background:
Angiogenic factors are critical to the initiation of angiogenesis and maintenance of the vascular network. VG5Q protein acts as a potent angiogenic factor in promoting angiogenesis, and suppression of VG5Q expression inhibits vessel formation. VG5Q shows strong expression in blood vessels and is secreted as vessel formation is initiated. VG5Q can bind to endothelial cells and promote cell proliferation, suggesting that it may act in an autocrine fashion. It also interacts with another secreted angiogenic factor, TWEAK (also known as TNFSF12). VG5Q is defective in patients with the vascular disease Klippel-Trenaunay syndrome (KTS).
Function:
Promotes angiogenesis and the proliferation of endothelial cells. Able to bind to endothelial cells and promote cell proliferation, suggesting that it may act in an autocrine fashion.
Subunit:
Interacts with the secreted angiogenic factor TNFSF12.
Subcellular Location:
Cytoplasm. Secreted. Note=Cytoplasmic in microvascular endothelial cells. Upon angiogenesis, when endothelial cell tube formation is initiated, it is secreted.
Tissue Specificity:
Widely expressed. Expressed in endothelial cells, vascular smooth muscle cells and osteoblasts. Expressed in umbilical vein endothelial cells and microvascular endothelial cells.
DISEASE:
Defects in AGGF1 are a cause of Klippel-Trenaunay syndrome (KTS) [MIM:19800]. KTS is a congenital disease characterized by malformations of capillary (98% of KTS patients), venous (72%) and lymphatic (11%) vessels, and bony and soft tissue hypertrophy that leads to large cutaneous hemangiomata with hypertrophy of the related bones and soft tissues.
Similarity:
Contains 1 FHA domain.
Contains 1 G-patch domain.
Database links:
UniProtKB/Swiss-Prot: Q8N302.2
Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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