Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.69 (APC)
 16,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuropilin-1 (NRP1) is a transmembrane protein expressed on neuronal and endothelial cells where it plays a crucial role in guiding axons and regulating angiogenesis. We have recently shown that NRP1 also is expressed on dendritic cells (DC) in the human immune system and have proposed a role for NRP1 in the first stages of the immune response. In these studies, we show that NRP1 can be transferred with a high efficiency from human DC to T lymphocytes by trogocytosis. The NRP1 transfer can occur independently of T lymphocyte activation; the amount of NRP1 transferred depends on the NRP1 expression level on APC and is enhanced when T cells are activated through the TCR. Moreover, the NRP1 transfer occurs between specific donor and recipient cells, because no NRP1 transfer is observed between endothelial cells and T lymphocytes or between APCs and CD34(+) hemopoietic cells. Finally, we show that a major NRP1 ligand, vascular endothelial growth factor (VEGF)(165), is secreted by mature human DCs and binds to NRP1 captured by T lymphocytes. These results show that NRP1 transfer to T lymphocytes during the immune synapse can convert T lymphocytes into VEGF(165)-carrying cells. Together with the enhanced signaling of VEGF-R2 on endothelial cells in the presence, in trans, of the NRP1-VEGF(165) complex, our results suggest that the intercellular transfer of NRP1 might participate in the Ag-independent remodelling of the endothelial vessels in secondary lymphoid organs during inflammation.
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PMID:Dendritic cells can turn CD4+ T lymphocytes into vascular endothelial growth factor-carrying cells by intercellular neuropilin-1 transfer. 1684 52

Wnt signaling is essential for the maintenance of adult stem cells and its aberrant activation is a stimulator of carcinogenesis. The transmembrane protein, Wntless, is an essential Wnt signaling component through regulating the secretion of Wnt ligands. Here, we generated a mouse model with specific Wntless knockout in intestinal epithelium to study its function in the intestinal epithelium. Wntless knockout exhibits no obvious defects in mice but significantly disrupted proliferation and differentiation of small intestinal organoids. We also discovered that these deficiencies could be partially rescued by Wnt3a supplement but not Wnt9b. To further investigate the role of Wntless in tumorigenesis, APC-deficient spontaneous intestinal tumors and chemical induced colorectal cancer mouse models were employed. To our surprise, intestinal epithelium-specific knockout of Wntless did not cause significant differences in tumor number and size. In summary, our data demonstrated that epithelial Wntless was required for the growth and differentiation of small intestinal organoids but not in live animals, suggesting the other tissues, such as mesenchymal tissue, play critical role for Wnt secretion in both intestinal homeostasis as well as tumorigenesis.
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PMID:Epithelial Wntless is dispensable for intestinal tumorigenesis in mouse models. 3154 88


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