VEGF165, Human Protein
- Known as:
- VEGF165, Human Protein
- Catalog number:
- z02689-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- VEGF165 Human Protein
Related genes to: VEGF165, Human 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
- Gene:
- NRP2 NIH gene
- Name:
- neuropilin 2
- Previous symbol:
- -
- Synonyms:
- VEGF165R2
- Chromosome:
- 2q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-23
- Date modifiied:
- 2015-09-01
Related products to: VEGF165, Human Protein
Related articles to: VEGF165, Human Protein
- Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy in which liver metastasis represents the principal determinant of poor prognosis. Although metastatic dissemination is thought to be driven by highly plastic tumor cells, the transcriptional features of liver metastasis-related initial cell (LMIC) and its spatial crosstalk with the metastatic microenvironment during PDAC progression remain incompletely defined. - Source: PubMed
Publication date: 2026/06/16
Li YangLiu Ya-DieJiang Zhi-YingLu Hong-Xiang - Neuropilins (NRPs), particularly NRP-1, are multifunctional co-receptors involved in neuroinflammatory and neuroprotective processes. Altered NRP expression has been observed in multiple sclerosis (MS) lesions and peripheral circulation, suggesting early involvement in disease progression. This review addresses the dual role of NRPs in MS and experimental autoimmune encephalomyelitis (EAE), emphasizing expression patterns, signaling pathways, and therapeutic interventions. NRP-1 is expressed by endothelial cells, microglia, and macrophages, while Sema3A, a key ligand, is produced by reactive astrocytes and contributes to a non-regenerative microenvironment. NRP-1 is involved in regulating blood-brain barrier (BBB) integrity, contributes to leukocyte trafficking, and modulates inflammatory signaling via the IFN-γ-STAT1-CXCL10 axis. In EAE, endothelial-specific NRP-1 deletion reduces disease severity, demyelination, and immune infiltration. Immunologically, NRP-1 governs interactions among T cells, dendritic cells, and macrophages, facilitating regulatory T cell (Treg) function and peripheral tolerance. Trogocytosis-mediated NRP-1 transfer from dendritic cells to T cells and polysialylated NRP-2 on dendritic cells further influence immune modulation. Tuftsin, a tetrapeptide targeting NRP-1, promotes anti-inflammatory microglial polarization and Treg activation, improving EAE outcomes. Therapeutic interventions, such as Bu-Shen-Yi-Sui Capsule (BSYSC), FTX-101 (a Sema3A-NRP-1 inhibitor), and tuftsin restore BBB function, reduce inflammation, enhance remyelination, and improve clinical scores. NRP-1 signaling thus exhibits context-dependent dual roles: promoting inflammatory cascades while enabling neuroprotection through regulatory immune networks and oligodendrocyte precursor cell support, highlighting NRP-1 as a therapeutic target in MS. - Source: PubMed
Publication date: 2026/05/28
Goleij PouyaBabamohamadi MehreganHeidari Mohammad MahdiKhazeei Tabari Mohammad AminAbolfazli SajadMohammadi SoroushMajma Sanaye PanteaArefnezhad RezaAschner MichaelKhan HaroonRezaei Tavirani MostafaMovafagh Abolfazl - H2A.Z is a conserved histone variant that plays essential roles in various DNA-templated processes. Although both histone H3 acetylation and H2A.Z enrichment levels are important epigenetic marks that regulate gene expression, their functional interplay remains incompletely understood. This study integrates genetic, molecular, and genomic approaches to investigate how GCN5 - a conserved histone acetyltransferase - couples H3 acetylation with H2A.Z dynamics in Arabidopsis, and how this interplay shapes gene expression and plant development. We found that the increase in H2A.Z levels observed in the nrp1-1 nrp2-2 double mutant (defective in NAP1-RELATED PROTEIN 1 and 2) suppresses the morphological and molecular phenotypes of gcn5-7. Conversely, H2A.Z-depleted mutants aggravate these phenotypes of gcn5-7/c1. Notably, the reduction in H3 acetylation caused by GCN5 loss promotes the decrease in H2A.Z level, and this requires the function of NRPs. The integrated analysis of ChIP-Seq and RNA-Seq data revealed that the differential gene expression in the GCN5 deletion mutant is correlated with H2A.Z distribution and enrichment levels. Moreover, H2A.Z overaccumulation at genes in the nrp1-1 nrp2-2 mutant promotes increased H3 acetylation in a GCN5-dependent manner. In conclusion, our findings support a model in which GCN5-mediated H3 acetylation shapes H2A.Z occupancy, linking chromatin dynamics to precise gene expression control and proper plant development. - Source: PubMed
Publication date: 2026/04/26
Su YingpeiHu QinLiu MinQian WeiyeXu ChaoXu JunjieAusin IsraelWang Yafei - Cardiometabolic and inflammatory pathways may play important roles in Alzheimer's disease (AD) pathogenesis contributing to neuronal dysfunction even in the absence of cognitive symptoms. Our objective is to characterize proteomic signatures of these pathways in AD. - Source: PubMed
Publication date: 2026/03/25
Hajjar Ihab MNeal ReemSingh NamrataYang ZhiyiObideen MalikShah Amil MDammer Eric B - The guinea pig with guinea pig cytomegalovirus (GPCMV) is the only small-animal model for congenital cytomegalovirus, a leading cause of cognitive impairment and hearing loss in newborns. GPCMV encodes human cytomegalovirus (HCMV) homologues of viral entry glycoprotein complexes, which are neutralizing-antibody vaccine targets. As with HCMV, GPCMV has two pathways of cell entry (direct and endocytic). Specific viral gH/gL-based complexes are necessary for receptor interaction and cell entry: gH/gL/gO trimer (direct) and pentamer complex (PC) (endocytic). Both pathways also require gB as the fusogenic protein. Direct GPCMV cell entry requires platelet-derived growth factor receptor alpha (PDGFRA), but an endocytic PC receptor remains unknown. We hypothesized that cellular knockout of direct and endocytic receptors would completely block infection, which cannot be achieved by gB-based antibodies. Candidate receptors including neuropilin proteins (NRP1, NRP2) and CD147 present on all established guinea pig cell lines were selected based on importance as common virus receptors or in fetal development. Results demonstrated that NRP2 interacted with PC, unlike NRP1 or CD147, in immunoprecipitation assays and eliminated NRP1/NRP2 heterodimer receptor interaction. The viral trimer only interacted with PDGFRA. Double knockout of PDGFRA/NRP2 completely blocked GPCMV infection. In contrast, the CD147/PDGFRA double knockout had limited GPCMV inhibition, and the single knockout of CD147 had no impact. Knockout of the various receptors had no effect on control HSV-1 infection. Ectopic expression of guinea pig cell receptors restored GPCMV infection but not human NRP2/PDGFRA, indicating a basis for the species-specific barrier for GPCMV and HCMV infection. Overall, results increase the translational relevance of GPCMV for the development of CMV intervention strategies. - Source: PubMed
Qin YushuChoi K YeonEl-Hamdi NadiaMcGregor Alistair