Gene interactions and pathways from curated databases and text-mining

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AGTR1 — IGF1

Text-mined interactions from Literome

van Eickels et al., Br J Pharmacol 2000 : IGF-I induced expression was completely inhibited by ACE inhibition or AT(1) receptor blockade ... The IGF-I induced overexpression of the IGF-IR was reduced by ACE inhibition with moexiprilat ( 10 ( -7 ) M ) by 79+/-7 % and by AT(1) receptor blockade with CV11974 ( 10 ( -7 ) M ) by 79+/-5 %
Ahmad et al., Clin Endocrinol (Oxf) 2001 (Growth Disorders) : IGF-I and IGF-I SDS increased significantly at 1 and 3 months ( P < 0.001 ) after commencing GHR
Müller et al., J Renin Angiotensin Aldosterone Syst 2000 : Insulin-like growth factor induces up-regulation of AT(1)-receptor gene expression in vascular smooth muscle cells ... In order to assess relevant interactions of both systems, the effect of IGF-1 on AT1-receptor expression was evaluated in vascular smooth muscle cells ... Experiments under transcriptional blockade showed that AT1-receptor mRNA stability was not altered by IGF-1, suggesting that transcriptional mechanisms may be involved in IGF-1 induced AT1-receptor regulation ... Preincubation with various pharmacological inhibitors revealed that IGF-1 up-regulated AT1-receptor expression via activation of p42/44 MAP kinase, whereas tyrosine phosphorylation and Pl-3 kinase seemed not to participate in this regulative pathway ... IGF-l induced up-regulation of the AT1-receptor maybe an important interaction by which cellular grow this modulated in the heart as well as in the vasculature
Yin et al., Int J Biochem Cell Biol 2003 : Besides coupling with heterotrimeric G proteins to activate phospholipase C-beta (PLC-beta), AT1R also activates receptor tyrosine kinases ( PDGF-R, EGF-R and IGF-R ) and non-receptor tyrosine kinases ( Src, Fyn, Yes, proline-rich tyrosine kinase 2 (Pyk2), focal adhesion kinase ( FAK ) and JAK2 )
Bäck et al., Growth Horm IGF Res 2009 : In PA both the IR and the IGF-IR was phosphorylated by their own ligand at 1 nM and in dPA the activation of both receptors was stimulated by IGF-I, but not insulin, at 1 nM
Germinario et al., AIDS Res Hum Retroviruses 1995 : Epidermal growth factor from 1.6 x 10 ( -10 ) to 1.6 x 10 ( -8 ) M demonstrated no inhibition of HIV-1 replication, while IGF-1 inhibited p24 antigen production 49 and 42 % at 1.3 x 10 ( -9 ) and 1.3 x 10 ( -8 ) M IGF-1, respectively
Langlois et al., Endocrinology 1994 : Insulin, Insulin-like growth factor and basic Fibroblast growth factor increased AT1 receptors ( mRNA and binding sites ) as well as the alpha subunit of Gq ( mRNA and protein ) and G11 ( protein )
Al-Shoumer et al., Eur J Endocrinol 1996 (Hypopituitarism) : Compared to baseline, IGF-I levels increased significantly at 1 ( p = 0.0001 ), 2 ( p = 0.0004 ), 3 ( p = 0.006 ) and 4 years ( p = 0.002 )
Wyse et al., Endocrinology 1997 : The hypothesis, based on previous in vivo data, that angiotensin AT1 receptors are regulated by GH or insulin-like growth factor I (IGF-I) has been investigated in this study using primary cultures of rat astrocytes as a model of AT1 receptor expression
Franchimont et al., Endocrinology 1997 : IL-6 did not modify IGF-I messenger RNA ( mRNA ) levels, but when tested in the presence of IL-6sR, IL-6 at 1 to 100 ng/ml increased IGF-I transcripts by up to 3.2-fold after 24 h. IL-6sR caused a small increase in IGF-I mRNA levels when tested alone