogenesis. By targeting the acceleration of high-density lipoprotein-mediated cellular cholesterol efflux, a new therapeutic approach for PD may become possible.

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