INT42251

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Context Info
Confidence 0.44
First Reported 1980
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 10
Total Number 10
Disease Relevance 5.25
Pain Relevance 3.45

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

mitochondrion (Gad1) lyase activity (Gad1) intracellular (Gad1)
cytoplasm (Gad1)
Anatomy Link Frequency
spinal 1
amacrine cells 1
spinal cord 1
piriform cortex 1
granule cell 1
Gad1 (Mus musculus)
Pain Link Frequency Relevance Heat
gABA 142 100.00 Very High Very High Very High
Glutamate 80 100.00 Very High Very High Very High
Spinal cord 9 99.58 Very High Very High Very High
GABAergic 33 98.28 Very High Very High Very High
Neuropathic pain 4 97.64 Very High Very High Very High
qutenza 6 96.00 Very High Very High Very High
unmyelinated 2 90.00 High High
bDMF 9 89.36 High High
hyperexcitability 5 88.80 High High
Hyperalgesia 2 87.48 High High
Disease Link Frequency Relevance Heat
Targeted Disruption 36 99.32 Very High Very High Very High
Frailty 10 98.20 Very High Very High Very High
Generalized Anxiety Disorder 71 98.00 Very High Very High Very High
Spasticity 80 97.96 Very High Very High Very High
Cerebral Palsy 172 97.64 Very High Very High Very High
Neuropathic Pain 4 97.64 Very High Very High Very High
Death 6 94.92 High High
Dyskinesias 4 93.04 High High
Epilepsy 40 92.24 High High
Neurological Disease 12 91.48 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We have identified a GAD1 sequence change G(36)C, which segregates with autosomal recessive spastic CP in 4 affected siblings.
Regulation (change) of GAD1 associated with spasticity and cerebral palsy
1) Confidence 0.44 Published 2004 Journal BMC Neurol Section Body Doc Link PMC544830 Disease Relevance 1.23 Pain Relevance 0.23
Two separate, independently-regulated genes, GAD1 and GAD2 (at chromosome 10p11, encoding a 65 kDa GAD isoform), have presumably arisen by duplication and been conserved during evolution, as indicated by their sequence homology [17] and the retention of common intron-exon boundary splice sites [18].
Regulation (regulated) of GAD1 associated with generalized anxiety disorder
2) Confidence 0.44 Published 2004 Journal BMC Neurol Section Body Doc Link PMC544830 Disease Relevance 0.66 Pain Relevance 0.33
Therefore the presence of an N-terminal mutation would affect both GAD25 and GAD67, and may disrupt a complex regulatory mechanism for GAD67.


Regulation (affect) of GAD25
3) Confidence 0.27 Published 2004 Journal BMC Neurol Section Body Doc Link PMC544830 Disease Relevance 0.68 Pain Relevance 0.10
Therefore the presence of an N-terminal mutation would affect both GAD25 and GAD67, and may disrupt a complex regulatory mechanism for GAD67.


Regulation (affect) of GAD67
4) Confidence 0.27 Published 2004 Journal BMC Neurol Section Body Doc Link PMC544830 Disease Relevance 0.68 Pain Relevance 0.10
Concordantly, reductions in both GAD65 and GAD67 and GAT1 immunoreactivity also support the observation of a loss of GABAergic inhibition and the associated spinal interneurons.
Regulation (immunoreactivity) of GAD67 in spinal associated with gabaergic
5) Confidence 0.26 Published 2010 Journal J. Neurotrauma Section Abstract Doc Link 20059302 Disease Relevance 1.52 Pain Relevance 1.05
BBX had only moderate effects on glutamic acid decarboxylase in the limbic areas, and enzyme activity increased 25% in the olfactory tubercle and the piriform cortex 4 weeks after BBX.
Regulation (effects) of glutamic acid decarboxylase in piriform cortex
6) Confidence 0.26 Published 1980 Journal Brain Res. Section Abstract Doc Link 6250669 Disease Relevance 0 Pain Relevance 0.30
As expected there was an up-regulation of GAD67 after kainate treatment (Fig. 3f), thus reproducing another granule cell characteristic in vitro.
Regulation (regulation) of GAD67 in granule cell
7) Confidence 0.22 Published 2007 Journal PLoS ONE Section Body Doc Link PMC1849968 Disease Relevance 0.09 Pain Relevance 0.54
GAD67 and GAT-1 immunoreactivities were localized in numerous amacrine and displaced amacrine cells, with somata in the INL and GCL, respectively, and in densely distributed immunoreactive processes and puncta in all laminae of the IPL (Figure 7) [37,51-56].
Regulation (immunoreactivities) of GAD67 in amacrine cells
8) Confidence 0.22 Published 2008 Journal Molecular Vision Section Body Doc Link PMC2519030 Disease Relevance 0.13 Pain Relevance 0.09
The aim of this study was to further establish, in vivo, evidence for a link between the maturation of spinal cord innervation and the regulation of several isoforms of the synthetic enzymes of GABA, the glutamic acid decarboxylases GAD65, GAD67, and EP10, the embryonic truncated form of GAD67.
Regulation (regulation) of EP10 in spinal cord associated with gaba and spinal cord
9) Confidence 0.05 Published 1998 Journal Perspect Dev Neurobiol Section Abstract Doc Link 9777631 Disease Relevance 0.16 Pain Relevance 0.58
Also, we have preliminary data (not shown) of a co-localization of CB1 and green fluorescent protein (GFP) in alBNST of knock-in mice expressing GFP under the control of the glutamate decarboxylase 67 (GAD67) promoter [38].
Regulation (control) of decarboxylase 67 associated with targeted disruption and glutamate
10) Confidence 0.01 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2810340 Disease Relevance 0.10 Pain Relevance 0.12

General Comments

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