◀ Back to ANGPT2

ANGPT2 — RAC1

Text-mined interactions from Literome

Murasawa et al., J Biol Chem 2000 (Calcium Signaling) : These results suggest that 1 ) in cardiac fibroblasts activation of JNK and c-Jun by Ang II is initiated by Pyk2 dependent signalings but not by downstream signals of EGF-R or Ras, 2 ) Rac1 but not Cdc42 is required for JNK activation by Ang II upstream of MEKK1, and 3 ) ATF-2/c-Jun binding to the activator protein-1 sequence at -190 plays a key role for induction of c-Jun gene by Ang II
Seshiah et al., Circ Res 2002 : These results suggest that c-Src, EGF receptor transactivation, phosphatidylinositol-3-kinase, and Rac play important roles in the sustained Ang II-mediated activation of vascular smooth muscle cell NAD ( P ) H oxidases and provide insight into the integrated signaling mechanisms whereby Ang II stimulation leads to activation of the growth related NAD ( P ) H oxidases
Zimmerman et al., Circ Res 2004 : Ang II induced a time dependent increase in Rac1 activation and O ( 2 ) ( *- ) production in Neuro-2A cells, and this was abolished by pretreatment with AdN17Rac1 or the NADPH oxidase inhibitors apocynin or diphenylene iodonium
Fujii et al., J Biol Chem 2005 : Ang II-induced NFAT activation was suppressed by diphenyleneiodonium ( an NADPH oxidase inhibitor ), dominant negative ( DN ) -Rac , DN-p47(phox), and an inhibitor of Galpha(12/13) ( Galpha(12/13)-specific regulator of G protein signaling domain of p115RhoGEF, p115-regulator of G protein signaling (RGS) )
Hingtgen et al., Physiol Genomics 2006 (Hypertrophy) : ANG II caused a significant time dependent increase in Rac1 activation and O2-* production in primary neonatal rat cardiomyocytes, and these responses were abolished by adenoviral ( Ad ) -mediated expression of a dominant negative Rac1 ( AdN17Rac1 ) or cytoplasmic Cu/ZnSOD ( AdCu/ZnSOD )