Gene interactions and pathways from curated databases and text-mining

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JUN — NGF

Text-mined interactions from Literome

Haas et al., Int J Dev Neurosci 1998 : Role of NGF in axotomy induced c-Jun expression in medial septal cholinergic neurons
Tong et al., Neurochem Res 1999 : While NGF somewhat increased c-Fos and c-Jun protein levels transiently, it had a more robust and persistent stimulatory effect on Jun B protein levels
Minneman et al., J Neurochem 2000 : In cells stably expressing alpha ( 1A ) -adrenergic receptors, norepinephrine activated all five reporters [ AP1 ( activator protein-1 ), SRE ( serum response element ), CRE ( cyclic AMP response element ), NFkappaB ) ( nuclear factor-kappaB ), and NFAT ( nuclear factor of activated T cells ) ], whereas nerve growth factor (NGF) and epidermal growth factor activated only AP1 and SRE
Wooten et al., Mol Cell Biol 2000 : Inhibitors of PKC-iota activity and PI3K had no effect on NGF induced MAPK or p38 activation but reduced NGF stimulated c-Jun N-terminal kinase activity
Pflug et al., J Neurosci Res 2001 (Glioma) : Moreover, NGF increased AP-1 binding activity in C6trk cells, suggesting that NGF may induce differentiation
Bruckner et al., J Neurochem 2001 : To evaluate directly the apoptotic role of the JNK isoform that is selectively expressed in neurons, JNK3, we isolated sympathetic neurons from JNK3-deficient mice and quantified nerve growth factor (NGF) deprivation induced neuronal death, oxidative stress, c-Jun phosphorylation, and c-jun induction ... In contrast, NGF-deprivation induced increases in the levels of phosphorylated c-Jun , c-jun, and apoptosis are each inhibited in JNK3-deficient mice
Zentrich et al., J Biol Chem 2002 : Truncation analysis and electromobility shift assays established the requirement for a cAMP-response element/activating transcription factor-like site in the NFLC promoter that minimally interacts with constitutively expressed cAMP-response element binding protein and JunD as well as c-Jun which is induced by NGF in an ERK dependent manner
Baskey et al., J Neurochem 2002 : Transfection with an AP-1 luciferase reporter gene revealed that PC12 but not B5P cells expressed nerve growth factor induced functional AP-1 activity ... Using DNA-protein gel shift assays we determined that nerve growth factor stimulates AP-1 binding in both PC12 and B5P cells, and identified c-Fos, FosB, Fra-1, Fra-2, c-Jun, JunB and JunD in AP-1 complexes
Ohki et al., Brain Res Dev Brain Res 2002 : NGF mediated activation of the transcription factor AP-1 was found to be suppressed in the NDRG4 protein diminished clone and enhanced in the NDRG4 protein upregulated clone as compared with those in the control cells ... These results suggest that NDRG4 plays a role in neurite outgrowth and has an influence on an NGF stimulated AP-1 activation by an undefined mechanism in PC12 cells
Levkovitz et al., J Neurosci 2002 : Furthermore, mutations of ZnEgr that greatly impair or abolish its ability to bind to the ERE do not block its ability to suppress c-Jun activation or neurite outgrowth induced by NGF
Oh et al., J Toxicol Environ Health 2004 : Co-treatment of OTA with NGF resulted in inhibition of NGF induced p38 MAP kinase and AP-1 activation
Marek et al., J Cell Physiol 2004 : We previously demonstrated that neurofilament light chain ( NFLC ) gene induction by NGF requires collaborative extracellular signal regulated kinase ( ERK ) and c-Jun N-terminal kinase (JNK) signaling
Kamata et al., Arch Biochem Biophys 2005 : Conversely, incubation of the cells with a reductant, N-acetyl-L-cysteine (NAC), inhibited NGF induced neuronal differentiation and AP-1 activation
Waetzig et al., Biochem Pharmacol 2008 : The mitogen activated protein kinases ( MAPKs ) extracellular signal regulated kinase 1/2 ( ERK1/2 ) and c-Jun N-terminal kinases (JNKs) were activated in response to NGF and both significantly contributed to neurite re-growth
Leugers et al., J Biol Chem 2010 (MAP Kinase Signaling System) : In addition, we demonstrate that Tau potentiates AP-1 transcription factor activation in response to nerve growth factor (NGF)
Mullenbrock et al., J Biol Chem 2011 (MAP Kinase Signaling System) : Expression of several AP-1 family members was induced by both EGF and NGF , but their induction was more robust and sustained in response to NGF
Gold et al., Neurosci Lett 1993 : Regulation of the transcription factor c-JUN by nerve growth factor in adult sensory neurons
Colangelo et al., Brain Res Mol Brain Res 1996 (Glioma) : Correlation between increased AP-1NGF binding activity and induction of nerve growth factor transcription by multiple signal transduction pathways in C6-2B glioma cells ... All of these stimuli increased NGF mRNA levels within 3 h. Cycloheximide pretreatment blocked the TPA and ISO mediated binding to AP-1NGF suggesting that de novo synthesis of c-Fos/c-Jun may be required for the transcriptional regulation of NGF gene
Tong et al., J Neurosci Res 1996 : Effect of nerve growth factor on AP-1 , NF-kappa B, and Oct DNA binding activity in apoptotic PC12 cells : extrinsic and intrinsic elements
Casaccia-Bonnefil et al., Nature 1996 : NGF binding to mature oligodendrocytes expressing the p75 neurotrophin receptor, but not trkA, resulted in a sustained increase of intracellular ceramide and c-Jun amino-terminal kinase (JNK) activity, which are thought to participate in a signal transduction pathway leading to cell death
Kamata et al., J Biol Chem 1996 : NAC suppressed NGF induced c-fos gene expression and AP-1 activation
Kontny et al., J Mol Neurosci 1997 : On the role of the low-affinity neurotrophin receptor p75LNTR in nerve growth factor induction of differentiation and AP 1 binding activity in PC12 cells ... NGF stimulated AP 1 binding activity in all clones
Courtney et al., J Neurosci 1997 : No TrkA is detected, although p75 ( NTR ) protein is expressed and NGF induces depolarization dependent elevation of c-Jun levels
Hughes et al., Neuroscience 1997 : In addition, since neither nerve growth factor nor neurotrophin-4/5 induced c-Jun in medial septum/diagonal band cholinergic neurons, it seems unlikely that the neurotrophic effects of nerve growth factor and neurotrophin-4/5 on cholinergic neurons are mediated via c-Jun expression
Unlap et al., Biol Psychiatry 1997 : Lithium attenuates nerve growth factor induced activation of AP-1 DNA binding activity in PC12 cells ... NGF induced large, time dependent increases in AP-1 DNA binding activity ... Pretreatment with 5 mmol/L lithium for 24 h reduced AP-1 induction by NGF by 42 % ; shorter treatments and lower concentrations of lithium had smaller inhibitory effects on AP-1
Furukawa et al., J Neurosci Res 1998 : Induction of DNA binding activity of the transcription factor AP-1 by NGF was markedly suppressed in cells expressing mutant PS-1
Colangelo et al., Proc Natl Acad Sci U S A 1998 : Our data suggest that, while AP-1 may regulate basal levels of NGF expression, C/EBPdelta is a critical component determining the area-specific expression of NGF in response to BAR stimulation
Haas et al., Neuroscience 1998 : Axotomy induced c-JUN expression in young medial septal neurons is regulated by nerve growth factor ... In the present study we investigated the axotomy induced expression of the proto-oncogene c-jun in young rat medial septal neurons and its regulation by nerve growth factor ... With the concept that nerve growth factor suppresses c-JUN expression, slice cultures of the medial septum were treated with antibodies against nerve growth factor ... These data suggest an age independent induction of c-JUN in axotomized medial septal neurons and its regulation by nerve growth factor