Gene interactions and pathways from curated databases and text-mining

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IGF1 — MYLIP

Text-mined interactions from Literome

Wang et al., Clin Exp Pharmacol Physiol 2009 (Diabetes Mellitus, Experimental...) : In addition, the miR-320 inhibitor significantly increased the expression of IGF-1 protein, but had no effect on the expression of IGF-1R
La Rocca et al., J Cell Physiol 2009 (Colonic Neoplasms) : An IGF-IR resistant to miR145 ( again by elimination of its 3 ' UTR ) is not down-regulated by miR145 but fails to rescue colon cancer cells from growth inhibition
Ning et al., Differentiation 2009 : Because Pitx3 is important for the maturation and function of dopaminergic neurons and has been shown to be regulated by microRNA miR-133b, we also examined the effects of IBMX and IGF-I on miR-133b expression ... Thus, IGF-I signaling and miR-133b co-regulate potential neural differentiation of ADSC through a feedback mechanism, in which IGF-I upregulates miR-133b while miR-133b in turn downregulates IGF-IR
Elia et al., Circulation 2009 : On the basis of bioinformatics tools, biochemical assays, and in vivo models, we demonstrate that ( 1 ) insulin-like growth factor-1 (IGF-1) and IGF-1 receptor are targets of miR-1 ; ( 2 ) miR-1 and IGF-1 protein levels are correlated inversely in models of cardiac hypertrophy and failure as well as in the C2C12 skeletal muscle cell model of differentiation ; ( 3 ) the activation state of the IGF-1 signal transduction cascade reciprocally regulates miR-1 expression through the Foxo3a transcription factor ; and ( 4 ) miR-1 expression correlates inversely with cardiac mass and thickness in myocardial biopsies of acromegalic patients, in which IGF-1 is overproduced after aberrant synthesis of growth hormone
Huang et al., PloS one 2011 : Our results elucidate a negative feedback circuit in which IGF-1 stimulated miR-133 in turn represses IGF-1R expression to modulate the IGF-1R signaling pathway during skeletal myogenesis
Knezevic et al., J Biol Chem 2012 (Anoxia...) : Additionally, our data show that miR-378 expression is inhibited by IGF1 in cardiomyocytes