LYVE1 antibody
- Known as:
- LYVE1 (anti-)
- Catalog number:
- orb11006
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- LYVE1 antibody
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
- Fatty liver diseases are highly prevalent worldwide, driven by hepatocyte metabolic dysfunction and alcohol consumption. Both cell-autonomous and non-cell-autonomous mechanisms contribute to hepatic lipid accumulation. Here, we investigated the role of liver endothelial cell-hepatocyte communication in regulating lipid metabolism. - Source: PubMed
Publication date: 2026/05/11
Rao XiyunZhao QianqianChen JinbiaoZheng MinXing MingyueFeng YuChen JiayuanZhu ShichaoHan ZhimingMcCaughan Geoffrey WZheng Xiangjian - Kaposiform lymphangiomatosis (KLA) is an ultrarare disease characterized by abnormal lymphatic vessel proliferation due to hyperactivation of the Rat sarcoma virus (RAS) signaling pathway, resulting in multifocal lymphatic malformations (LMs) that can potentially involve multiple organ systems. Its distinctive histologic features include the presence of clusters of spindle cells expressing clusters of differentiation 31 (CD31), cluster of differentiation 34 (CD34), podoplanin (D2-40), prospero homeobox protein 1 (PROX1), and lymphatic vessel endothelial hyaluronan receptor 1 (LYVE1), along with abnormal lymphatic vessels. Sirolimus is recommended as a treatment option, particularly for patients without known mutations. This study aimed to examine the long-term therapeutic effects of sirolimus treatment in adult patients with KLA. - Source: PubMed
Publication date: 2026/04/23
Bilny-Paluch MagdalenaPiekarczyk PiotrBłasińska KatarzynaSzołkowska MałgorzataPolaczek MateuszRadzikowska Elżbieta - The purpose of this study was to compare the effects of riboflavin-ultraviolet A (RF/UVA) cross-linking (CXL) and rose bengal-green light (RB/green light) CXL on corneal neovascularization (CNV) in rat eyes. - Source: PubMed
Oral MerveDayanir DuyguArik Erol Gökce NurÖzmen Mehmet Cüneyt - Dysregulation of Mo/M activity is known to contribute to impaired healing in diabetes; however, the mechanisms underlying this dysregulation are not well understood. In this study, we used a variety of bioinformatics approaches along with our time series scRNA-seq data on wound Mo/M from non-diabetic and diabetic mice to identify transcriptional regulators (TRs) that drive Mo/M state transitions during normal and impaired healing. First, we used the Lamian framework and our newly developed Pseudotime Graph Diffusion method to show that state transitions from early stage phenotypes to later stage reparative and antigen presenting phenotypes characteristic of normally healing wounds are impaired and that transitions to inflammatory, foam cell-like, and Lyve-1 M phenotypes are enhanced during impaired healing of diabetic mice. Using our BITFAM model, we identified a broad range of TRs predicted to be preferentially active in each cell state and using CellOracle, we performed in silico perturbation to identify groups of TRs predicted to drive cell state transitions along multiple trajectories (e.g. CEBPA, IRF8), whereas other TRs were predicted to drive cell state transition towards reparative phenotypes (e.g. NR1H3, NR3C1) or towards an antigen-presenting phenotype (e.g. IRF4, OGT). Selected findings were validated using existing experimental data, confirming the usefulness of this approach. In conclusion, we identified TRs that likely drive Mo/M state transitions towards desirable and undesirable phenotypes for wound healing. These findings provide insight into novel targets for altering Mo/M phenotypes to promote healing of diabetic wounds. - Source: PubMed
Publication date: 2026/04/24
Lukas BrandonPang JingboDai YangKoh Timothy J - Cholangiocarcinoma (CCA) is an aggressive malignancy with poor prognosis and limited treatment options. Molecular heterogeneity and the tumor immune microenvironment play crucial roles in CCA progression and therapeutic response, but comprehensive stratification remains insufficient for guiding treatment decisions. - Source: PubMed
Publication date: 2026/02/26
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