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ANGPT1 — MAPK3

Text-mined interactions from Literome

Fujikawa et al., Exp Cell Res 1999 : In contrast to VEGF mediated biological effects, inhibition of MAPK/ERKs by PD98059 in endothelial cells did not affect angiopoietin-1 mediated survival or migration
Zhu et al., Am J Pathol 2002 (MAP Kinase Signaling System) : Both VEGF and Ang-1 induced rapid, monophasic ( 15 minutes ) phosphorylation of p38 MAPK
Krikun et al., Am J Pathol 2002 (Uterine Hemorrhage) : To further examine the effects of progestin, hypoxia, and reactive oxygen species ( ROS ) on the regulation of Ang-1 and Ang-2 as well as the activation of MAPK , SAPK/JNK, and p38 by the relevant cell types, we conducted in vitro studies with cultured human endometrial stromal cells ( HESCs ) and human endometrial endothelial cells ( HEECs )
Xu et al., Cancer Res 2004 (Carcinoma, Lewis Lung...) : In addition, we have demonstrated that the binding of Ang-3 to the cell surface is required for the effective inhibition of Ang-3 on tumor metastasis and that Ang-3 inhibits endothelial cell proliferation and survival and blocks Ang-1- and vascular endothelial growth factor induced activation of extracellular signal regulated kinase 1/2 and Akt kinases, which likely underlie the Ang-3 mediated inhibition on tumor angiogenesis and metastasis
Samuel et al., Diabetes 2010 (Diabetes Mellitus, Experimental...) : We also observed increased phosphorylated mitogen activated protein kinase activated protein kinase-2, 2 days after the treatment and increased expression of vascular endothelial growth factor ( VEGF ), Flk-1, angiopoietin-1 (Ang-1) , Tie-2, and survivin, 4 days after treatment in the diabetic animals ... We also observed increased phosphorylated mitogen activated protein kinase activated protein kinase-2, 2 days after the treatment and increased expression of vascular endothelial growth factor ( VEGF ), Flk-1, angiopoietin-1 (Ang-1), Tie-2, and survivin, 4 days after treatment in the diabetic animals
Babu et al., Infect Immun 2012 (Elephantiasis, Filarial...) : TLR2 mediated enhancement of angiogenic growth factor production in CP individuals was shown to be dependent on mitogen activated protein kinase ( MAPK ) and NF-?B signaling, as pharmacologic inhibition of either extracellular signal regulated kinase 1/2 ( ERK1/2 ), p38 MAPK , or NF-?B signaling resulted in significantly diminished production of VEGF-A and Ang-1