HUGO ID Detailed Result 7808


HUGO ID 7808
Symbol NGF
Name nerve growth factor (beta polypeptide)
#Occurrence 124
#Paper 6

 


PMID Match String Actual String Score Flanking text Edited by Edit
10077670NGFNGF1.2phosphatase activity in cells expressing SODV148G or SODWT or after NGF withdrawal was normalized to activity of mock-infected cells 
10077670NGFNGF-removal1.2was no decline in calcineurin activity of PC12 cells after NGF-removal a procedure that also leads to apoptotic cell death (Fig 
10077670NGFNGF1.2after mock infection (Fig Fig 2 C lane 1 after NGF removal (Fig Fig 2 C lane 2 or 72 hr 
10077670NGFNGF1.2Analogs on Cell Death Induced by Mutant SOD Expression or NGF Withdrawal 
10077670NGFNGF1.2811 and PSC 833 protected PC12 cells from death after NGF withdrawal (Fig Fig 3 B 
10077670NGFNGF1.2dansylated CsA had relatively little effect on cell death after NGF withdrawal (Fig Fig 3 B 
10077670NGFNGF-differentiated1.2cyclophilin rotamase activity on mutant SOD-induced cell death we transfected NGF-differentiated PC12 cells with wild-type CyPA (CyPAWT) CyPAWT cDNA or CyPA(R55A) 
10077670NGFNGF1.2R55A did not significantly protect cells from death induced by NGF withdrawal (Fig Fig 5 B indicating that the apoptotic pathway 
10077670NGFNGF-differentiated1.2adenovirus as a vector to express SODWT or SODV148G in NGF-differentiated PC12 cells and hippocampal neurons to test whether calcineurin was 
10077670NGFNGF-withdrawal1.2Both NGF-withdrawal and expression of SOD mutations have been associated with the 
10077670NGFNGF1.2For NGF withdrawal and NMDA toxicity the ability of CsA and its 
10077670NGFNGF1.2addition CsA actually decreased cell death in PC12 cells after NGF withdrawal 
10077670NGFNGF1.2assayed 3 days after AdV infection or 1 day after NGF withdrawal 
10077670NGFNGF1.2PC12 cells ( A and show a protective effect after NGF removal ( B 
10077670NGFNGF1.2cell death induced by SODV148G expression ( A or after NGF withdrawal ( B 
10077670NGFNGF1.2Zn superoxide dismutase-1 FALS familial ALS CyP cyclophilin WT wild-type NGF nerve growth factor AdV adenovirus CsA cyclosporin A NMDA N 
10077670NGFNGF1.2expression of FALS-associated mutant SOD in nerve growth factor (NGF)-differentiated NGF -differentiated PC12 cells primary sympathetic neurons and hippocampal neurons leads 
12901835NGFNGF1.2is not causative of death in nerve growth factor (NGF)-differentiated NGF -differentiated PC12 cells transfected with mutant SOD1s (SODMT, SODMT V148G 
17191135NGFNGF0.6Recent work suggests that Trx-1 play a key role in NGF signaling pathways 74 
17191135NGFNGF0.6NGF a neurotrophic factor regulating development maintenance and function of the 
17634371NGFNGF1.2Nerve growth factor (NGF) NGF can induce apoptosis by signaling through the p75 neurotrophin receptor 
17634371NGFNGF1.2Cultured embryonic motor neurons expressing p75 are not vulnerable to NGF unless they are exposed to an exogenous flux of nitric 
17634371NGFNGF-induced1.2prevented neuronal loss further evidencing the role of mitochondria in NGF-induced apoptosis 
17634371NGFNGF1.2sclerosis (ALS)-linked ALS -linked superoxide dismutase 1 (SOD1 SOD1 mutation NGF induced apoptosis even in the absence of an external source 
17634371NGFNGF1.2The increased susceptibility of SOD1 motor neurons to NGF was associated to decreased nuclear factor erythroid 2-related factor 2 
17634371NGFNGF1.2reproduced the effect of SOD1 expression increasing their sensitivity to NGF 
17634371NGFNGF-induced1.2In contrast rising antioxidant defenses by Nrf2 activation prevented NGF-induced apoptosis 
17634371NGFNGF1.2Nerve growth factor (NGF) NGF has a key role on the development and function of 
17634371NGFNGF1.2In addition to promoting neuronal differentiation and survival NGF can induce apoptosis of neurons during development and may also 
17634371NGFNGF1.2NGF exerts its actions through two nonhomologous transmembrane receptors the tyrosine 
17634371NGFNGF1.2Adult motor neurons had been thought to be unresponsive to NGF because they lack both TrkA and p75 receptors (Henderson Henderson 
17634371NGFNGF-induced1.2Induction of p75 renders motor neurons vulnerable to NGF-induced apoptosis p75 has been implicated in motor neuron death occurring 
17634371NGFNGF-induced1.2Pure motor neuron cultures expressing p75 are sensitive to NGF-induced apoptosis only when physiological concentrations of exogenous nitric oxide ( 
17634371NGFNGF1.2Mouse NGF (2.5S) 2.5S was obtained from Harlan (Madison, Madison WI recombinant 
17634371NGFNGF1.2Blocking antibodies to NGF and p75 were from Chemicon (Temecula, Temecula CA 
17634371NGFNGF1.2Treatments with NGF and inhibitors were performed 3 h after motor neuron plating 
17634371NGFNGF1.2mito-HE incubation cells were treated with 100 ng/ml ng ml NGF and then imaged every 15 min 
17634371NGFNGF1.2GDNF (1 1 ng/ml) ng ml and then treated with NGF (100 100 ng/ml) ng ml in the presence or absence 
17634371NGFNGF1.2Consistent with our previous results (Pehar Pehar et al. 2004 NGF reduced motor neuron survival by 40% only in the presence 
17634371NGFNGF-induced1.2The extent of NGF-induced reduction in motor neuron survival was similar to that induced 
17634371NGFNGF-induced1.2NGF-induced motor neuron death was blocked by manumycin A (10 10 
17634371NGFNGF1.2of p75 under pathological conditions renders motor neurons vulnerable to NGF (Ferri Ferri et al. 1998 Wiese et al. 1999 Lowry 
17634371NGFNGF1.2In the present study we show that the NGF/p75 NGF p75 -mediated motor neuron apoptosis involved increased production of mitochondrial 
17634371NGFNGF-mediated1.2Moreover ALS-linked SOD1 overexpression increases motor neuron vulnerability to NGF-mediated apoptosis by reducing antioxidant defenses 
17634371NGFNGF1.2In accordance pharmacological activation of Nrf2 prevented NGF/p75 NGF p75 -induced motor neuron apoptosis suggesting a potential target to 
17634371NGFNGF1.2Therefore NGF signaling through p75 and the subsequent increase in ceramide production 
17634371NGFNGF1.2an important source of superoxide in motor neurons exposed to NGF 
17634371NGFNGF1.2and peroxynitrite scavengers completely prevent motor neuron death induced by NGF through p75 (Pehar Pehar et al. 2004 
17634371NGFNGF-mediated1.2(mitoCP) mitoCP supports a role for mitochondrial oxidative damage in NGF-mediated apoptosis 
17634371NGFNGF1.2prevent mitochondrial oxidative damage and neuronal death induced by NGF/p75 NGF p75 -signaling in vivo 
17634371NGFNGF-mediated1.2to nontransgenic motor neurons SOD1 motor neurons are sensitive to NGF-mediated apoptosis in the absence of exogenous nitric oxide 
17634371NGFNGF-induced1.2Although an external source of nitric oxide is not required NGF-induced apoptosis in SOD1 transgenic motor neurons requires endogenous production of 
17634371NGFNGF-induced1.2The increased susceptibility of SOD1 motor neurons to NGF-induced apoptosis was not mediated by increased expression of p75 or 
17634371NGFNGF-mediated1.2nitric oxide production was counteracted by endogenous antioxidant defenses and NGF-mediated apoptosis only proceeds in the presence of an exogenous source 
17634371NGFNGF-mediated1.2NGF-mediated apoptosis will be executed only in the presence of surrounding 
17634371NGFNGF1.2the increased susceptibility of SOD1 motor neurons not only to NGF but also to Fas-mediated apoptosis which also involves ROS and 
17634371NGFNGF-1.2Accordingly pharmacological activation of Nrf2 by tBHQ treatment completely prevented NGF- and Fas-mediated motor neuron apoptosis in nontransgenic and SOD1 motor 
17634371NGFNGF-induced1.2NGF-induced apoptosis in motor neurons involves nSMase activation and triggers cytochrome 
17634371NGFNGF1.2with GDNF (1 1 ng/ml) ng ml were exposed to NGF (100 100 ng/ml) ng ml plus 10 micro M DETA-NONOate 
17634371NGFNGF1.2SMase inhibitors were added 1 h before NGF and DETA-NONOate 
17634371NGFNGF1.2motor neurons maintained with GDNF (control) control or exposed to NGF plus DETA-NONOate (NGF+NO) NGF NO 
17634371NGFNGF1.2GDNF (control) control or exposed to NGF plus DETA-NONOate (NGF+NO) NGF NO 
17634371NGFNGF1.2In the absence of NGF motor neurons showed a punctuate (mitochondrial) mitochondrial labeling of cytochrome 
17634371NGFNGF1.2labeling of cytochrome c whereas 12 h after treatment with NGF NO motor neurons showed a diffuse cytoplasmic labeling 
17634371NGFNGF1.2100 n M GW prevented cytochrome c release induced by NGF NO 
17634371NGFNGF1.21 ng/ml) ng ml were exposed to vehicle (Ctrl), Ctrl NGF (100 100 ng/ml), ng ml DETA-NONOate (10 10 micro M 
17634371NGFNGF1.2NGF increases superoxide production by mitochondria 
17634371NGFNGF1.20.1 micro M mito-HE and after washing were exposed to NGF (100 100 ng/ml) ng ml 
17634371NGFNGF1.2fluorescence emission of mito-HE ( exc 405 nm immediately after NGF addition ( t = 0 min and 40 min later 
17634371NGFNGF1.2min in cultures maintained with GDNF in the absence of NGF (data data not shown 
17634371NGFNGF1.2The increased mito-HE fluorescence emission induced by NGF was not observed in cultures preincubated for 24 h with 
17634371NGFNGF1.2Preincubation with missense oligonucleotides did not prevent the effect of NGF 
17634371NGFNGF1.2with GDNF (1 1 ng/ml) ng ml were exposed to NGF (100 100 ng/ml) ng ml plus DETA-NONOate (10 10 micro 
17634371NGFNGF1.2ng/ml) ng ml plus DETA-NONOate (10 10 micro M (NGF+NO) NGF NO in the presence of vehicle (white white bar or 
17634371NGFNGF1.2mean _amp_#177 SD * p _lt_ 0.05 significantly different from NGF NO 
17634371NGFNGF-induced1.2Motor neurons overexpressing SOD1 show increase susceptibility to NGF-induced apoptosis 
17634371NGFNGF1.21 ng/ml) ng ml and exposed to increasing concentrations of NGF 
17634371NGFNGF1.2gray bars represent motor neuron survival in cultures exposed to NGF (100 100 ng/ml) ng ml in the presence of DETA-NONOate 
17634371NGFNGF1.2B SOD1 transgenic motor neurons were exposed to NGF in the presence of vehicle GW4869 (100 100 n M 
17634371NGFNGF1.2mean _amp_#177 SD * p _lt_ 0.05 significantly different from NGF 
17634371NGFNGF1.2maintained with GDNF and exposed to vehicle (control) control or NGF (100 100 ng/ml) ng ml 
17634371NGFNGF1.2In the absence of NGF motor neurons showed a punctuate labeling of cytochrome c and 
17634371NGFNGF1.2labeling of cytochrome c and 12 h after treatment with NGF a diffuse labeling was observed in affected motor neurons 
17634371NGFNGF1.2( exc 405 nm in SOD1 motor neurons immediately after NGF addition ( t = 0 min and 40 min later 
17634371NGFNGF1.2E SOD1 transgenic motor neurons were exposed to NGF in the presence of vehicle mitoQ (10 10 p M 
17634371NGFNGF1.2mean _amp_#177 SD * p _lt_ 0.05 significantly different from NGF 
17634371NGFNGF-induced1.2Glutathione levels modulate NGF-induced motor neuron apoptosis 
17634371NGFNGF1.210 n M and 24 h later were exposed to NGF (100 100 ng/ml) ng ml 
17634371NGFNGF1.2Motor neuron survival was determined 48 h after NGF treatment 
17634371NGFNGF1.2NGF did not affect motor neuron survival in cultures preincubated with 
17634371NGFNGF1.2vehicle (control) control tBHQ prevented motor neuron death induced by NGF (100 100 ng/ml) ng ml plus DETA-NONOate (10 10 micro 
17634371NGFNGF1.2100 ng/ml) ng ml plus DETA-NONOate (10 10 micro M NGF NO 
17634371NGFNGF1.2Increased Nrf2 activation prevents SOD1 motor neuron death induced by NGF or sFasL 
17634371NGFNGF1.2with GDNF (1 1 ng/ml) ng ml were exposed to NGF (100 100 ng/ml) ng ml in the presence of vehicle 
17634371NGFNGF1.2In the absence of NGF motor neurons showed a punctate pattern of cytochrome c immunoreactivity 
17634371NGFNGF1.2NGF (100 100 ng/ml) ng ml or DETA-NONOate (10 10 micro 
17634371NGFNGF1.2In contrast after 12 h of NGF treatment in the presence of DETA-NONOate ~27% of motor neurons 
17634371NGFNGF1.2Cytochrome c release induced by NGF in the presence of nitric oxide was prevented by the 
17634371NGFNGF-mediated1.2tested for the potential involvement of mitochondrial ROS production in NGF-mediated motor neuron death 
17634371NGFNGF1.2NGF (100 100 ng/ml) ng ml treatment induced a 1.7 _amp_#177 
17634371NGFNGF-induced1.2Kelso et al. 2001 Dhanasekaran et al. 2005 also blocked NGF-induced motor neuron death ( Fig 2 B strengthening the role 
17634371NGFNGF-induced1.2nontransgenic motor neurons SOD1 -expressing motor neurons were sensitive to NGF-induced apoptosis in the absence of the nitric oxide donor DETA-NONOate 
17634371NGFNGF1.2donor DETA-NONOate even at concentrations of 10 ng/ml ng ml NGF ( Fig 3 
17634371NGFNGF-induced1.210 micro M which renders nontransgenic motor neurons sensitive to NGF-induced apoptosis did not further decrease the survival of SOD1 -expressing 
17634371NGFNGF-induced1.2NGF-induced apoptosis in SOD1 -expressing motor neurons was prevented by blocking 
17634371NGFNGF-induced1.2p M and mitoCP (1 1 n M also prevented NGF-induced apoptosis in SOD1 motor neurons ( Fig 3 E 
17634371NGFNGF1.2an exogenous source of nitric oxide is not required for NGF to induce SOD1 motor neuron death N -nitro-L -arginine methyl 
17634371NGFNGF-induced1.2a specific inhibitor of the neuronal isoform of NOS prevented NGF-induced apoptosis in SOD1 motor neurons ( Fig 3 E 
17634371NGFNGF1.2These results indicate that the apoptotic pathway induced by NGF in SOD1 motor neurons required endogenous nitric oxide production by 
17634371NGFNGF1.2The increased sensitivity of SOD1 motor neurons to NGF could not be explained by differential expression of p75 or 
17634371NGFNGF1.2n M increased the sensitivity of nontransgenic motor neurons to NGF ( Fig 5 A 
17634371NGFNGF-induced1.2Nontransgenic motor neurons previously exposed to BSO were sensitive to NGF-induced apoptosis even in the absence of DETA-NONOate ( Fig 5 
17634371NGFNGF1.2et al. 2002 completely prevented motor neuron death induced by NGF in the presence of NO ( Fig 5 B 
17634371NGFNGF-induced1.2Nrf2 activation by tBHQ also prevented NGF-induced apoptosis in SOD1 motor neurons ( Fig 6 A 
10077670nerve growth factornerve growth factor1.0als amyotrophic lateral sclerosis sod cu/zn superoxide dismutase 1 fals familial als cyp cyclophilin wt wild type ngf nerve growth factor adv adenovirus csa cyclosporin a nmda n methyl d aspartate mptp mitochondrial permeability transition pore  
10077670nerve growth factornerve growth factor1.0it recently has been reported that the expression of fals associated mutant sod in nerve growth factor ngf differentiated pc12 cells primary sympathetic neurons and hippocampal neurons leads to altered o 2 content and an apoptotic cell death 12 .  
12901835nerve growth factornerve growth factor1.0this is in line with the recent report [ lee et al 2002 ] that aggregation of fals sod1 is not causative of death in nerve growth factor ngf differentiated pc12 cells transfected with mutant sod1s sodmt v148g or a4v .  
17105868nerve growth factornerve growth factor1.0the neurotrophins nerve growth factor brain derived neurotrophic factor neurotrophin 3 nt 3 and nt 4/5 promote neuronal survival by preventing programmed cell death or apoptosis but they markedly enhance necrotic degeneration of neurons  
17634371nerve growth factornerve growth factor1.0nerve growth factor ngf can induce apoptosis by signaling through the p75 neurotrophin receptor p75 in several nerve cell populations.  
17634371nerve growth factornerve growth factor1.0key words: amyotrophic lateral sclerosis; mitochondria; motor neurons; nerve growth factor; nrf2; p75 ; superoxide  
17634371nerve growth factornerve growth factor1.0nerve growth factor ngf has a key role on the development and function of the nervous system snider 1994 ; chao 2003 .  
17634371nerve growth factornerve growth factor1.0enzyme inhibitors|nf e2 related factor 2|nfe2l2 protein rat|nitric oxide donors|nitroso compounds|oligodeoxyribonucleotides antisense|reactive oxygen species|receptor nerve growth factor|2 2'|cytochromes c|nerve growth factor|sod1 g93a protein|superoxide dismutase|sphingomyelin phosphodiesterase|  
17634371nerve growth factornerve growth factor1.0|2 2'|cytochromes c|nerve growth factor|sod1 g93a protein|superoxide dismutase|sphingomyelin phosphodiesterase|  
18210200nerve growth factornerve growth factor1.0another study also suggested that cnts functionalized with growth factors such as nerve growth factor or brain derived neurotrophic factor can stimulate growth of neurons on the nanotube scaffold matsumoto et al 2007 .