Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
Weitere Synonyme anzeigen
Wählen Sie die gewünschte Spezies
Long noncoding RNA ANRIL regulates endothelial cell activities associated with coronary artery disease by up-regulating CLIP1, EZR, and LYVE1 genes
The mRNA high expression levels of both podoplanin and LYVE-1 genes had a statistically significantly higher rate of LN metastasis (p<0.01) and histological grade (p<0.01 for podoplanin, p<0.05 for LYVE-1).
LYVE1 was up-regulated in the malignant Middle Cerebral Artery Infarction.
this study shows up-regulation of LYVE-1 expression in the fetal circulation of conducting and exchange villi of HIV-infected pre-eclamptics
Dendritic cells (DCs) docked to the basolateral surface of lymphatic vessels and transited to the lumen through hyaluronan-mediated interactions with the lymph-specific endothelial receptor LYVE-1. Targeted deletion of the gene Lyve1, antibody blockade or depletion of the DC hyaluronan coat not only delayed lymphatic trafficking of dermal DCs but also blunted their capacity to prime CD8(+) T cell responses in LNs.
These findings reveal binding is dependent not just on clustering but also on the biochemical properties of LYVE-1 homodimers. They also mark LYVE-1 as the first Link protein superfamily member requiring covalent homodimerization for function and suggest the interchain disulfide acts as a redox switch in vivo.
LYVE1 expression is significantly upregulated in human masticatory mucosa during wound healing
Immunostaining analyses in psoriasis skin lesions suggested that the ectodomain shedding of LYVE-1 occurred in lymphatic vessels undergoing chronic inflammation. These results indicate that the ectodomain shedding of LYVE-1 might be involved in promoting pathological lymphangiogenesis.
These results demonstrate the prerequisite of a critical LYVE-1 threshold density and show that hyaluronan binding may be elicited in lymphatic endothelium by surface clustering with divalent LYVE-1 mAbs.
We have established a novel, three-protein biomarker panel that is able to detect patients with early-stage pancreatic cancer in urine specimens:LYVE-1, REG1A, and TFF1 were selected as candidate biomarkers
Data (including data from studies in knockout mice) suggest LYVE1 mediates adhesion of group A Streptococci (GAS) to lymphatic vesicular endothelium via capsular hyaluronan; this appears to be critical factor for lymphatic trafficking of GAS in vivo.
High expression of LYVE-1 is associated with atherosclerotic arteries.
High LYVE expression is associated with visceral pleural invasion and lymphatic thromboembolism in non-small-cell lung cancer.
Data indicate that detection of lymphatic vascular invasion (LVI) can be optimized by specific D2-40 or LYVE-1 staining.
High-low cell surface HA content of tumor cells through the interaction with LYVE-1 leads to adhesion differences.
FGF2 binds to LYVE-1 with a higher affinity than any other known LYVE-1-binding molecules, such as hyaluronan or PDGF-BB. Glycosylation of LYVE-1 is important for FGF2 binding.
CRSBP-1-associated fibrillar structures are identical to the ER network as evidenced by the co-localization of CRSBP-1 and BiP in these cells
LYVE-1 may have value as predictor of outcome in neuroblastoma
Significant correlation between LYVE-1 and Prox-1 expression was observed in non-small cell lung cancer. Expression was also correlated with lymph node metastasis.
LYVE-1, VEGFR-3 and CD44 all play an important role in lymphangiogenesis, invasion and metastasis
This study has unveiled a hitherto unknown homeostatic contribution of arterial LYVE-1(+) macrophages through the control of collagen production by smooth muscle cells and has identified a function of LYVE-1 in leukocytes.
Study in metastatic MDA-MB-231 xenograft models shows that LYVE-1 is involved in primary tumor formation and metastasis, and it may be a promising molecular target for cancer therapy.
lymphatic vessel endothelial hyaluronan receptor-1 (LYVE1) is identified as a marker of yolk sac (YS) endothelium and definitive hematopoietic stem and progenitor cells.
the LYVE-1-expressing cells might be involved in the uptake of hyaluronan and other waste products as well as foreign particles circulating in the blood and lymph while participating in the subsequent degradation in relay with adjacent macrophage populations.
Immunostaining analyses in VEGF-A transgenic skin suggested that the ectodomain shedding of LYVE-1 occurred in lymphatic vessels undergoing chronic inflammation. These results indicate that the ectodomain shedding of LYVE-1 might be involved in promoting pathological lymphangiogenesis.
Endogenous hyaluronan on the surface of macrophages can engage LYVE-1, facilitating their adhesion and transit across lymphatic endothelium.
MT1-MMP directly cleaves LYVE-1 on lymphatic endothelial cells to inhibit LYVE-1-mediated lymphangiogenic responses and restrains the production of VEGF-C.
Data (including data from studies in knockout mice) suggest Lyve1 mediates adhesion of group A Streptococci (GAS) to lymphatic vesicular endothelium via capsular hyaluronan; this appears to be critical factor for lymphatic trafficking of GAS in vivo.
Data show that the expression of lymphatic vessel endothelial hyaluronan receptor 1 (LYVE 1) was similar with vascular endothelial growth factor C (VEGF-C), but its peak appeared 1-2 d later than that of VEGF-C.
LMW-HA may play a critical role in the processes required for lymphangiogenesis through interactions with its receptor LYVE-1 and triggering intracellular signal cascades.
Studied the specific targeting property of lymphatic vessel endothelial hyaluronan receptor-1 binding polyethylene glycol-coated ultrasmall superparamagnetic iron oxide (LYVE-1-PEG-USPIO) nanoparticles to mouse lymphatic endothelial cells.
Reelin-deficient mice showed abnormal collecting lymphatic vessels, characterized by a reduced number of SMCs, abnormal expression of lymphatic capillary marker lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1), and impaired function
report intact CD31(+) corneal lymphatic capillary endothelial cells that do not express LYVE-1. The number of LYVE-1(-) gaps initially increased until 8 wk of age but was significantly reduced in aged mice.
Adrenomedullin and SB431542 enhance the induction of LYVE-1-positive endothelial cells during late phase differentiation.
CRSBP-1 ligands induce disruption of VE-cadherin-mediated intercellular adhesion and opening of intercellular junctions in lymphatic endothelial cell.
Expression of lymphatic endothelium-specific hyaluronan receptor LYVE-1 in the developing mouse kidney
the expression of lymphatic vessel endothelial hyaluronan receptor-1 is dramatically reduced early in Lama2-deficient muscle pathogenesis
This study provides the first evidence that the hyaloid vascular system contains a LYVE-1(+) cellular component in both physiological and pathologic conditions.
LYVE-1 is not exclusive to the lymph vessels
CRSBP-1 plays a role in autocrine regulation of cell growth mediated by growth regulators containing cell surface retention sequence.
This gene encodes a type I integral membrane glycoprotein. The encoded protein acts as a receptor and binds to both soluble and immobilized hyaluronan. This protein may function in lymphatic hyaluronan transport and have a role in tumor metastasis.
lymphatic vessel endothelial hyaluronan receptor 1
, extracellular link domain containing 1
, lymphatic endothelial hyaluronan receptor LYVE-1
, lymphatic vessel endothelial hyaluronic acid receptor 1
, cell surface retention sequence binding protein-1
, cell surface retention sequence-binding protein 1
, extracellular link domain-containing 1
, extracellular link domain-containing protein 1
, hyaluronic acid receptor
, extra cellular link domain-containing 1
, lymphatic vessel endothelial HA receptor-1
, lymphatic vessel endothelial HA recptor-1