Ask about this productRelated genes to: PBEF1 antibody
- Gene:
- NAMPT NIH gene
- Name:
- nicotinamide phosphoribosyltransferase
- Previous symbol:
- PBEF1
- Synonyms:
- PBEF
- Chromosome:
- 7q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-02
- Date modifiied:
- 2014-11-19
Related products to: PBEF1 antibody
Related articles to: PBEF1 antibody
- Neonatal hypoxic-ischemic (HI) brain injury remains a major cause of death and long-term neuro-disability leading to hypoxic-ischemic encephalopathy (HIE), and current hypothermia therapy is only partially effective. Curcumin is a polyphenolic compound with antipyretic and neuroprotective activities, but its role in thermos-metabolic control after neonatal HI has not been defined. Using the Rice-Vannucci model in postnatal day-7 mice, we found that curcumin administered either before HI (100-300 µg/g, i.p.) or after HI (200 µg/g within 3 h) significantly reduced infarct volume, improved survival and body-weight recovery, and accelerated restoration of sensorimotor and cognitive functions. Infrared thermography and rectal monitoring showed that HI induced focal, lesion-side brain hyperthermia, accompanied by a rise in core temperature, whereas curcumin lowered both parameters during the acute post-insult phase. Text-mining, protein-protein interaction, and GO enrichment analyses of 191 HI-related genes identified a thermometabolic-centered mitochondrial signature, with glutaminase 2 (GLS2) and nicotinamide phosphoribosyltransferase (NAMPT) ranked as central nodes. Docking analyses demonstrated favorable binding of curcumin to GLS2 and NAMPT, consistent with curcumin-mediated restraint of mitochondrial energy/heat production and with the observed reductions in microglial activation, caspase-dependent apoptosis, and neuronal loss. These findings define mitochondrial thermos-metabolic regulation as a druggable target in neonatal HI and support the further development of curcumin-based pharmacological interventions within this pathway. Targeting the mitochondrial thermogenesis pathway for neuroprotection in neonatal HIE by curcumin. - Source: PubMed
Publication date: 2026/05/20
Wang XianxuanZhang BoEide SarahZhang Xin-YangYang MengFeng Zhong-PingSun Hong-Shuo - Vascular endothelial cells maintain vascular homeostasis by releasing mediators with vasoconstrictive and vasorelaxant effects. Prostanoids are bioactive substances synthesised by cyclooxygenase2 (COX2); they preserve vascular function and can increase the risk of cardiovascular disease (CVD) associated with ageing. Age-related reductions in nicotinamide adenine dinucleotide (NAD) have been implicated in CVD pathogenesis. However, the relationship between intracellular NAD levels and prostanoid production in vascular endothelial cells is unclear. Herein, reduced intracellular NAD levels upregulated COX2 protein expression by activating the p38 mitogen-activated protein kinase (MAPK) signalling pathway, increasing the production of prostaglandin F (PGF) and thromboxane B (TXB) in human umbilical vein endothelial cells (HUVECs). Treatment with the nicotinamide phosphoribosyltransferase (NAMPT) inhibitor, FK866, decreased intracellular NAD levels, induced a cellular senescence-like phenotype characterised by the suppression of cell proliferation without cell death and promoted PGF and TXB production in HUVECs. FK866 treatment increased phosphorylated p38 and COX2 protein levels, whereas treatment with the p38 inhibitor, PD169316, suppressed the FK866-induced increase in COX2 expression. Supplementation with nicotinamide mononucleotide (NMN), a precursor of NAD, following FK866 treatment restored intracellular NAD levels, reduced the cellular senescence-like phenotype and attenuated the production of PGF and TXB. These results suggest that intracellular NAD appears to regulate prostanoid production in HUVECs under conditions of acute depletion. - Source: PubMed
Kitajima NatsukoNakajo TakahisaKatayoshi TakeshiTsuji Kentaro - Dysregulation of Cholesterol homeostasis(CH) and NK cells proportion can increase risk of ST-Elevated Myocardial Infarction(STEMI) for Coronary atherosclerotic heart disease(CAD) patients. Hence, it is necessary for the investigation of CH and MC in pathogenesis of STEMI for CAD patients, providing additional choice for the prevention of STEMI for CAD patients. - Source: PubMed
Publication date: 2026/05/14
Chen XuemeiZhao YifanGuo XixiMan QiushanWang MingWang ZhouCheng JunChen Shijian - Metastatic cutaneous melanoma (MCM) is primarily treated with BRAF/MEK inhibitors and immune checkpoint inhibitors (ICIs), but the long-term efficacy of these therapies is often limited by acquired resistance. Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in NAD biosynthesis, is frequently upregulated in MCM, supporting metabolic rewiring and targeted therapy resistance. Interferon-γ (IFN-γ) signaling plays a central role in melanoma biology, exerting both antitumor and immunoregulatory effects, linked with the onset of therapeutic resistance. Emerging evidence suggests that metabolic pathways may critically modulate IFN-γ responses; however, the functional interplay between NAD/NAMPT metabolism and IFN-γ signaling in melanoma cells remains poorly defined. - Source: PubMed
Publication date: 2026/05/14
Fiorilla IreneGhezzi BeatricePonzano AlessiaMoiso EnricoRiccardo FedericaTommasi NicolettaAvalle LidiaCarrà GiovannaUgolini FilippoCalussi EdoardoTodesco Alberto MariaDigiovanni SabrinaCasone FilippoRizza GiuliaPonzone LucaSzumera-Ciećkiewicz AnnaCavaletto MariaPorporato Paolo EttoreConti LauraRiganti ChiaraMassi DanielaCalautti EnzoAudrito Valentina - Mitochondrial dysfunction and insufficient mitophagy are central to cisplatin-induced acute kidney injury (AKI). Tirzepatide, a dual GLP‑1/GIP receptor agonist, exhibits reno-protective effects, but its mechanism related to mitochondrial homeostasis remains unclear. Here, we used metabolomics, in vivo mouse AKI model, and in vitro cisplatin-injured HK‑2 cells to explore the protective effects and underlying mechanisms. Tirzepatide pretreatment significantly alleviated renal dysfunction, tubular injury, and mitochondrial damage caused by cisplatin. Metabolomic analysis revealed that tirzepatide strongly regulated energy metabolism and autophagy , particularly NAD + homeostasis. Mechanistically, tirzepatide boosted NAD levels by nicotinamide phosphoribosyl transferase (NAMPT), the rate-limiting enzyme for NAD + synthesis , which in turn activating the Pink1-Parkin mitophagy pathway. Inhibition of autophagy or NAMPT abolished the mitochondrial and reno-protective effects of tirzepatide. Taken together, our findings demonstrate that tirzepatide protects against cisplatin‑induced AKI by enhancing NAMPT‑dependent NAD + restoration and promoting mitophagy, highlighting a promising therapeutic strategy for chemotherapy‑related nephrotoxicity. - Source: PubMed
Publication date: 2026/05/09
Han ChongyangTan ZhichengWang YuJing XuanCui XiangrongZhang YuyuYan PanCheng YaoYue HongyuWang BaodongGuo Hui