HUGO ID Detailed Result 5464

HUGO ID 5464
Symbol IGF1
Name insulin-like growth factor 1 (somatomedin C)
#Occurrence 55
#Paper 3

 

PMID Match String Actual String Score Flanking text Edited by Edit
16194581IGF1IGF-11.8localized expression of ERK and insulin-like growth factor 1 (IGF-1) IGF-1 and its receptor (IGF-1R) IGF-1R was also assayed by immunohistochemistry 
16194581IGF1IGF-11.8aged rats showed significant increases in the protein levels of IGF-1 IGF-1R and ERK and these increases were also inversely correlated 
16194581IGF1IGF-11.8and cognitive performance via concerted mechanisms involving neurogenesis neurotrophic factor IGF-1 and its receptor and MAP kinase signal transduction cascades 
16877542IGF1IGF12.0products damage proteins such as insulin-like growth factor 1 (IGF1) IGF1 receptors which are located on motor neurons 
16877542IGF1IGF12.0data indicate that such an oxidative modification hinders the IGF1/Akt IGF1 Akt survival pathway in motor neurons 
16877542IGF1IGF12.0Phosphorylation of Akt and cell viability in response to IGF1 recombinant and to H 2 O 2 or activated BV2 
16877542IGF1IGF12.0NADPH Oxidase Impairs the Insulin-Like Growth Factor 1 (IGF1)/Akt IGF1 Akt Pathway in Transgenic SOD1 G93A Mice 
16877542IGF1IGF12.0by damaging essential surviving pathways for motor neurons such as IGF1 
16877542IGF1IGF12.0After IGF1 was immunoprecipitated from spinal cord extracts it was probed for 
16877542IGF1IGF12.0This approach failed to reveal evidence of IGF1 oxidation in any of the studied mouse genotypes (data data 
16877542IGF1IGF12.0carbonyl adducts were evident in the _amp_#x003b1 -chain of the IGF1 tyrosine kinase cognate receptor in the spinal cord of symptomatic 
16877542IGF1IGF12.0B similar results were obtained for the _amp_#x003b2 -chain of IGF1 receptor (data data not shown 
16877542IGF1IGF12.0This finding might be quite significant because IGF1 receptors in mouse spinal cords were detected almost exclusively on 
16877542IGF1IGF12.0Contrasting with the IGF1 receptor findings oxidation indices in the intracellular serine/threonine serine threonine 
16877542IGF1IGF12.0in the intracellular serine/threonine serine threonine kinase Akt which transduces IGF1 receptor signaling ( 15 did not differ between symptomatic transgenic 
16877542IGF1IGF12.0These results suggest that the entire IGF1 molecular pathway is not oxidatively modified by inflammation in this 
16877542IGF1IGF12.0Next we compared selected IGF1 transduction events among the different mouse groups 
16877542IGF1IGF12.0Although mutant SOD1 is expressed in all cells markers of IGF1 transduction such as phospho-IGF1 receptor phospho-Akt (data data not shown 
16877542IGF1IGF12.0These data further support the idea that oxidative modification of IGF1 receptor in symptomatic transgenic SOD1 G93A /gp91 gp91 phox mice 
16877542IGF1IGF12.0Microglial-Derived ROS Recapitulate the IGF1/Akt IGF1 Akt Pathway Defect in Vitro 
16877542IGF1IGF12.0To test the idea that NADPH oxidase-derived ROS could impair IGF1 pathway function an in vitro cell system using the neuron-like 
16877542IGF1IGF12.0were briefly incubated with 0.1_amp_#x02013 100 _amp_#x003bc M human recombinant IGF1 in the presence of overnight-preconditioned serum-free medium supplemented with or 
16877542IGF1IGF12.0to provide a constant flux of H 2 O 2 IGF1 pathway responsiveness was monitored by Akt phosphorylation 
16877542IGF1IGF12.0Exposure to IGF1 caused a dose-dependent phosphorylation of Akt in SH-SY5Y cells ( 
16877542IGF1IGF12.0Conversely IGF1 barely increased Akt phosphorylation in the neuroblastoma cell lines that 
16877542IGF1IGF1-mediated1.5of H 2 O 2 ( Fig 5 E attenuated IGF1-mediated Akt phosphorylation in the neuroblastoma cell line ( Fig 5 
16877542IGF1IGF12.0to LPS-activated microglial-conditioned medium the Akt phosphorylation response to the IGF1 recombinant remained depressed and at 72 h a reduction of 
16877542IGF1IGF12.0a reduction of cell viability indistinguishable from the condition without IGF1 was observed ( Fig 5 F 
16877542IGF1IGF1-mediated1.5However both the alteration of IGF1-mediated Akt phosphorylation and the loss of cell viability mediated by 
16877542IGF1IGF12.0Relevant to the latter scenario are our results for IGF1 a trophic factor that is known to promote motor neuron 
16877542IGF1IGF12.0In this study we indeed found that receptors for IGF1 were primarily expressed on motor neurons in mouse spinal cords 
16877542IGF1IGF12.0in mouse spinal cords (Fig Fig 8 and that the IGF1 signaling pathway was impaired by a NADPH oxidase-dependent mechanism in 
16877542IGF1IGF12.0Although IGF1 per se did not seem to be damaged by inflammation 
16877542IGF1IGF12.0by inflammation NADPH oxidase did stimulate the oxidative modification of IGF1 receptors ( Fig 4 
16877542IGF1IGF12.0The ligand-dependent kinase activation of IGF1 receptor relies on its arrangement into a heterotetrameric 2_amp_#x003b1;/2_amp_#x003b2;-chain 2_amp_#x003b1 
16877542IGF1IGF12.0It may thus be predicted that oxidation of the IGF1 receptor main extracellular domains (i.e., i.e. the _amp_#x003b1 -chains could 
16877542IGF1IGF12.0molecular events that are normally elicited by ligation of the IGF1 receptor including autophosphorylation and Akt phosphorylation were indeed abated by 
16877542IGF1IGF12.0data also show that microglial NADPH oxidase by impairing the IGF1 signaling pathway renders SH-SY5Y cells in our in vitro system 
16877542IGF1IGF12.0Muscle-specific expression of IGF1 stabilizes neuromuscular junctions reduces inflammation in the spinal cord and 
16877542IGF1IGF12.0did not find any evidence that the rescue of the IGF1 pathway by abrogating NADPH oxidase was associated with muscle hypertrophy 
16877542IGF1IGF12.0transgenic SOD1 G93A mice with an adeno-associated virus carrying an IGF1 gene prolongs survival in these animals ( 20 24 
16877542IGF1IGF12.0but instead may blunt the motor neuron survival response to IGF1 in ALS 
16877542IGF1IGF12.0progression that is seen in patients treated with human recombinant IGF1 ( 25 may be related to the issue raised above 
16877542IGF1IGF12.0It may thus be argued that optimal therapeutic response to IGF1 in diseases such as ALS may rely on a concomitant 
16877542IGF1IGF12.0Modulation of the IGF1/Akt IGF1 Akt pathway by NADPH oxidase-derived ROS 
16877542IGF1IGF12.0( A Immunoprecipitation of IGF1 receptor _amp_#x003b1 -chain followed by OxyBlot (upper upper blot and 
16877542IGF1IGF12.0by OxyBlot (upper upper blot and immunoblot for spinal cord IGF1 receptor _amp_#x003b1 -chain (lower lower blot 
16877542IGF1IGF12.0Glucose oxidase- and microglial-derived ROS impair the IGF1 Akt pathway in vitro 
16877542IGF1IGF1-treated1.5upper blot and total Akt (lower lower blot immunoblots of IGF1-treated SH-SY5Y cells exposed or not exposed to 75 _amp_#x003bc M 
16877542IGF1IGF12.0ROS reactive oxygen species SOD1 superoxide dismutase 1 IGF1 insulin-like growth factor 1 
16194581insulin-like growth factor 1insulin like growth factor 11.0the localized expression of erk and insulin like growth factor 1 igf 1 and its receptor igf 1r was also assayed by immunohistochemistry.  
16877542insulin-like growth factor 1insulin like growth factor 11.0we also show that nadph oxidase derived oxidant products damage proteins such as insulin like growth factor 1 igf1 receptors which are located on motor neurons.  
16877542insulin-like growth factor 1insulin like growth factor 11.0nadph oxidase impairs the insulin like growth factor 1 igf1 /akt pathway in transgenic sod1 g93a mice.  
16877542insulin-like growth factor 1insulin like growth factor 11.0ros reactive oxygen species sod1 superoxide dismutase 1 igf1 insulin like growth factor 1  
17105868insulin-like growth factor 1insulin like growth factor 11.0surprisingly insulin like growth factor 1 prevents neuronal cell apoptosis and protects spinal motor neurons in als mice ryu et al. 1999 ; kaspar et al. 2003 but markedly potentiates neuronal cell necrosis induced by hydroxyl radical or glut