LYVE1 antibody - N-terminal region (ARP46761_P050)
- Known as:
- LYVE1 (anti-) - N-terminal region (ARP46761_P050)
- Catalog number:
- arp46761_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- LYVE1 antibody - N-terminal region (ARP46761_P050)
Related genes to: LYVE1 antibody - N-terminal region (ARP46761_P050)
- Gene:
- LYVE1 NIH gene
- Name:
- lymphatic vessel endothelial hyaluronan receptor 1
- Previous symbol:
- XLKD1
- Synonyms:
- LYVE-1
- Chromosome:
- 11p15.4
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-21
- Date modifiied:
- 2015-07-22
Related products to: LYVE1 antibody - N-terminal region (ARP46761_P050)
Related articles to: LYVE1 antibody - N-terminal region (ARP46761_P050)
- Diminished lymphocyte infiltration and activation in ovarian cancer are attributable to the malignancy and irresponsiveness to immunotherapy. We show here that treatment of a murine model of ovarian cancer with recombinant tumor necrosis factor superfamily-15 (TNFSF15) results in a marked inhibition of peritoneal dissemination of the cancer cells and a substantial reduction of ascites. The treatment leads to normalization of the tumor vasculature judged by enhanced coverage of the neo-blood vessels with PDGFβ pericytes and diminished levels of the hypoxia-responsive cancer stem cell marker CD133. Additionally, the treatment gives rise to accumulation of Lyve-1 lymphatic endothelial cells and PNAd high endothelial venules (HEV) in the tumors, consistent with the formation of tertiary lymphoid structures (TLS). Moreover, the treatment results in facilitated tumor infiltration of T cells, B cells, macrophages, and dendritic cells, the latter exhibit upregulated expression of TLS-associated cytokines and chemokines, including Lt-α, Lt-β, IFN-β, TNF-α, CCL19, CCL21, CXCL13, and CXCL10. Furthermore, there is an enhanced responsiveness in TNFSF15-treated tumors toward PD-1 blockade treatment. These findings suggest that TNFSF15 is capable of facilitating vascular normalization and TLS formation, and thus promoting a reinstitution of the immune microenvironment in ovarian cancer. - Source: PubMed
Wang Jing-YingWang Yu-YingZhang Li-SongWeng Shi-TingCui Hai-YanZhang Zhi-SongLi Lu-Yuan - -related overgrowth spectrum (PROS) comprises a group of rare genetic disorders caused by de novo, mosaic, postzygotic gain-of-function mutations in the gene. These mutations arise during embryogenesis, affect multiple organ systems, and result in heterogeneous clinical phenotypes. We previously showed that primary cells derived from a PROS mouse model exhibit a metabolic shift toward aerobic glycolysis (a Warburg-like effect), accompanied by altered secretion of metabolites. Here, we observed that this metabolic reprogramming was associated with the up-regulation of key transcription factors, including cellular myelocytomatosis and hypoxia-inducible factor 1 alpha. PIK3CA hyperactivation induces a distinct microenvironment marked by metabolic dysregulation, extracellular matrix remodeling, increased cellular proliferation, elevated phosphorylated form of the histone variant H2AX levels, and enhanced macrophage infiltration, hallmarks commonly associated with increased lactate production. To further examine immune infiltration dynamics, we used a mouse model expressing a constitutively active mutation selectively in adipose tissue (Adipo), a tissue frequently affected in PROS. Single-cell transcriptomics and flow cytometry profiling revealed that macrophages adopt an immunomodulatory phenotype, with increased infiltration of TREM2 and Lyve1MHCII macrophages, along with myeloid-derived suppressor cells, and a concurrent reduction in T-cell populations. These immune alterations parallel those observed in tumor microenvironments and may contribute to tissue overgrowth and impaired immune surveillance. Multiplex immunofluorescence analysis of tissue samples from individuals with PROS confirmed these findings, underscoring the translational relevance of the mouse model. Together, our results demonstrate that mutations in PROS profoundly remodel the tissue microenvironment and reprogram macrophage function in a manner reminiscent of tumor biology. - Source: PubMed
Publication date: 2026/05/13
Galasso IlariaBayard CharlesBlériot CamilleLadraa SophiaKong Wan TingCassaca RubinaHoguin ClémentProtic SanelaMegret JérômeGoudin NicolasSignolle NicolasScoazec Jean-YvesNemazanyy IvanBalducci EstelleVillarese PatrickAsnafi VahidFraitag SylvieVenteclef NicolasGinhoux FlorentCanaud Guillaume - The omentum is a vascularized, immune-active tissue with regenerative potential, particularly when activated by intraperitoneal stimuli. Its secreted factors may promote lymphangiogenesis, offering a novel approach to lymphedema treatment. - Source: PubMed
Publication date: 2026/05/29
Hojo MasahiroSeo DongkyungIto RiriIshikawa KosukeMiura TakahiroFunayama EmiYamamoto YuheiMaeda Taku - During alcoholic liver disease (ALD), alcohol induces functional impairment of LSECs, thereby exacerbating inflammation and fibrosis. This research aims to investigate whether P38γ drives aerobic glycolysis in LSECs via the PFKFB3 signaling axis, thereby participating in the progression of ALD. - Source: PubMed
Publication date: 2026/05/27
Zhang QianYang MiaoZhang YunHu Jing - This study aims to analyze the dynamic changes in lymphatic endothelial cell (LEC) markers during the progression of intervertebral disk degeneration (IDD) and to investigate their association with the progression of IDD. In this study, intervertebral disk (IVD) specimens were first collected from patients who underwent open lumbar fusion surgery for spinal fractures (control group, = 10) and lumbar disk herniation (IDD group, = 10). Concurrently, a mouse IDD model was established, and IVD specimens were collected from mouse in the Sham group and the IDD group 1, 3, and 6 weeks after modeling ( = 5 per group at each time point). Pathological morphological changes in human and mouse IVD specimens were observed using Hematoxylin and Eosin (H&E) and Masson's Trichrome staining. The degree of degeneration in the mouse IVD specimens was quantified using a histopathological scoring system. Subsequently, real-time quantitative polymerase chain reaction (RT-qPCR), immunohistochemistry (IHC), and immunofluorescence (IF) staining were employed to examine LEC markers in IVD tissue, including lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1), podoplanin (PDPN), prospero homeobox protein 1 (PROX-1), and vascular endothelial growth factor receptor 3 (VEGFR-3), as well as matrix metabolism-related markers such as matrix metalloproteinase 13 (MMP-13) and collagen II (Col II). Finally, we performed Spearman's rank correlation analysis between the histopathological scores of all mouse IVD specimens and the corresponding expression levels of LEC markers. In human IVD tissue, expression levels of LYVE-1, PDPN, PROX-1, and VEGFR-3 were extremely low in the normal group. In contrast, expression of these markers was significantly upregulated in the IDD group. In the mouse IDD model, compared with the Sham group at the same time point, the IDD group exhibited higher histopathological scores in IVD tissue, accompanied by upregulation of LYVE-1, PDPN, PROX-1, and MMP-13, as well as downregulation of Col II. In-depth analysis revealed that these differences between the Sham and IDD groups were not static but exhibited a dynamic pattern of increasing magnitude over time. Concurrently, as the modeling period progressed, the histopathological scores of mouse IVD in the IDD group, as well as the expression levels of LYVE-1, PDPN, PROX-1, and MMP-13, showed a progressive upward trend, while Col II expression progressively decreased. In addition, Spearman's rank correlation analysis revealed that the expression levels of LYVE-1, PDPN, and PROX-1 in mouse IVD tissue were all significantly positively correlated with histopathological scores. In the process of IDD, the dynamic upregulation of LEC markers is highly consistent with its severity in the time dimension. At the same time, there was also a significant positive correlation between the expression level of LEC markers and the severity of IDD. Taken together, these findings suggest that the dynamic upregulation of LEC markers may be potentially associated with the pathological progression of IDD. - Source: PubMed
Publication date: 2026/04/27
Zhang QiangLin MaoqiangYan ShishunHuang FeiZhou Haiyu