INT217094

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Context Info
Confidence 0.69
First Reported 2007
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 17
Total Number 17
Disease Relevance 5.31
Pain Relevance 1.87

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

nucleus (Egr2) intracellular (Egr2) DNA binding (Egr2)
ligase activity (Egr2) cytoplasm (Egr2)
Anatomy Link Frequency
brain 4
jaw 2
neuronal 1
neurons 1
peripheral nerve 1
Egr2 (Mus musculus)
Pain Link Frequency Relevance Heat
long-term potentiation 80 98.96 Very High Very High Very High
withdrawal 20 96.84 Very High Very High Very High
opiate 20 96.62 Very High Very High Very High
dopamine receptor 20 96.18 Very High Very High Very High
fifth nerve 10 95.92 Very High Very High Very High
Hippocampus 100 91.00 High High
medulla 33 73.64 Quite High
Pyramidal cell 10 63.68 Quite High
unmyelinated 2 57.08 Quite High
amygdala 20 54.88 Quite High
Disease Link Frequency Relevance Heat
Shock 200 99.84 Very High Very High Very High
Anxiety Disorder 200 98.84 Very High Very High Very High
Convulsion 40 98.36 Very High Very High Very High
Brain Hemorrhage 20 95.76 Very High Very High Very High
Targeted Disruption 127 90.56 High High
Syndrome 10 89.24 High High
Disease 10 88.08 High High
Charcot Marie Tooth Disease 20 87.24 High High
Neuropathic Pain 12 86.64 High High
Peripheral Neuropathy 30 84.68 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Like other Egr members, Egr2 can be induced in brain by various stimuli, including electroconvulsive shock inducing seizure activity (Bhat et al., 1992, this study), focal cerebral ischaemia (An et al., 1992), dopamine receptor activation and opiate withdrawal (Bhat et al., 1992) and in hippocampal neurons following kainic acid injection (Gass et al., 1994) or LTP-inducing stimuli (Williams et al., 1995), although Egr2 is less robustly induced and is not induced by weaker patterns of stimuli despite induction of long-lasting LTP along with Egr1 expression (Worley et al., 1993).
Neg (not) Positive_regulation (induced) of Egr2 in brain associated with brain hemorrhage, convulsion, dopamine receptor, shock, long-term potentiation, opiate and withdrawal
1) Confidence 0.69 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525857 Disease Relevance 0.47 Pain Relevance 0.33
For example, induction of Egr2 mRNA or protein has been observed after seizure activity (Bhat et al., 1992, but see Mack et al., 1992), focal cerebral ischaemia (An et al., 1992), kainic acid injection (Gass et al., 1994), dopamine receptor activation and opiate withdrawal (Bhat et al., 1992), and in hippocampal neurons following LTP-inducing stimuli (Williams et al., 1995; Worley et al., 1993).
Positive_regulation (induction) of Egr2 in neurons associated with brain hemorrhage, convulsion, dopamine receptor, long-term potentiation, opiate and withdrawal
2) Confidence 0.69 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525857 Disease Relevance 0.60 Pain Relevance 0.28
Furthermore, NFAT c4 complexes with Sox-10, a transcription factor required for myelination [17], to activate the promoter and myelin-specific enhancer of the Krox-20 gene, which globally regulates peripheral myelination [11,18-20], and also with the promoter of the myelin protein zero (P0) gene, all of which underline the involvement of NFAT proteins in myelination.
Positive_regulation (activate) of Krox-20 in NFAT
3) Confidence 0.58 Published 2010 Journal F1000 Biol Rep Section Body Doc Link PMC2948355 Disease Relevance 0 Pain Relevance 0.03
The consequences of Egr2 inactivation were explored in conventional Egr2-null mutant mice and these studies revealed a prominent role of Egr2 in the regulation of peripheral nerve myelination (Topilko et al., 1994) as well as in hindbrain segmentation (Giudicelli et al., 2001; Schneider-Maunoury et al., 1993; Swiatek and Gridley, 1993) and endochondreal bone formation (Levi et al., 1996).
Positive_regulation (role) of Egr2 in peripheral nerve
4) Confidence 0.50 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525857 Disease Relevance 0.63 Pain Relevance 0.09
In contrast, in the cKO mice, presence of the deleted allele was attested by this analysis in all these tissues (Figure 1B), establishing that recombination occurred as expected, leading to complete inactivation of Egr2 in at least part of the cells.


Positive_regulation (inactivation) of Egr2
5) Confidence 0.50 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525857 Disease Relevance 0.23 Pain Relevance 0
Control of the oro-buccal reflex requires both Hoxa2 and Krox20
Positive_regulation (requires) of Krox20
6) Confidence 0.49 Published 2007 Journal Neural Develop Section Body Doc Link PMC2098766 Disease Relevance 0.07 Pain Relevance 0.05
The hypomorphic Krox20 mutant was obtained by combining two previously developed Krox20 alleles: the Krox20Cre allele consists of an insertion of the gene for the Cre recombinase into the Krox20 locus, resulting in Krox20 inactivation and expression of the Cre gene with a pattern that faithfully recapitulates the normal Krox20 pattern [46]; in the Krox20flox allele, the second Krox20 exon is flanked by loxP sites – this allele behaves like the wild-type until excision of the floxed exon by the Cre recombinase results in inactivation of Krox20 [30,46].
Positive_regulation (inactivation) of Krox20
7) Confidence 0.49 Published 2007 Journal Neural Develop Section Body Doc Link PMC2098766 Disease Relevance 0.15 Pain Relevance 0
We found that inactivation of either Hoxa2 or Krox20 impairs the rhythmic control of the jaw opening in agreement with HOXA2-dependent trigeminal defects and direct regulation of Hoxa2 by KROX20 in r3.
Positive_regulation (inactivation) of Krox20 in jaw
8) Confidence 0.49 Published 2007 Journal Neural Develop Section Body Doc Link PMC2098766 Disease Relevance 0 Pain Relevance 0
Like other Egr members, Egr2 can be induced in brain by various stimuli, including electroconvulsive shock inducing seizure activity (Bhat et al., 1992, this study), focal cerebral ischaemia (An et al., 1992), dopamine receptor activation and opiate withdrawal (Bhat et al., 1992) and in hippocampal neurons following kainic acid injection (Gass et al., 1994) or LTP-inducing stimuli (Williams et al., 1995), although Egr2 is less robustly induced and is not induced by weaker patterns of stimuli despite induction of long-lasting LTP along with Egr1 expression (Worley et al., 1993).
Positive_regulation (induced) of Egr2 in brain associated with brain hemorrhage, convulsion, dopamine receptor, shock, long-term potentiation, opiate and withdrawal
9) Confidence 0.47 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525857 Disease Relevance 0.63 Pain Relevance 0.31
Egr2 was significantly upregulated by MECS in WT and HT mice (t?
Positive_regulation (upregulated) of Egr2 associated with shock
10) Confidence 0.47 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525857 Disease Relevance 0.53 Pain Relevance 0.06
Egr2 was also significantly upregulated in both WT (t?
Positive_regulation (upregulated) of Egr2
11) Confidence 0.47 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525857 Disease Relevance 0.46 Pain Relevance 0.04
As opposed to Egr1, however, which is rapidly induced in different brain structures after a variety of learning (Guzowski et al., 2001; Hall et al., 2001; Malkani and Rosen, 2000; Maviel et al., 2004; Okuno and Miyashita, 1996; Thomas et al., 2002), there is as yet no firm evidence for Egr2 induction after learning, at least in fear conditioning (Malkani and Rosen, 2000).
Positive_regulation (induction) of Egr2 in brain structures associated with anxiety disorder
12) Confidence 0.47 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525857 Disease Relevance 0.37 Pain Relevance 0.29
Like other Egr members, Egr2 can be induced in brain by various stimuli, including electroconvulsive shock inducing seizure activity (Bhat et al., 1992, this study), focal cerebral ischaemia (An et al., 1992), dopamine receptor activation and opiate withdrawal (Bhat et al., 1992) and in hippocampal neurons following kainic acid injection (Gass et al., 1994) or LTP-inducing stimuli (Williams et al., 1995), although Egr2 is less robustly induced and is not induced by weaker patterns of stimuli despite induction of long-lasting LTP along with Egr1 expression (Worley et al., 1993).
Neg (not) Positive_regulation (induced) of Egr2 in brain associated with brain hemorrhage, convulsion, dopamine receptor, shock, long-term potentiation, opiate and withdrawal
13) Confidence 0.47 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525857 Disease Relevance 0.47 Pain Relevance 0.33
Interestingly, mutations affecting rostral hindbrain segmentation differentially affect the control of jaw opening in neonates, which requires Krox20 [17] but not Hoxa1 expression [18].
Positive_regulation (requires) of Krox20 in jaw
14) Confidence 0.43 Published 2007 Journal Neural Develop Section Body Doc Link PMC2098766 Disease Relevance 0.17 Pain Relevance 0.04
The hypomorphic Krox20 mutant was obtained by combining two previously developed Krox20 alleles: the Krox20Cre allele consists of an insertion of the gene for the Cre recombinase into the Krox20 locus, resulting in Krox20 inactivation and expression of the Cre gene with a pattern that faithfully recapitulates the normal Krox20 pattern [46]; in the Krox20flox allele, the second Krox20 exon is flanked by loxP sites – this allele behaves like the wild-type until excision of the floxed exon by the Cre recombinase results in inactivation of Krox20 [30,46].
Positive_regulation (inactivation) of Krox20
15) Confidence 0.43 Published 2007 Journal Neural Develop Section Body Doc Link PMC2098766 Disease Relevance 0.13 Pain Relevance 0
In cKO mice, there was a very small increase in Egr2 following MECS that may be due to activation in non-neuronal cells that are not supposed to have undergone Cre-recombination; however, this did not reach statistical significance (t?
Positive_regulation (increase) of Egr2 in neuronal associated with shock
16) Confidence 0.41 Published 2007 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2525857 Disease Relevance 0.40 Pain Relevance 0.03
EGR2 is expressed in r3 and r5, and is required for the development of both of these segments [41].
Positive_regulation (required) of EGR2
17) Confidence 0.39 Published 2010 Journal Neural Dev Section Body Doc Link PMC2843687 Disease Relevance 0 Pain Relevance 0

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