Ask about this productRelated genes to: LYVE1 antibody
- 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
Related articles to: LYVE1 antibody
- Almost all human tissues are supplied with lymphatic vessels, yet histological structure and function of lymphatic vessels is still elusive. Most immunocytochemical studies have been performed with the routinely formalin-fixed and paraffin-embedded tissue. This study aimed to investigate lymphatic and blood vessels immunocytochemically with frozen sections to explore the masked lymphatic and blood vessels in the routinely processed normal tissues. Several normal monkey tissues were frozen in liquid propane, and frozen sections were immunostained for lymphatic and blood vessels using LYVE-1 for lymphatic vessels and von Willebrand factor for blood vessels. In the liver, sinusoids were immunostained panlobularlly for LYVE-1 compared to LYVE-1 immunostaining limited in the pericentral lobe with the routinely processed liver. In the Jejunal villi, lacteals were surrounded by scattered mall venous capillaries. In the large intestines, a few longitudinal lymphatic vessels were detected in lamina propria. Pancreatic islets were surrounded by baskets of rich venous capillaries. Glomerular capillaries were diffusely positive for von Willebrand factor, suggesting leaking capillaries for von Willebrand factor. Prostate had scattered lymphatic and numerous blood vessels in the stroma with nerve bundles in the fibrous capsule. Many lymphatic and blood vessels were immunostained only in frozen sections, which were not immunostained in the routinely processed tissues. Routine processing masks antigen sites of lymphatic and blood vessels. Therefore, immunocytochemical staining with frozen sections is superior to routinely embedded tissues and this immunostaining would further add histopathological information on tumor spread and liver and kidney biopsies. - Source: PubMed
Publication date: 2026/07/31
Tomita TatsuoMah Kunie - Stroke is a well-established risk factor for dementia, and many patients with Alzheimer's disease exhibit mixed neuropathology that includes both ischemic injury and amyloid-β (Aβ) accumulation. Breathing disturbances, such as apnea, have also been linked to cognitive dysfunction and accelerated dementia progression. - Source: PubMed
Publication date: 2026/08/17
Zhang Yu-XingEl Hamamy AhmadIqbal ZahidRanjan AryaSumani DestinyDe Souza Karienn ALee JuneyoungMarrelli SeanMcCullough Louise DLi Jun - Here, we report the identification of a previously unrecognized population of tumor-induced podoplanin-positive (PDPN) cells in clear-cell renal cell carcinoma (ccRCC) that exhibit features of under-differentiated lymphatic endothelial cells (LECs). These PDPN cells lack a complete repertoire of canonical LEC markers, including VE-cadherin, LYVE1, and VEGFR3, and fail to form functional lymphatic vessels, indicating a dysplastic phenotype. We termed these cells dysLECs and found that these cells are induced by BMP10 produced specifically by tumor cells. In turn, dysLECs secrete CXCL13, which promotes tumor cell proliferation and metastasis. Ligand-receptor analyses revealed a highly tumor-specific reciprocal signaling circuit: kidney tubule cells deficient in the von Hippel-Lindau () tumor suppressor gene uniquely express BMP10, a TGF-β family cytokine, whereas its receptor ALK1 is restricted to dysLECs; conversely, dysLECs produce CXCL13, while mutant kidney tubule cells uniquely express its receptor, CXCR5. Pharmacological inhibition of ALK1 reduced CXCL13 production and suppressed the hyperplastic phenotype of mutant tumor cells in vivo, whereas BMP10 neutralization inhibited tumor growth and metastasis in an orthotopic ccRCC xenograft model. Collectively, these findings identify a dysplastic population of PDPN lymphatic-like endothelial cells and define a tumor-specific BMP10-CXCL13 signaling axis that drives ccRCC progression, uncovering a previously unrecognized therapeutic vulnerability in this disease. - Source: PubMed
Publication date: 2026/08/04
Nguyen Tuong-ViNguyen-Tran Hieu-HuyNguyen Thi-NgocHsu Tien - - Source: PubMed
Publication date: 2026/08/04
Gao YuxiangLi LanRao XiaohuaZhao LutingXiao Lin - Mitochondria activate immunity, but the role in cancer is unknown. Here, we report that transgenic expression of Parkin, a regulator of mitochondrial fitness, induces inflammation and interferon (IFN) gene signatures, suppresses prostate cancer formation and generates CD8 and CD20 intraprostatic immune aggregates. These had hallmarks of mature tertiary lymphoid structures (TLS), expressing markers of B cell maturation (CXCL13, CCL21), germinal center formation (BCL6, GL7), mature dendritic cells (MHC-II/CD208) and high endothelial venules (LYVE-1). Parkin TLS showed high Ig gene expression, recruitment of CXCR5 follicular T helper cells and expansion of CD69/KLRG1 effector T cells. Conditioned medium from Parkin-positive cells expanded memory B and plasma cells, increased IgG1 production, and sustained B and T cell migration. Finally, conditional expression of Parkin induced TLS formation, upregulated Ig chains and inhibited prostate cancer growth, in vivo, whereas Parkin reconstitution in IFNAR1, CD8 or CD20 knockout mice had no effect. Therefore, mitochondrial immunity orchestrates antitumor responses, and TLS formation contributes to tumor suppression. - Source: PubMed
Publication date: 2026/08/07
Perego MichelaKossenkov Andrew VGhosh Jagadish CCamisaschi ChiaraTursi Nicholas JWeiner David BAltieri Dario C