Literature summary for 2.7.1.91 extracted from

Hayashi, H.; Nakagami, H.; Takami, Y.; Koriyama, H.; Mori, M.; Tamai, K.; Sun, J.; Nagao, K.; Morishita, R.; Kaneda, Y.
FHL-2 suppresses VEGF-induced phosphatidylinositol 3-kinase/Akt activation via interaction with sphingosine kinase-1 (2009), Arterioscler. Thromb. Vasc. Biol., 29, 909-914.

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Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
endothelial cell	vascular and aorta endothelial cell	Homo sapiens	-

Subunits

Subunits	Comment	Organism
More	isoform Sk1 interacts with four-and-a-half LIM only protein FHL-2. Overexpression of FHL-2 in endothelial cells inhibits VEGF-induced Sk1 activity, phosphatidylinositol 3-kinase activity, and phosphorylation of Akt and eNOS. Overexpression of FHL-2 has no effect on sphinganine 1-phosphate induced Akt phosphorylation. VEGF stimulation decreases the binding of FHL-2 and Sk1. Depletion of FHL-2 by siRNA increases endothelial cell migration accompanied with Sk1 and Akt activation	Homo sapiens

General Information

General Information	Comment	Organism
physiological function	isoform Sk1 interacts with four-and-a-half LIM only protein FHL-2. Overexpression of FHL-2 in endothelial cells inhibits VEGF-induced Sk1 activity, phosphatidylinositol 3-kinase activity, and phosphorylation of Akt and eNOS. Overexpression of FHL-2 has no effect on sphinganine 1-phosphate induced Akt phosphorylation. VEGF stimulation decreases the binding of FHL-2 and Sk1. Depletion of FHL-2 by siRNA increases endothelial cell migration accompanied with Sk1 and Akt activation	Homo sapiens

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Release 2023.1 (January 2023)