PBEF1 Blocking Peptide
- Known as:
- PBEF1 Blocking Peptide
- Catalog number:
- 33r-1818
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- PBEF1 Blocking Peptide
Related genes to: PBEF1 Blocking Peptide
- 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 Blocking Peptide
Related articles to: PBEF1 Blocking Peptide
- Cerebral ischemia-reperfusion (I/R) injury constitutes a pivotal pathological driver in cerebrovascular disorders such as stroke, yet effective therapeutic interventions remain scarce. This study explored whether hydrogen sulfide (HS) mitigates endothelial cell damage in the cerebral vasculature during I/R by modulating nicotinamide phosphoribosyltransferase (NAMPT) activity and its S-sulfhydration status, consequently restoring mitochondrial integrity and energetic homeostasis. Primary cerebrovascular endothelial cells (ECs) were subjected to hypoxia/reoxygenation (H/R) conditions in vitro, while rats experienced middle cerebral artery occlusion/reperfusion (MCAO/R) in vivo. The HS donor sodium hydrosulfide (NaHS) was administered, and outcomes were evaluated through Western blot analysis, S-sulfhydration assays, mitochondrial functional tests, autophagy profiling, and neurobehavioral assessments. The contributions of NAMPT and S-sulfhydration were validated using FK866 and dithiothreitol (DTT), respectively. LC-MS/MS was employed to identify candidate S-sulfhydration sites on NAMPT triggered by HS. In cellular models, NaHS substantially boosted NAMPT enzymatic activity, elevated NAD and ATP levels, and enhanced cell survival. These protective benefits were nullified upon NAMPT inhibition with FK866 or reversal of S-sulfhydration via DTT. In animal studies, NaHS treatment significantly diminished infarct volume and ameliorated neurological deficits in MCAO/R rats; however, pretreatment with FK866 or DTT attenuated these benefits. Mechanistic investigations revealed that NaHS promoted S-sulfhydration of NAMPT, thereby activating autophagy of dysfunctional mitochondria. LC-MS/MS analysis confirmed enhanced S-sulfhydration at Cys39 and Cys397 residues of NAMPT following HS exposure. HS exerts neuroprotection against cerebral I/R injury in rats through S-sulfhydration-mediated activation of NAMPT, which improves mitochondrial performance and stimulates autophagy in cerebrovascular ECs. - Source: PubMed
Publication date: 2026/05/08
Jiang LaLiang ShuaiJiang YuJiang Jia-RongWang ShanYin XiaojiaoChen ZhiwuWen Ji-YueChen Shuo - NAD+ plays crucial roles in various biological processe and its aberrant regulation has been suggested to be critical in the pathogenesis of diverse diseases. Intracellular NAD+ is synthesized largely from nicotinamide mononucleotide (NMN), which is the product of reaction catalyzed by nicotinamide phosphoribosyltransferase (NAMPT). Thus, the development of specific inhibitors targeting NAMPT has been suggested as a promising treatment strategy. In this study, we developed a pharmacophore-based QSAR model to discover novel NAMPT inhibitors based on diverse structural features. By virtual screening using the conformation model, we could identify eight novel active analogs having distinct pharmacophores. The biological activity of these candidates on cell viability were further examined. Our study proves the efficiency of our novel screening model and demonstrates its usefulness in the application of drug discovery process. - Source: PubMed
Publication date: 2026/05/21
Lee SujinZheng MeiKim KangChun Kwang-Hoon - Amino acids are key regulators of metabolism, their coordinated effects on skeletal muscle signaling and metabolic remodeling under physiological conditions remain incompletely understood. Here, we investigated whether 14 weeks of combined histidine and proline supplementation (HISPRO; 700 mg/kg) enhances skeletal muscle function through metabolic reprogramming in normal ICR mice. HISPRO significantly improved muscle performance compared with the control group, including grip strength, rota-rod, and treadmill. Histological and biochemical analyses revealed a shift toward oxidative muscle phenotype compared with the control group, with larger muscle fibers and succinate dehydrogenase-positive fibers. Consistently, HISPRO promoted mitochondrial biogenesis and oxidative metabolism compared with the control group, as evidenced by upregulation of mitochondrial regulatory genes, mitochondrial DNA copy number, citrate synthase activity, and oxidative phosphorylation (OXPHOS) complex levels in skeletal muscles. Mechanistically, HISPRO was associated with activation of the SIRT1-PGC1α-AMPK signaling axis compared with the control group, as evidenced by increased and expression, an elevated NAD/NADH ratio, and enhanced AMPK phosphorylation. SIRT1 inhibition markedly attenuated HISPRO-induced increases in mitochondrial biogenesis markers but did not fully suppress OXPHOS protein expression, suggesting the involvement of both SIRT1-dependent and -independent mechanisms. Notably, HISPRO also improved muscle function in dexamethasone-induced muscle atrophy model. It restored mitochondrial biogenesis and function, and suppressed atrophy-related markers compared with the dexamethasone-treated group. HISPRO may contribute to improving muscle quality through coordinated metabolic regulation and could represent a complementary nutritional for supporting muscle metabolic health. - Source: PubMed
Publication date: 2026/05/13
Lee DohyunJeon JongsuHuh GyuwonBaek SeoyeongKim DaehunKang Hyeon-JiLee HoyulLee In-KyuJeon Jae-HanJung Hoe-Yune - Juvenile Polyposis Syndrome (JPS) is an autosomal dominant disorder characterized by multiple gastrointestinal polyps and an increased risk of cancer, most commonly associated with mutations in the tumor suppressor gene . However, substantial phenotypic variability exists among individuals carrying identical mutations, suggesting the presence of genetic modifiers. In this study, we used the genetically diverse Collaborative Cross (CC) mouse population crossed with Smad4 knockout mice to identify loci influencing intestinal polyp development. A cohort of 260 F1 mice derived from 14 CC lines was assessed for polyp number and size across intestinal segments. Quantitative trait locus (QTL) mapping revealed several significant loci, including regions on chromosomes 16, 14, and 12, which were designated 1, 2, and 3 for Intestinal Polyposis Susceptibility locus (), respectively, in the full population, as well as additional sex-specific loci in male and female cohorts. Pathway enrichment analysis of genes within these regions highlighted functional associations with immune signaling, ubiquitin-proteasome degradation, and metabolic regulation. Candidate genes, including , , , and , emerged as potential modifiers of polyp susceptibility. These findings highlight the complex genetic architecture underlying JPS phenotypes and provide candidate loci for future functional and translational investigations. - Source: PubMed
Publication date: 2026/05/07
Zohud OsaydMidlej KreemLone Iqbal MNashef AysarAbu-Elnaaj ImadIraqi Fuad A - Deoxynivalenol (DON) is a globally prevalent mycotoxin that threatens food and feed safety via severe multi-organ toxicity. Previous studies indicate that DON induces cellular energy metabolism dysregulation by triggering oxidative stress and impairing mitochondrial function. During this process, nicotinamide adenine dinucleotide (NAD), a central coenzyme in cellular energy metabolism, frequently exhibits significantly decreased intracellular levels or even complete depletion. However, the molecular mechanisms underlying the disruption of NAD homeostasis by DON exposure, as well as the development of targeted countermeasures, remain elusive. Using human embryonic kidney 293T (HEK293T) cells as an in vitro renal toxicity model, we dissected DON-induced NAD dysregulation and evaluated the protective potential of nicotinamide (NAM). DON caused significant NAD depletion in porcine serum (in vivo) and HEK293T cells (in vitro), which was confirmed as a key driver of cytotoxicity. Mechanistically, although DON binds and inhibits nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme of the NAD salvage pathway, neither NAMPT knockdown and overexpression nor nicotinamide mononucleotide (NMN) supplementation rescued DON-induced toxicity. Instead, DON dose-dependently activated poly(ADP-ribose) polymerase 1 (PARP1), the primary intracellular NAD-consuming enzyme, to accelerate NAD depletion. PARP1 knockdown markedly attenuated DON-induced cytotoxicity, identifying PARP1 hyperactivation as the core toxic mechanism. NAM dose-dependently suppressed PARP1 activity, replenished NAD pools, and reversed cell injury. These findings establish PARP1-driven NAD depletion as an important mechanism of DON-induced renal toxicity, providing a promising intervention candidate for mitigating DON toxicity in food safety. - Source: PubMed
Publication date: 2026/05/10
Chen ChaoQin YifanLuo ZijunMu PeiqiangWen JikaiDeng Yiqun