◀ Back to FOS

ANG — FOS

Text-mined interactions from Literome

Chen et al., Blood 2004 : Angiotensin II (Ang II) stimulation increased c-Fos , c-Jun, and Sp1 binding to the MRE by 100-, 4.9-, and 1.9-fold, respectively, and these responses were inhibited by PD98059 and AT1 receptor antagonist candesartan
Blume et al., Am J Physiol Regul Integr Comp Physiol 2005 : Similar to ANG II, ANG III induced the expression of c-Fos , c-Jun, and Krox-24 in four brain regions, subfornical organ, median preoptic area, paraventricular nucleus, and supraoptic nucleus of the hypothalamus, with the same efficacy
Li et al., Regul Pept 2007 (Liver Cirrhosis, Experimental) : However, the signal transduction mechanism underlying effects of Angiotensin II (Ang II) and Aldosterone ( Aldo ) on Nuclear Factor-kappaB (NF-kappaB) and active protein-1 (AP-1) pathway in hepatic fibrogenesis remains to be fully elucidated
Hattori et al., Diabetes 2007 : gAd also activated AP-1 and enhanced angiotensin II (Ang II) induced AP-1 activity
Lu et al., Neuroscience 2009 : Results showed that the Fos immunoreactivity (Fos-ir) expression in forebrain areas such as subfornical organ ( SFO ), paraventricular hypothalamic nuclei ( PVN ), supraoptic nucleus (SON) and organum vasculosum laminae terminalis ( OVLT ) all increased significantly and that the levels of ANG I, ANG II and ALD also increased in plasma and forebrain in rats fed with low sodium diet
Naftilan et al., Mol Cell Biol 1990 : This study demonstrated that Ang II also activated c-jun and, in addition, could activate the AP-1 enhancer element
McKinley et al., Brain Res Bull 1995 : By contrast, ICV ANG II caused intense Fos immunoreactivity predominantly in the median preoptic nucleus and juxtaventricular neurons of the SFO and OVLT
Badoer et al., Am J Physiol 1997 : In the medulla, ANG II did not significantly increase Fos production in the nucleus of the solitary tract (NTS) or ventrolateral medulla ( VLM )
Rowland et al., Pharmacol Biochem Behav 1997 : Fos-IR induced in brain by Ang I was not markedly affected by either acute or chronic treatment with captopril
Xu et al., Brain Res 1999 : Pretreatment of the SFO with either captopril, an ANG converting enzyme inhibitor, or losartan, an AT1 receptor antagonist, abolished both drinking and Fos-ir induced by ANG I. Water intake partially decreased ANG I-induced Fos-ir in the SON and PVN, but not in the other areas