Human Furin ELISA kit
- Known as:
- Human Furin Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- lf-ek50799
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Abfrontier
- Gene target:
- Human Furin ELISA kit
Related genes to: Human Furin ELISA kit
- Gene:
- FURIN NIH gene
- Name:
- furin, paired basic amino acid cleaving enzyme
- Previous symbol:
- PCSK3, FUR, PACE
- Synonyms:
- SPC1
- Chromosome:
- 15q26.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-08
- Date modifiied:
- 2016-02-22
Related products to: Human Furin ELISA kit
Related articles to: Human Furin ELISA kit
- Neuropilin-1 (NRP1) is a developmentally conserved cell surface receptor that functionally acts to bind various ligands like class 3 semaphorins and several members of the VEGF family to engage in different signaling pathways that control cell migration and motility. Due to its widespread expression, NRP1 is implicated in immune function, axonal guidance, viral entry, tumor progression and angiogenesis. NRP1 is dysregulated across multiple cancer types and promotes tumor progression in a context-dependent manner in tumor cells and the tumor microenvironment, including endothelial, stromal, and immune-cell compartments. NRP1 is also involved in different autoimmune disorders, anosmia, and cardiovascular disorders. Phage display studies revealed that peptides containing C-terminal CendR motifs engage NRP1 for tissue penetration. Apart from cell-penetrating peptides, monoclonal antibodies against NRP1 also present a promising target for cancer therapeutics. Importantly, NRP1 in SARS-CoV-2 infection act as an auxiliary host factor, and furin cleavage of the viral spike protein exposes a C-terminal CendR motif that can bind NRP1, thereby facilitating viral entry. However, NRP1 is not an independent receptor comparable to ACE2, thus, NRP1-targeted antiviral strategies need further investigations. Given the above, the review provides comprehensive narrative of different signaling mechanisms of NRP1 in different diseases and how this cell surface receptor can be utilized in various therapeutic approaches to combat these diseases. - Source: PubMed
Publication date: 2026/09/15
Aashaq SabreenaRakhshan RabiaRafiq AsmaAli MahvishBeigh Mushtaq A - Fluoroquinolones (FQs) are a cornerstone of most all-oral, shorter regimens endorsed by the World Health Organization for the treatment of rifampicin-resistant or multidrug-resistant tuberculosis (RR/MDR-TB). Knowledge of resistance to FQs can help guide regimen selection at the point of care. In settings where rapid testing for FQ resistance is unavailable, prediction models could support treatment decisions by identifying FQ resistance based on patient characteristics observable at the point of care. These prediction models have been typically developed and evaluated within a single country, and their generalizability across different geographic settings is unclear. - Source: PubMed
Publication date: 2026/09/15
Shao TianfangNeves Mariana RFranke MollyMitnick CaroleFurin JenniferCohen TedYaesoubi Reza - Fibroblast growth factor 23 (FGF23), a bone-derived hormone, regulates phosphorus (P) homeostasis by modulation of renal P excretion and vitamin D metabolism. Physiological roles of FGF23 have been mainly characterized in human disorders of P metabolism and murine models. This study aimed to validate roles of FGF23 in P homeostasis in a large animal, healthy swine model. Juvenile pigs fed a low-P diet (LP) for 4 d were fasted overnight then fed a high-P diet (HP) for 5 d. Blood was collected to determine plasma concentrations of P, calcium (Ca), PTH, and vitamin D metabolites, and urine was collected to assess P and Ca concentrations. Femur and kidney tissues were collected to assess gene and protein expression related to FGF23 synthesis, signaling, and vitamin D metabolism. The rapid increase in plasma P (5 to 18 mg/dL) within 12 h of HP intake was lagged by increased urinary P. At maximal urinary P concentration (108 h), plasma P had returned to physiological ranges. The initial increase in plasma PTH with HP intake returned to baseline levels by 108 h. At 108 h, HP consumption upregulated bone mRNA expression (250-fold increase relative to LP). Sodium-phosphate co-transporters ( and ) mRNA and NaPi2a protein expression decreased with HP intake, consistent with FGF23-mediated phosphaturia, independent of circulating PTH. Bone mRNA expression of post-translational FGF23 regulators ( and ) was unaffected by HP consumption, whereas kidney FGF23 receptors ( and ) slightly increased. High P intake downregulated renal 1α-hydroxylase () mRNA expression at 108 h, consistent with decreased circulating 1,25(OH)D concentrations. In conclusion, HP consumption stimulated bone expression and renal adaptive responses in healthy pigs, consistent with roles of FGF23-mediated phosphaturia and regulation of vitamin D metabolism for maintenance of P homeostasis, as previously described in humans and rodents. - Source: PubMed
Publication date: 2026/08/08
Grez-Capdeville MariolaKokinos Brittney PAmundson Laura ACrenshaw Thomas D - Paramyxoviruses such as respiratory syncytial virus (RSV) and human parainfluenza virus 3 (HPIV3) spread in the airway by releasing virions and by forming syncytia. Spread phenotypes are typically attributed to the fusion protein cleavage site, yet it remains unclear whether, and if so, how, host protease context biases syncytial versus cell-free spread. We compared RSV and HPIV3-two closely related viruses with overlapping epithelial tropism but distinct F cleavage-site composition (polybasic, furin-type for RSV versus a distinct, less polybasic cleavage-site motif for HPIV3)-in respiratory cell lines and primary airway cells under defined protease conditions. In multi-cycle infections, furin-dominant, trypsin-like-low environments produced the largest syncytia, whereas trypsin-like-high environments favored smaller syncytia and more cell-free spread. Adding exogenous TMPRSS2 shifted HPIV3 toward cell-free spread with minimal impact on RSV. Using serine protease inhibitors (SERPINs) as protease-selective inhibitors, we show that inhibiting specific proteases restricts infection and remodels syncytium architecture, consistent with protease switching. Together, these results indicate that host protease availability is a reversible control point for respiratory virus dissemination. This framework has direct implications for protease-targeting therapeutics. Selective inhibition may reroute fusion activation and shift spread modality toward more syncytia-associated cytopathic effects rather than uniformly suppressing dissemination. - Source: PubMed
Publication date: 2026/09/14
Rodriguez Galvan Joaquinde Vries MarenBelblidia ShirazFisher AshleyDittmann Meike - Recently, research has revealed that the Golgi apparatus is involved in the development process of cancer; however, the specific effect of Golgi apparatus-related genes (GAGs) in lung adenocarcinoma (LUAD) remains unclear. This study aims to construct a more concise and practical risk model in LUAD using GAG. - Source: PubMed
Publication date: 2026/07/21
Li HaoranCao PeijunLi JialongWang PeiyuYi Ying