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Endothelial receptor that acts as an essential regulator of CNS angiogenesis. Additionally we are shipping GPR124 Antibodies (79) and GPR124 Proteins (7) and many more products for this protein.
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Data suggest that GPR124 promotes cell adhesion via interaction with Elmo1-Dock180 and intersectin 1/2; this constitutes a previously unrecognized heteromeric complex that is putatively involved in GPR124-dependent adhesive/angiogenic responses in vascular endothelial cells. (GPR124 = G-protein coupled receptor 124; Elmo1 = ELMO domain-containing protein 1; Dock180 = dedicator of cytokinesis protein 1 180 kDa)
Observed an inverse correlation between the expression of miR-138-5p and GPR124 in lung adenocarcinoma specimens. Knockdown of GPR124 mimicked the effects of miR-138-5p on the sensitivity to gefitinib.
Thrombin-induced shedding of tumour endothelial marker 5 and exposure of its RGD motif are regulated by cell-surface protein disulfide-isomerase.
TEM5 expression during capillary morphogenesis is induced by the small GTPase Rac and mediates contact inhibition of proliferation in endothelial cells.
Proteolytically processed soluble tumor endothelial marker TEM5 mediates endothelial cell survival during angiogenesis by linking integrin alpha(v)beta3 to glycosaminoglycans
experiments indicate that Reck and Gpr124 are part of the cell surface protein complex that transduces Wnt7a- and Wnt7b-specific signals in mammalian CNS Epithelial Cells to promote angiogenesis and regulate the BBB.
Gpr124 is an endothelial GPCR specifically required for endothelial Wnt signaling and BBB integrity under pathological conditions in adult mice.
Vital role for GPR124 is potentiation of WNT7-induced canonical beta-catenin signaling with important implications for understanding and manipulating CNS-specific angiogenesis.
Gpr124 functions as coactivator of Wnt7a- and Wnt7b-stimulated canonical Wnt signaling via Frizzled receptor and Lrp coreceptor and that Gpr124-stimulated signaling functions in concert with Norrin/Frizzled4 signaling to control CNS vascular development
GPR124, an orphan G protein-coupled receptor, is required for CNS-specific vascularization and establishment of the blood-brain barrier.
TGF-beta stimulates Gpr124 expression which is required for angiogenic sprouting into neural tissues.
study shows that complete null or endothelial-specific GPR124 deletion resulted in embryonic lethality from CNS-specific angiogenesis arrest in forebrain and neural tube; results demonstrate CNS-specific angiogenesis regulation by an endothelial receptor
Whole mount in situ hybridization approaches visualized adgra2 expression in many tissues during Xenopus embryogenesis such as the cardiovascular system including the heart, the migrating neural crest cells and the developing eye including the periocular mesenchyme; results indicate a role of Adgra2 for embryogenesis and are a good starting point for further functional studies during early vertebrate development.
Ouchless mutants fail to complement previously characterized adgra2 mutants and exhibit highly penetrant cerebrovascular defects. The aberrantly spliced adgra2 transcript found in ouchless mutants encodes a receptor lacking a single leucine-rich repeat (LRR) within its N-terminus.
The GPI-anchored MMP inhibitor Reck and the adhesion GPCR Gpr124 are integral components of the Wnt7a/Wnt7b-specific signaling complex required for brain angiogenesis and dorsal root ganglia neurogenesis.
Endothelial receptor that acts as an essential regulator of CNS angiogenesis. Required for normal endothelial cell sprouting and migration in the forebrain and neural tube.
G-protein coupled receptor 124
, tumor endothelial marker 5
, G protein-coupled receptor 124
, probable G-protein coupled receptor 124-like