Gene interactions and pathways from curated databases and text-mining

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IGF1 — NFKB1

Text-mined interactions from Literome

Remacle-Bonnet et al., Cancer Res 2000 (Adenocarcinoma...) : These findings indicate that the antiapoptotic function of IGF-I in HT29-D4 cells is based on the enhancement of the survival pathways initiated by TNF, but not Fas, and mediated by MAPK/p38, MAPK/ERK, and NF-kappaB , which act in concert to suppress the proapoptotic signals
Mitsiades et al., Oncogene 2002 (Multiple Myeloma) : In contrast, the Akt inhibitor IL-6-Hydroxymethyl-chiro-inositol 2- ( R ) -2-O-methyl-3-O-octadecylcarbonate induced cell death of both Dex- and Doxo-sensitive and -resistant cells ; opposed the protective effect of constitutive Akt activity against Apo2L/TRAIL ; and abrogated the NF-kappaB activation, increase of anti-apoptotic proteins and protection against Apo2L/TRAIL induced by IGF-1
Poulaki et al., Am J Pathol 2002 (Retinoblastoma) : Inhibition of the p38 kinase sensitized cells to SN50 induced cell death, whereas insulin-like growth factor-1 activated NF-kappaB and attenuated the proapoptotic effect of SN50
Vallée et al., Biochem Biophys Res Commun 2003 (Adenocarcinoma...) : Indeed, TNF alpha induced NF-kappa B translocation was not sufficient to support enhancement of the transcription and des-IGF-1 did not promote but partly inhibited both the TNF alpha induced NF-kappa B activation and I kappa B alpha degradation through a PI-3K dependent pathway
Kim et al., Mol Cells 2003 : IGF-1 increased the activity of signal transducer and activator of transcription 6 ( STAT6 ) in response to IL-4, and activated NF-(kappa)B
Eichten et al., Virology 2004 : Expression of two insulin-like growth factor-1 binding proteins, IGFBP-2 and -5, is increased presumably in response to enhanced NF-kappaB activity in HPV-16 E7-expressing serum starved cells
Kim et al., Biochem Biophys Res Commun 2004 (MAP Kinase Signaling System) : Furthermore, IGF-II remarkably increased the DNA binding activities of NF-kappaB and AP-1, and the IL-8 promoter activity
Eisner et al., FEBS Lett 2006 : Hyperosmotic stress dependent NFkappaB activation is regulated by reactive oxygen species and IGF-1 in cultured cardiomyocytes ... NFkappaB activation and procaspase-3 and -9 fragmentation were prevented by NAC and IGF-1 ... IGF-1 prevents NFkappaB activation by a ROS independent mechanism
Ren et al., J Mol Endocrinol 2007 : Further study demonstrated that IGF-I induced the DNA binding activity of NF-kappaB in association with decreased expression of the NF-kappaB inhibitory protein IkappaBalpha ... Using a specific phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002, we also found that PI3K was involved in the pathway by which IGF-I activated NF-kappaB and increased FLIP expression
Wu et al., J Biol Chem 2008 : In rat growth plate chondrocytes, IGF-I induced NF-kappaB-p65 nuclear translocation ... Moreover, the inhibition of the phosphatidylinositol 3-kinase and Akt abolished the effects of IGF-I on NF-kappaB activation
Ren et al., Acta Pharmacol Sin 2009 : Further studies showed that IGF-1 specifically induced NF-kappaB activity
Salminen et al., Cell Signal 2010 : We will discuss the evidence that insulin/IGF-1 signaling can enhance the NF-kappaB signaling and subsequently potentiate the aging process and aggravate age related degenerative diseases