NUCB1 antibody - C-terminal region (P101699_T100)
- Known as:
- NUCB1 (anti-) - C-terminal region (P101699_T100)
- Catalog number:
- p101699_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- NUCB1 antibody - C-terminal region (P101699_T100)
Related genes to: NUCB1 antibody - C-terminal region (P101699_T100)
- Gene:
- NUCB1 NIH gene
- Name:
- nucleobindin 1
- Previous symbol:
- -
- Synonyms:
- NUC, Calnuc
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1996-09-13
- Date modifiied:
- 2014-11-19
Related products to: NUCB1 antibody - C-terminal region (P101699_T100)
Related articles to: NUCB1 antibody - C-terminal region (P101699_T100)
- Visceral hypersensitivity (VH) is acknowledged as a critical pathogenic mechanism underlying functional gastrointestinal disorders (FGIDs), which is influenced by dysregulation of the gut-brain axis. Transauricular vagus nerve stimulation (taVNS) is a clinically used intervention for the relief of visceral pain; however, its underlying neural mechanisms remain poorly understood. Drawing on the pathogenesis of VH and our team's previous research, we hypothesized that taVNS mitigates VH through the nesfatin-1/corticotropin-releasing factor (CRF) pathway. This study aims to elucidate the potential central regulatory mechanisms that contribute to the analgesic effects of taVNS. - Source: PubMed
Xu WanliZhou ZiqinZhou ShuaiZhao RuiruiZhu WeijianChen HuanZhou JingzhuZhang Zhaohui - Nesfatin-1 is a peptide hormone derived from the precursor protein Nucleobindin-2 (NUCB2) and was discovered recently in the rat hypothalamus. Nesfatin-1 is primarily expressed in the brain, particularly in the hypothalamus. It regulates food intake, body weight, gastrointestinal and cardiovascular functions, cell proliferation, protection against neurotoxicity, and energy homeostasis. Nesfatin-1 acts through an unidentified GPCR, activating key downstream signaling cascades such as MAPKs, JAK/STAT, and PI3K/AKT. - Source: PubMed
Publication date: 2026/02/22
Rai Akhila BalakrishnaCodi Jalaluddin Akbar KandelBhat SowrabhaAmmankallu ShruthiParate Sakshi SanjayUpadhyay Shubham SukerndeoNarayana Vanya KadlaVerghese SusmiJisha Tinta IzabelleShaji VineethaAnwitha K Jagannath R S Babu Neeraja SKinra SanjayMallinson PoppyDagamajalu ShobhaPrasad Thottethodi Subrahmanya Keshava - Nesfatin-1 assumes a crucial role in the regulation of appetite and glucose metabolism. The present study aimed to determine the effect of LPBN nesfatin-1 on food intake and blood glucose in type 1 diabetes (T1DM) rats and underlying mechanisms. Catheter implantation and nucleus microinjection were employed to investigate the effect of LPBN nesfain-1 on the regulation of food intake and blood glucose in Rats with T1DM. In vivo electrophysiological technique was used to record LPBN glucose-sensitive (GS) neurons to explore central underlying mechanisms. ELISA kits were utilized to assess the plasma levels of nesfatin-1, norepinephrine (NE), and epinephrine (E). We found LPBN nesfatin-1 inhibited nocturnal feeding in Rats with T1DM. The glucose regulation of LPBN nesfatin-1 is closely associated with insulin. LPBN nesfatin-1 increased the firing rate of glucose-excited neurons in Rats with T1DM and the firing rate of glucose-inhibited neurons in Wistar Rats. LPBN nesfatin-1 increased plasma NE levels in Wistar Rats under hypoglycemia and decreased plasma E levels in Rats with T1DM with hyperglycemia. These findings suggested that LPBN nesfatin-1 was involved in food intake and blood glucose regulation in Rats with T1DM, which may be achieved by influencing GS neurons and subsequent putative modulation of sympathetic nervous system activity, a pathway that requires further mechanistic validation. - Source: PubMed
Publication date: 2026/02/04
Zhang CaishunZhang QingWang LiuxinWang HaidanLin QianWang YuxuanYu JiaqingZhu KunXia YunqiuDong Jing - Nesfatin1, a multifunctional peptide involved in energy homeostasis and neural regulation, has emerged as a promising candidate for modulating neurodevelopmental disorders. The anti-inflammatory, antioxidant, and neuroprotective properties of Nesfatin1 have been proven in the central nervous system (CNS). Therefore, it has emerged as a candidate for targeted therapy of various neurological condition. Autism Spectrum Disorder (ASD) is a significant neurological disorder. Considering the importance of these mechanisms demonstrated by Nefastine1, The current study aimed to investigate the therapeutic potential and mechanisms of Nesfatin1 in a rat model of autism. This study evaluated the therapeutic potential of Nesfatin1 in a rodent model of autism induced by prenatal exposure to valproic acid (VPA). Pregnant Wistar rats received VPA on embryonic day 12.5, and male offspring were subsequently assessed for autism-like behaviors using a comprehensive battery of tests, including the three-chamber social interaction test, marble burying, shuttle box passive avoidance, and the elevated plus maze. Following behavioral testing, rats were euthanized, and blood samples were collected via transcardial perfusion. Serum oxytocin levels were measured, and hippocampal tissues were analyzed for inflammatory markers (IL-6, TNF-α) using ELISA. Additionally, total antioxidant capacity (TAC) and the activities of glutathione peroxidase (GPx) and superoxide dismutase (SOD) were assessed. VPA-exposed rats exhibited significant social deficits, increased repetitive behaviors, and impaired cognitive performance, accompanied by heightened neuroinflammation and oxidative stress. Notably, treatment with Nesfatin1 markedly improved social engagement and preference, reduced anxiety and repetitive behaviors, and restored biochemical parameters toward normal levels. Results showed that possible therapeutic mechanism of Nefastin1 are by decreasing inflammation and reducing markers of oxidative stress, while concurrently elevating levels of oxytocin, in addition to the other unknown mechanisms. - Source: PubMed
Publication date: 2025/09/13
Farbin MitraHajisoltani RaziehBaluchnejadmojarad TourandokhtHejazi AnahitaAhmed TouqeerParsian HeshmatollahMehrabi Soraya - Autism spectrum disorders (ASD) are neurodevelopmental pathologies. Investigating both sexes is crucial for understanding sex-specific manifestations of ASD. This study aims to examine ASD-like behaviours and metabolic alterations in male and female rats prenatally exposed to valproic acid (VPA). Pregnant Wistar albino rats were administered 400 mg/kg VPA or saline on embryonic day 12. Pups were subjected to various behavioural tests, including olfactory discrimination, sociability, locomotion, anxiety and exploratory behaviour assessments. On postnatal day 35, pups were sacrificed, and blood glucose levels were measured. Serum and brain leptin, orexin-A, nesfatin-1 and ghrelin levels were assessed by the ELISA method. VPA-exposed pups exhibited increased latency to reach maternal bedding, reduced sociability, decreased locomotion and increased immobility in both sexes. In the elevated plus maze, VPA-exposed females showed an increase in open-arm entries, while males showed a reduction compared to control groups. Blood glucose levels were significantly elevated in VPA-exposed males but not females. Significant sex-independent changes were observed in serum and brain levels of leptin and nesfatin-1 in the VPA groups. Brain orexin-A and serum ghrelin levels were altered in the VPA group in a sex-dependent manner. Prenatal VPA exposure induces ASD-like symptoms in both sexes, with notable sex-specific differences in behaviour and metabolic regulation. These findings highlight the importance of including both sexes in ASD research to better understand sex-dependent characteristics of the disorder, particularly concerning metabolic dysregulation. - Source: PubMed
Publication date: 2025/09/10
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