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ANGPT2 — GRAP2

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Lai et al., Beijing Da Xue Xue Bao 2004 : ANG II promoted podocyte apoptosis in a time- and dose dependent manner ; ANG II stimulated p38MAPK , but inhibited JNK ; SB202190 inhibited both ANG II-induced podocyte apoptosis and p38MAPK phosphorylation ; Inhibition of ERK by PD98059 had no effect on ANG II-induced cell apoptosis
Kiribayashi et al., Kidney Int 2005 (Peritonitis) : Ang II-induced fibronectin expression was mediated by the activation of extracellular signal regulated kinase 1/2 ( ERK1/2 ) and p38 mitogen activated protein kinase ( p38 MAPK ), but not c-Jun N-terminal kinase
Fukuyama et al., Arterioscler Thromb Vasc Biol 2006 (Hyperthyroidism) : 3,3',5-triiodo-L-thyronine ( T3 ) did not show a significant effect on Ang II-induced activation of extracellular signal regulated protein kinase or p38 mitogen activated protein kinase in vascular smooth muscle cells ( VSMCs ), whereas T3 inhibited Ang II-induced activation of cAMP response element ( CRE ) binding protein ( CREB ), a nuclear transcription factor involved in the vascular remodeling process
Wu et al., Zhongguo Ying Yong Sheng Li Xue Za Zhi 2007 (MAP Kinase Signaling System) : ( 3 ) Ang II significantly activated ERK1/2, JNK and P38 , only JNK activation was inhibited by Que and DPI but not ERK1/2 and P38 activation
Ren et al., Am J Hypertens 2011 (Fibrosis...) : Furthermore, Ang II activation of nuclear factor-?B ( NF-?B ), JNK and p38 mitogen activated protein kinases ( MAPKs ) in WT macrophages was reduced in CARD9 ( -/- ) macrophages
Yu et al., Molecules (Basel, Switzerland) 2012 (MAP Kinase Signaling System) : The results showed that Ang II ( 10 ( -7 ) M ) stimulated the cardiac fibroblast proliferation which was inhibited by NAC ( an antioxidant ), SB203580 ( a p38MAPK inhibitor ) or enalaprilat ; Ang II caused an burst of intracellular ROS level within thirty minutes, an increase in p-p38MAPK ( 3.6-fold of that in the control group ), as well as an elevation of TGF-ß ( 1 ) meantime ; NAC, an antioxidant, and enalaprilat treatment attenuated cardiac fibroblast proliferation induced by Ang II and decreased ROS and p-p38MAPK protein levels in rat cardiac fibroblast ; SB203580 lowered TGF-ß ( 1 ) protein expression in rats ' CFb in a dose dependent manner
Morales et al., Int J Biochem Cell Biol 2012 (Fibrosis) : These results strongly suggest that the fibrotic response to Ang-II is mediated by the AT-1 receptor and requires the p38MAPK phosphorylation, NOX induced ROS, and TGF-ß1 expression increase mediated by Ang-II in skeletal muscle cells