◀ Back to IGF1
IGF1 — NOX4
Text-mined interactions from Literome
Tsukamoto et al., J Neurosci Res 2003
(Alzheimer Disease) :
Further investigation suggested that Abeta neurotoxicity via p75NTR involved JNK,
NADPH oxidase , and caspases-9/3 and was
inhibited by activity dependent neurotrophic factor,
insulin-like growth factor-I , basic fibroblast growth factor, and Humanin, as observed in primary neuron cultures
Meng et al., Cardiovasc Res 2008
:
Insulin-like growth factor-I induces reactive oxygen species production and cell migration through
Nox4 and Rac1 in vascular smooth muscle cells
Edderkaoui et al., J Biol Chem 2011
(Pancreatic Neoplasms) :
Here we investigate the mechanisms through which
insulin-like growth factor I and serum ( FBS )
activate NADPH oxidase in pancreatic cancer ( PaCa ) cells ...
Insulin-like growth factor I and FBS
activate NADPH oxidase through transcriptional up-regulation of p22(phox)
Handayaningsih et al., Endocrinology 2011
:
Nox4 knockdown, which is reportedly to produce ROS in insulin signaling, attenuated IGF-I induced IGF-IR phosphorylation, indicating that
Nox4 is
involved in the regulation of
IGF-I signaling
New et al., Am J Physiol Cell Physiol 2012
:
Expression of dominant negative adenovirus Nox4 inhibits
IGF-I induced
NADPH oxidase activity, Akt phosphorylation, and fibronectin protein expression
Xi et al., Diabetes 2012
(Hyperglycemia) :
Hyperglycemia induced
Nox4 , but not Nox1, and p22 phagocyte oxidase (p22phox) expression and
IGF-I stimulated Nox4/p22phox complex formation, leading to increased ROS generation