Ask about this productRelated genes to: NUCB1 antibody
- 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
Related articles to: NUCB1 antibody
- Proteomic profiling offers thorough insights into protein structure and function, as well as it acts as an essential approach for analyzing molecular changes at the tissue level. However, because of the proteome's diversity and dynamic nature, biomarker discovery remains challenging. By combining proteomics with bioinformatics, the level of understanding in relation to molecular interactions and disease processes can be improved. Through an integrative approach, few limitations can be addressed, thereby promoting proteomic profiling for the discovery of new therapeutic targets and novel biomarkers for a variety of disorders. - Source: PubMed
Publication date: 2026/06/18
Rao Bounika EsvanthNair Anju MRamesh PreethiRamshankar VijayalakshmiGopinath SAbhinand P ANdkoraj ArtnoraMazur MartaWarnakulasuriya SamanCatakapatri Venugopal Divyambika - Sex differences in metabolic physiology are widespread across species and are tightly linked to reproductive demands. Here, we identify nucleobindin 1 (Nucb1), a conserved calcium-binding protein, as a female-specific metabolic regulator in the adipokinetic hormone (Akh)-producing cells (APCs) of . APC-specific knockdown increased energy storage and body mass in females but not in males. Cellular sex reversal experiments revealed these female-specific functions of Nucb1 to be dependent on the intrinsic sexual identity of the APCs, rather than the sex of the organism. Furthermore, under nutrient restriction, females lacking in APCs failed to suppress oocyte maturation, indicating disrupted coupling between nutrient status and reproductive output. In contrast, we identified slowpoke-binding protein (Slob) in the APCs as a regulator of male-specific body fat storage. Together, these findings demonstrate that sex-specific metabolic and reproductive regulation arises from differential regulatory factors within the same neuroendocrine cell type. - Source: PubMed
Publication date: 2026/06/01
Pujari NarsimhaChevrier KameaTurriff NatalieAl-Tahir YonaShahi DipeshGorjan Aidin ShaikheiLi Alex S OJois Shreyas VDonà ErikaFerrari MaudUnniappan SurajLeung Adelaine K W - How perivascular adipose tissue (PVAT) controls vascular remodeling and perivascular inflammation during pulmonary hypertension progresses remains unknown. - Source: PubMed
Publication date: 2026/05/29
Liu JieGuo YuHuang JingGao ZhenqiangZhang MuzhiJia YufengLong HuanyuXue XinZhang HanxiaoShi WenhuaLi CongZhang YonghongYang ShuanyingLiu AijunWang Lei - Acute pancreatitis (AP) is an inflammatory disorder with no efficient therapy. Here we demonstrate that the anorexigenic peptide nesfatin-1 exerts potent and dose-dependent protection against both caerulein-induced and hypertriglyceridemic AP. Intraperitoneal administration of nesfatin-1 to restore its serum levels significantly reduced pancreatic necrosis, edema, and infiltration of immune cells, as well as circulating levels of amylase, lipase, and pro-inflammatory cytokines. RNA-seq revealed that nesfatin-1 down-regulated the ER-stress signature (Ddit3, Atf3, Ppp1r15a) and the NF-κB/NLRP3 signaling. Further studies in primary acinar cells confirmed that nesfatin-1 at the dose of 10 nM suppressed phosphorylated eIF2α, DDIT3, ATF3, p65, and NLRP3, thereby inhibiting pyroptosis. Consequently, nesfatin-1 attenuated macrophage/neutrophil infiltration, shifted M1 toward M2 macrophages, inhibited the release of inflammatory cytokines, and alleviated multi-organ injury in lung, intestine, and spleen. Collectively, nesfatin-1 limits AP severity by restraining ER-stress-driven pyroptosis and innate immune activation. Thus, nesfatin-1 may serve as a promising therapeutic candidate for acute pancreatitis. - Source: PubMed
Li HanWang XianfengNiu YuefengSun LijunYang YinmoZhang WeizhenYin Yue - 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