Recombinant Human LYVE1 Proteins
- Known as:
- Recombinant Human LYVE1 Proteins
- Catalog number:
- 228-11061-2
- Product Quantity:
- 5
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Recombinant Human LYVE1 Proteins
Related genes to: Recombinant Human LYVE1 Proteins
- 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: Recombinant Human LYVE1 Proteins
Related articles to: Recombinant Human LYVE1 Proteins
- 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
Chen LuHe YuchaoSu HongTian XiangdongLiao HaotianLiu DongmingZhao MengSun HuichuanQi LishaCao ManqingLiu ZhiyongGuo LinLi GuangtaoZhou ChenhaoLuo YiChen LiweiWu QiangCui YunlongLi HuikaiZhu XiaolinFang FengZhang WeiZhang ShaojunSong TianqiangGuo Hua - - Source: PubMed
Takagaki Kazuki - To investigate the mechanism of Huiyang Shengji unguent (, HYSJ) for improving inflammation and promoting wound healing in patients with diabetic foot. - Source: PubMed
Fangning Y ULi LinXiao TangXiujuan H EBo ZhangYukun ChenYizhao M AZeyu LiuJinsheng Y EXuying X U - This study investigated the mechanism of pirfenidone (PFD) inhibiting metastasis of lung cancer in vivo.A nude mouse lung cancer model was established and treated with PFD (200, 400 μg/mL); lung metastatic tumor weight was recorded, Lyve-1 (lymphatic marker), LC3II (autophagy protein) and polo-like kinase 1 (PLK1) were detected. In human lung lymphatic endothelial cells (HMVEC-LLy) cells, PFD's effects on migration, apoptosis, lymphangiogenesis, and LC3II/LC3I/PLK1 levels were tested. PLK1-overexpressed HMVEC-LLy cells were treated with 400 μg/mL PFD to explore its mechanism. PFD inhibited the weight of lung metastases and down-regulated the expression levels of Lyve-1, LC3II/LC3I and PLK1. In cell experiments, PFD was found to inhibit HMVEC-LLy migration, apoptosis and lymph angiogenesis, as well as down-regulate LC3II/LC3I and PLK1 protein levels, and these effects could be reversed by PLK1 overexpression.PFD may inhibit lung cancer metastasis in vivo by regulating lymph angiogenesis through PLK1 signaling. - Source: PubMed
Publication date: 2026/04/21
Xia ZehaiWang QuanZheng LeiLv Qun