NRP1 _ Neuropilin_1 Protein
- Known as:
- NRP1 _ Neuropilin_1 Protein
- Catalog number:
- 10011-H02H
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- NRP1 _ Neuropilin_1 Protein
Related genes to: NRP1 _ Neuropilin_1 Protein
- Gene:
- NRP1 NIH gene
- Name:
- neuropilin 1
- Previous symbol:
- -
- Synonyms:
- NRP, VEGF165R, CD304
- Chromosome:
- 10p11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-23
- Date modifiied:
- 2016-10-05
Related products to: NRP1 _ Neuropilin_1 Protein
Related articles to: NRP1 _ Neuropilin_1 Protein
- In recent years, chilled chicken has emerged as a new market trend. Skin feather follicle density, an important carcass appearance trait characterized by "fine and dense" features, is increasingly preferred by consumers. This study analyzed hair follicle density in the leg and back regions of 1,382 yellow-feathered broiler. The results showed that back feather follicle density was significantly higher than that of the leg (P < 0.01), with a significant positive correlation between the two regions. Meanwhile, feather follicle density in both the leg and back showed negative correlations with abdominal fat weight, body weight, dressed weight, full-eviscerated weight, semi-eviscerated weight. mRNA-seq analysis of leg and back skin tissues from four individuals identified differentially expressed genes (DEGs) affecting feather follicle density traits across different anatomical locations, including GTF2A1, RPSA2, COX3, and CNKSR2. Furthermore, Genome-Wide Association Study (GWAS) analysis of 505 chickens identified 223 single-nucleotide polymorphisms (SNPs) significantly associated with leg feather follicle density and 107 SNPs associated with back feather follicle density, including candidate SNPs such as C19014967G, C17514817T, G1847078C, and C34389948G, as well as candidate genes including ELF5, MAP3K1, HIF1AN, and SERPINF1. mRNA-seq analysis of skin tissues from high and low feather follicle density groups in the leg (TG vs. TD) and back (BG vs. BD) identified 541 leg-related DEGs and 1,130 back-related DEGs, respectively. Joint analysis of TG vs. TD and BG vs. BD revealed 174 commonly DEGs, including candidate genes such as NSA2, IGF2, RPL17, and NRP1. Through integrated GWAS and RNA-seq analysis, five genes significantly associated with leg feather follicle density and twelve candidate genes associated with back feather follicle density were identified. Notably, individuals with the AA genotype at the SERPINF1 SNP locus Chr19:5636537 showed extremely significantly higher feather follicle density than those with the GG genotype, and both mRNA and protein expression levels of SERPINF1 were significantly upregulated in high feather follicle density individuals. - Source: PubMed
Publication date: 2026/07/31
Chao XiaohuanChen ShuyaOuYang TongYe ChutianChen JieWu JiongwenMa XueRongLiu AijunLiang WeimingCui TianxiXia LuluXiao KaifanHe YouchengZhang XiquanFang ChengLuo Qingbin - Sepsis-induced cardiac dysfunction is a primary contributor to mortality, and microRNAs (miRNAs) are recognized as crucial mediators in sepsis pathogenesis. This study aims to identify the key regulatory miRNAs involved in cardiac dysfunction stemming from sepsis. We developed a rat model of sepsis using cecal ligation and puncture (CLP). Myocardial tissue from these rats underwent miRNA sequencing and transcriptome sequencing. Echocardiography was utilized to assess heart function, while cardiac damage was evaluated through HE staining, analysis of inflammatory factors, and detection of tissue injury biomarkers. To model inflammation-induced cardiomyocyte injury, rat cardiomyocyte H9C2 cells were treated with lipopolysaccharide (LPS). Cellular viability was determined using CCK8, and apoptosis was assessed via TUNEL staining and flow cytometry. Oxidative stress levels were analyzed by flow cytometry, and related marker levels were quantified by ELISA. Our results demonstrated that the CLP group displayed substantial cardiac dysfunction, myocardial injury, and elevated inflammatory factor levels. MiR-221-5p was found to be upregulated in both the in vivo and in vitro models. Overexpression of miR-221-5p reduced cardiomyocyte survival while increased apoptotic activity and oxidative stress in LPS-stimulated H9C2 cell. Mechanistically, Neuropilin-1 (NRP1) was identified as a target of miR-221-5p. The cardioprotective effect of miR-221-5p inhibition was reversed by NRP1 knockdown. Furthermore, in vivo administration of a miR-221-5p antagomir mitigated cardiac dysfunction and myocardial damage associated with septic conditions. In conclusion, our findings indicate that miR-221-5p exacerbates septic cardiomyopathy by negatively regulating NRP1, suggesting that the miR-221-5p/NRP1 pathway could represent a novel therapeutic strategy for sepsis-related heart complications. - Source: PubMed
Zhu YikeWang JinjunZhang LingwenYao XiaozhouCai Xingjun - The specific role of Neuropilin-1 (NRP1) and its link to oxidative stress in Non-Small Cell Lung Cancer (NSCLC) progression remains unclear. - Source: PubMed
Publication date: 2026/08/11
Yang YaLi YingZhao YongjuanFeng WenwenYu PengchengLi ShanDing Zongli - Coronavirus disease 2019 (COVID-19) survivors frequently experience a wide range of symptoms known as post-acute sequelae of SARS-CoV-2 (PASC) or long COVID. Importantly, complications arising from microvascular dysfunction, blood-brain barrier (BBB) disruption, and chronic neuroinflammation have been implicated in driving PASC within the central nervous system (CNS), known as neuro-PASC. Notably, people with HIV (PWH), who suffer from chronic neuroinflammation, BBB impairment, and glial cell dysfunction, collectively known as neuro-HIV, are generally at higher risk of neuro-PASC. The overlap between neuro-PASC and neuro-HIV raises concerns that HIV and SARS-CoV-2 co-infection may exacerbate neurological dysfunctions among PWH. In this study, using an in-vitro cell culture model, we examine the effects of HIV and SARS-CoV-2 mono- and co-infection in microglia, astrocytes, and pericytes. Our results demonstrated that majority of brain cell types support SARS-CoV-2 replication, in the presence and absence of HIV infection. Furthermore, in both mono- and co-infected cells, there were varying degree of up- and downregulation of SARS-CoV-2 host cell entry factors, such as ACE2, TMPRSS2, NRP1, and TRIM28, and inflammatory cytokines including IL-6, TNF-α, and IL-1β. Moreover, conditioned media collected from HIV, SARS-CoV-2, and HIV/SARS-CoV-2 co-infected astrocytes and pericytes were shown to be neurotoxic. Additionally, proteomic analysis has revealed a unique set of proteins significantly up/down regulated in HIV/SARS-CoV-2 co-infected astrocytes and pericytes. The gene set enrichment analysis of these proteins indicates dysregulation of lipid, energy, and immune metabolism pathways linked to neurodegenerative disorders like Alzheimer's, Parkinson's, Huntington's disease, and amyotrophic lateral sclerosis. These in-vitro findings indicate that astrocytes and pericytes from HIV/SARS-CoV-2 co-infection exhibit altered protein expression profiles, implicating dysregulated signaling pathways associated with neurodegenerative dysfunction. - Source: PubMed
Acharya ArpanThurman MichellieSutar DebapriyaOlasunkanmi Oluwatayo IsraelMalik Johid RDyavar Shetty RaviVégvári ÁkosByrareddy Siddappa N - Membrane-bound neuropilin-1 (Nrp-1) has been implicated as a regulator of insulin resistance-related lipid metabolism, but little is known about its circulating form, soluble Nrp-1 (sNrp-1), in a metabolic context. Here we investigated the association between plasma levels of sNrp-1 and metabolic variables in 501 participants from the Prospective investigation of Obesity, Energy and Metabolism (POEM) study. Metabolic phenotyping included blood sampling, dual energy X-ray absorptiometry scan, magnetic resonance imaging for fat distribution, and a glucose tolerance test. Associations were examined using linear regression models and Spearman's rank correlation. Plasma sNrp-1 levels were inversely associated with levels of total fatty acids, triglycerides and lactate, and positively associated with markers of insulin sensitivity. In human Simpson-Golabi-Behmel Syndrome (SGBS) adipocytes, we showed that treatment with recombinant Nrp-1 reduced phosphorylation of hormone-sensitive lipase in the basal state and attenuated isoproterenol-stimulated glycerol release, a measure of total lipolytic activity. Based on these findings, we thus postulate that sNrp-1-mediated suppression of lipolysis could explain our observed association between plasma sNrp-1 and a favorable lipid profile in humans. Further studies are warranted to establish causality and to clarify the role of sNrp-1 in promoting insulin sensitivity in human adipose tissue. - Source: PubMed
Publication date: 2026/08/05
Fryk EmanuelSilva Vagner Ramon RodriguesBauzá-Thorbrügge MarcoStrindberg LenaKullberg JoelAhlström HåkanWabitsch MartinFischer-Posovszky PamelaPerkins RosieVujicic MilicaAsterholm Ingrid WernstedtLind LarsJansson Per-Anders