HUGO ID Detailed Result 7782

HUGO ID 7782
Symbol NFE2L2
Name nuclear factor (erythroid-derived 2)-like 2
#Occurrence 40
#Paper 2

 

PMID Match String Actual String Score Flanking text Edited by Edit
17191135NRF2Nrf22.1activation (via via acetylation of the redox sensitive transcription factor Nrf2 and its consequent binding to the antioxidant responsive element (ARE) 
17191135NRF2Nrf22.1factors Bach-2 (positive) positive and Keap (negative) negative in the Nrf2 activation as well as the redox cycling between Bilirubin and 
17191135NRF2Nrf22.1Nuclear factor-erythroid 2-related factor 2 (Nrf2) Nrf2 is a transcription factor responsible for the induction of several 
17191135NRF2Nrf22.1Under normal conditions Nrf2 is sequestered in the cytoplasm by an actin-binding protein Kelch-like 
17191135NRF2Nrf22.1(Keap1), Keap1 but upon exposure of cells to oxidative stress Nrf2 dissociates from Keap1 translocates to the nucleus binds to antioxidant 
17191135NRF2Nrf22.1AP-1 nuclear factor-kB (NFkB) NFkB and the more recently identified Nrf2 proteins 24 -26 (Fig Fig 1 B contain cysteine residues 
17191135NRF2Nrf-21.6up-regulation of HO-1 and nuclear translocation of the transcription factor Nrf-2 27 
17191135NRF2Nrf22.1evidence to suggest that heterodimers of NF-E2-related factors 2 (Nrf2) Nrf2 and one or another of the small Maf proteins (i.e 
17191135NRF2Nrf22.1A possible model centered on Nrf2 activity suggests that the heme protein Bach1 works as a 
17191135NF-E2NF-E21.6enhancers and allow activators such as heterodimer of Maf with NF-E2 related activators (Nrf2), Nrf2 to interact with the transcriptional promotionJunguk Hur
17191135NRF2Nrf22.1such as heterodimer of Maf with NF-E2 related activators (Nrf2), Nrf2 to interact with the transcriptional promotion of HO-1 33 
17191135NRF2Nrf22.1the induction of Prx-1 appears to involve the transcription factor Nrf2 
17191135NRF2Nrf22.1mechanism involving activation and nuclear translocation of the transcription factor Nrf2 27 
17634371NRF2Nrf23.1associated to decreased nuclear factor erythroid 2-related factor 2 (Nrf2) Nrf2 expression and downregulation of the enzymes involved in glutathione biosynthesis 
17634371NRF2Nrf23.1In contrast rising antioxidant defenses by Nrf2 activation prevented NGF-induced apoptosis 
17634371NRF2Nrf23.1the expression of ALS-linked SOD1 mutations and critically modulated by Nrf2 activity 
17634371NRF2Nrf23.1words amyotrophic lateral sclerosis mitochondria motor neurons nerve growth factor Nrf2 p75 superoxide 
17634371NRF2Nrf23.1the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), Nrf2 which increases antioxidant defenses (Vargas Vargas et al. 2006 
17634371NRF2Nrf23.1the p75 -activated apoptotic pathway which was associated to decreased Nrf2 expression and the consequent reduction in antioxidant defenses 
17634371NRF2Nrf23.1PCR primers specific to each gene are as follows Nrf2 5'-TTCCTCTGCTGCCATTAGTCAGTC-3' and 5'-GCTCTTCCATTTCCGAGTCACTG-3' (242 242 bp glutamate-cysteine ligase modifier subunit 
17634371NRF2Nrf23.1properties (Beckman Beckman et al. 2001 but also by reduced Nrf2 expression which leads to a downregulation of the key enzymes 
17634371NRF2Nrf23.1In accordance pharmacological activation of Nrf2 prevented NGF/p75 NGF p75 -induced motor neuron apoptosis suggesting a 
17634371NRF2Nrf23.1of the enzyme GCLC and GCLM are transcriptionally regulated by Nrf2 a redox-sensitive transcription factor and member of the Cap'n'Collar/basic-leucine Cap'n'Collar 
17634371NRF2Nrf23.1Compared with nontransgenic motor neurons SOD1 motor neurons showed reduced Nrf2 mRNA expression which correlated with a decreased transcription of GCLC 
17634371NRF2Nrf23.1A similar reduction in Nrf2 expression was previously observed in a motor neuron-like NSC34 cell 
17634371NRF2Nrf23.1This reduction in Nrf2 expression could explain the increased susceptibility of SOD1 motor neurons 
17634371NRF2Nrf23.1has been established to strongly activate gene expression mediated by Nrf2 and to subsequently increase GSH content by induction of GCL 
17634371NRF2Nrf23.1induction of GCL tBHQ causes increased GCL expression only when Nrf2 is present but it does not in Nrf2 knock-out cells 
17634371NRF2Nrf23.1only when Nrf2 is present but it does not in Nrf2 knock-out cells (Lee Lee et al. 2003 
17634371NRF2Nrf23.1Accordingly pharmacological activation of Nrf2 by tBHQ treatment completely prevented NGF- and Fas-mediated motor neuron 
17634371NRF2Nrf23.1Thus Nrf2 manipulation may be a target in the prevention of motor 
17634371NRF2Nrf23.1ng ml for 24 h and the expression level of Nrf2 GCLC and GCLM mRNA was determined by relative quantitative RT-PCR 
17634371NRF2Nrf23.1Increased Nrf2 activation prevents SOD1 motor neuron death induced by NGF or 
17634371NRF2Nrf23.1a ~30% decrease in the expression of the transcription factor Nrf2 was observed in SOD1 motor neurons compared with nontransgenic ones 
17634371NRF2Nrf23.1The decrease in Nrf2 expression correlated with a decrease in the expression of Nrf2 
17634371NRF2Nrf23.1Nrf2 expression correlated with a decrease in the expression of Nrf2 regulated genes including both subunits of glutamate-cysteine ligase (GCL), GCL 
17634371NRF2Nrf23.1In contrast tBHQ treatment a well known Nrf2 activator in neurons (Johnson Johnson et al. 2002 completely prevented 
17634371NRF2Nrf23.1Nrf2 activation by tBHQ also prevented NGF-induced apoptosis in SOD1 motor 
17191135nf e2nf e21.0there is now evidence to suggest that heterodimers of nf e2 related factors 2 nrf2 and one or another of the small maf proteins i.e mafk maff and mafg are directly involved in induction of ho 1 gene through these mares [ 53 ]. Junguk Hur
17191135nf e2nf e21.0mal physiological conditions expression of ho 1 is repressed by bach1/maf complex while increased levels of heme displace bach1 from the enhancers and allow activators such as heterodimer of maf with nf e2 related activators nrf2 to interact with the transcriptional promotion of ho 1 [ 33 ]. Junguk Hur