NMUR2 antibody - N-terminal region (ARP35300_P050)
- Known as:
- NMUR2 (anti-) - N-terminal region (ARP35300_P050)
- Catalog number:
- arp35300_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- NMUR2 antibody - N-terminal region (ARP35300_P050)
Related genes to: NMUR2 antibody - N-terminal region (ARP35300_P050)
- Gene:
- NMUR2 NIH gene
- Name:
- neuromedin U receptor 2
- Previous symbol:
- NMU2R
- Synonyms:
- -
- Chromosome:
- 5q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-08-24
- Date modifiied:
- 2014-11-19
Related products to: NMUR2 antibody - N-terminal region (ARP35300_P050)
Related articles to: NMUR2 antibody - N-terminal region (ARP35300_P050)
- Juvenile colorectal polyps (JP) are the most common polypoid lesions of the colon in children and the leading cause of lower gastrointestinal bleeding in pediatric patients. Although histologically classified as benign hamartomatous lesions, they arise in a context of allergic sensitization and IgE-mediated inflammation, suggesting that the epithelial compartment may play an active role in their pathogenesis. To date, most studies have focused on the immune cell infiltrate, leaving the molecular programs operating within the epithelium largely unexplored. Whole-transcriptome RNA sequencing (RNA-seq) was performed on epithelial cells isolated from pediatric JP ( = 8) and paired tissue circumjacent to polyp (TCP) ( = 7) obtained from children with a history of rectal bleeding and IgE sensitization to food allergens. Differential expression, functional enrichment (GO, KEGG, GSEA), and cross-dataset comparison with TCGA colorectal adenocarcinoma (CRC) was conducted. Candidate genes were validated by RT-qPCR in independent samples, including colorectal cancer (CRC) and inflammatory bowel disease (IBD) tissue. Differential expression analysis identified 3273 differentially expressed genes (2342 upregulated, 931 downregulated in JP vs. TCP), with 220 genes exceeding 32-fold change, including (log2FC = 12.16), (log2FC = 10.19), (log2FC = 10.08) and (log2FC = 8.87). JP epithelium displayed a coherent type 2 inflammatory signature, encompassing upregulation of the alarmin IL33, eosinophil-attracting chemokines (, ), IgE receptor subunits (, ), and a coordinately activated leukotriene and prostaglandin biosynthetic program (, , ). Concurrent alterations in epithelial identity were observed, including downregulation of absorptive enterocyte and intestinal stem cell markers (, , ) alongside upregulation of secretory and regenerative programs, including the ectopic gastric-type mucin . Tight junction dysregulation-notably upregulation of the pore-forming claudin and loss of barrier-sealing claudins (, , )-was consistent with impaired epithelial permeability. Pathway analyses confirmed activation of type 2 immune and extracellular matrix remodeling programs, with concurrent suppression of mitochondrial oxidative phosphorylation. Cross-dataset comparison with TCGA CRC data identified 381 co-upregulated and 87 co-downregulated genes shared between JP and CRC, including , , , and , several of which were associated with poorer disease-specific survival in CRC patients. RT-qPCR validation confirmed elevation of and in both JP and CRC, while appeared JP-specific. Epithelial cells from pediatric juvenile colorectal polyps associated with allergic sensitization display a comprehensive type 2 inflammatory transcriptome alongside profound alterations in lineage identity, barrier integrity, and metabolic programming. Partial convergence with CRC-associated gene expression programs-in the absence of histological dysplasia-suggests that chronic allergic inflammation activates conserved epithelial remodeling pathways shared across mucosal tissues. , , and are candidate biomarkers warranting validation in larger cohorts. - Source: PubMed
Publication date: 2026/09/07
Polo María BelénIlid ManuelaBernedo VivianaBorobia PaulaMenendez LorenaZosi AnabellaZubirí CeciliaFernández Rivas MaximilianoRecalde María FlorenciaAguilar Becher Barbara VirginiaGarcía MarcelaAltamirano EugeniaGuzmán LucianaAbba MartinMuglia CeciliaDocena Guillermo - Medial arterial calcification (MAC) is closely related to the morbidity and mortality in people with chronic kidney disease (CKD). Neuromedin U (NMU) is a group of highly conserved neuropeptides, and it exerts its peripheral effects mainly via NMU receptors, NMUR1. The present study was designed to explore the role and mechanism of NMU in MAC under condition of CKD. CKD rats with MAC were induced by feeding an adenine (0.75%) diet combined with high phosphorus (1.5%) for 4 weeks. Rat NMU (NMU-23, 1 nM/kg/h) infusion was applied subcutaneously via osmotic pump. The calcified vascular smooth muscle cells (VSMCs, A7r5 cell line) were induced by the calcifying media. In the aortic media of rats with CKD and in the calcifying media-treated VSMCs, the results showed that the endogenous protein levels of NMU and its receptors NMUR1 and NMUR2 were elevated, and NMU application further aggravated calcification and promoted osteogenic transformation and apoptosis. These effects were effectively inhibited by an inhibitor of ERK activation U0126 and NMUR1 antagonist CPN-351, but not NMUR2 antagonist R-PSOP, in the calcifying media-treated VSMCs. Moreover, the downregulation of NMUR1 expression using siRNA, but not NMUR2 downregulation, significantly attenuated the promoting effects of NMU on calcification, osteogenic transformation and apoptosis in cacified VSMCs. Our research suggests that the role of NMU in calcification of VSMCs partially through the activation of the receptor NMUR1-ERK signaling pathway. So downregulating the expressions of NMU and NMUR1 in aortic media may be a good strategy for the treatment of MAC in CKD. - Source: PubMed
Publication date: 2026/09/13
Chang RuiWang Hong-YuCao Wen-JuanZhu Han-XuTang Rong-JieGao QingZhou Ye-BoChen Lei-Lei - Glioma is a highly aggressive brain tumor with poor prognosis and limited therapeutic options. Although temozolomide (TMZ) remains the standard chemotherapeutic agent for glioma, frequent recurrence and the development of therapeutic resistance continue to limit clinical benefit, highlighting the need for new molecular targets and treatment strategies. Here, we identify neuromedin U receptor 2 (NMUR2) as a driver of glioma progression and a potential therapeutic target. NMUR2 expression was markedly elevated in glioma tissues and positively associated with tumor grade. Functional analyses showed that NMUR2 promoted glioma cell proliferation and migration, whereas NMUR2 silencing attenuated these malignant phenotypes. Mechanistically, NMUR2 activated Gαq-dependent Ca²⁺ signaling, leading to STAT5 phosphorylation and subsequent transcriptional upregulation of the cell cycle-associated genes PIM1 and FOXM1. Drug-repurposing screening of 6,331 compounds identified NNC 05-2090 as a candidate NMUR2 antagonist. NNC 05-2090 blocked NMUR2-mediated Gαq/Ca²⁺/STAT5 signaling, which was associated with reduced PIM1 and FOXM1 expression, cell cycle arrest, and suppression of glioma growth and . In addition, combination treatment with TMZ produced synergistic anti-tumor effects in glioma models. Collectively, our findings define a previously unrecognized NMUR2/Gαq/STAT5/PIM1-FOXM1 signaling axis in glioma and support pharmacological inhibition of NMUR2 as a potential therapeutic strategy. - Source: PubMed
Publication date: 2026/07/30
Roh YunaSon TaesangHan Tae-HeeKim SarangJung EunsunHwang Jin-SeongIm Joo-YoungKang Mi-JungCho Mun JeongLim Jung HwaJung Cho-RokLee Moo-SeungCho Hyun-SooKim Dae-SooSon Mi-YoungKim Seon-YoungKim Seon-KyuBan Hyun SeungKim Jang-SeongHan Tae-Su - Residual feed intake (RFI) is an indicator of feed efficiency that reflects variation in nutrient utilization independent of growth. This study characterized physiological traits and multi-omics profiles associated with divergent RFI in small-sized meat ducks. From an initial population of 500 1-day-old ducks, a total of 420 healthy ducks were individually housed from 21 to 42 d to record feed intake, and ducks with low RFI (LRFI) and high RFI (HRFI) were identified for further analyses. During the experiment, 30 ducks per group for growth performance, 15 ducks per group for plasma biochemical and 5 per group for multi-omics. Compared with HRFI ducks, LRFI ducks showed lower feed intake, lower feed conversion ratio (FCR), and lower plasma triglyceride concentrations, whereas body weight gain did not differ between groups. Shotgun metagenomic analysis showed that LRFI ducks were enriched in Bacteroides-related lineages and had higher predicted capacities for complex carbohydrate degradation, lipid and energy metabolism, and cofactor synthesis, whereas HRFI ducks were enriched in taxa including Subdoligranulum variabile and Clostridioides difficile. Untargeted cecal metabolomics revealed distinct lipid- and bile acid-related metabolic profiles between the 2 groups, including differences in long-chain lipid species and bile acid-associated metabolites. Hypothalamic transcriptomic analysis identified differentially expressed genes related to neuropeptide signaling, serotonin biosynthesis, intracellular signaling, and inflammatory regulation, including NMUR2, TPH1, and PTK2B. Correlation analysis integrating microbial taxa, metabolites, and hypothalamic transcripts further revealed coordinated associations among these features in small-sized meat ducks with divergent RFI. Overall, variation in feed efficiency in ducks was associated with differences in cecal microbiota, metabolite profiles, and hypothalamic gene expression, and these results highlight candidate microbial taxa, metabolites, and genes for further validation. - Source: PubMed
Publication date: 2026/06/17
Geng DandanDing YifanJiang YongWang ZhixiuChen GuohongChang GuobinBai Hao - The central neuromedin U receptor 2 (NMUR2) participates in regulating neuronal activity and synaptic transmission. This study aimed to explore the functional role of NMUR2 in climbing fiber-Purkinje cell synaptic transmission in mouse cerebellar slices. - Source: PubMed
Publication date: 2026/07/30
Li Mei-RuiPiao Ri-LongZhang Xu-DongWeng Wen-CaiChu Chun-PingQiu De-Lai