INT180240

Context Info Confidence 0.47 First Reported 2004 Last Reported 2010 Negated 0 Speculated 0 Reported most in Body Documents 7 Total Number 7 Disease Relevance 2.99 Pain Relevance 0.86

mitochondrion (Gad1) lyase activity (Gad1) intracellular (Gad1) cytoplasm (Gad1)

Anatomy Link Frequency neurons 1 brain 1 synaptic vesicles 1 palate 1 Gad1 (Mus musculus)

Pain Link Frequency Relevance Heat gABA 118 100.00 GABAergic 90 100.00 adenocard 3 100.00 ketamine 7 98.32 Hippocampus 15 86.64 Glutamate 45 79.60 Action potential 20 75.28 Spinal cord 17 73.52 medulla 2 72.24 long-term potentiation 3 66.96

Disease Link Frequency Relevance Heat Cleft Palate 24 100.00 Targeted Disruption 61 99.60 Umbilical Hernia 24 96.20 Cognitive Disorder 38 92.80 Aging 23 92.32 Cerebral Palsy 86 89.80 Spasticity 40 89.68 Dyskinesias 2 79.60 Epilepsy 21 78.80 Neurological Disease 6 78.04

Sentences Mentioned In

Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

The association of GAD67 with membranes requires formation of heteromeric links with GAD65, which are mediated via their N-terminal domains.

GAD67 Binding (association) of

1) Confidence 0.47 Published 2004 Journal BMC Neurol Section Body Doc Link PMC544830 Disease Relevance 0.86 Pain Relevance 0.17

These N-terminal domains are thought to be responsible for sub-cellular targeting and the formation of GAD65–GAD67 heterodimers [26].

GAD67 Binding (formation) of

2) Confidence 0.35 Published 2004 Journal BMC Neurol Section Body Doc Link PMC544830 Disease Relevance 0.23 Pain Relevance 0.03

Concerning the mechanism of onset of cleft palate, studies using knockout mice have revealed associations between cleft palate and mutation of genes related to GABA signaling, such as GAD67 and GABRB3 [8,23,38].

GAD67 Binding (associations) of in palate associated with targeted disruption, gaba and cleft palate

3) Confidence 0.34 Published 2010 Journal Mol Brain Section Body Doc Link PMC3023674 Disease Relevance 1.25 Pain Relevance 0.23

The VTM neurons of HDC-KO mice showed no histamine immunoreactivity, but were immunoreactive for the histaminergic (HA) neuron markers adenosine deaminase and glutamic acid decarboxylase 67.

glutamic acid decarboxylase Binding (immunoreactive) of in neurons associated with adenocard

4) Confidence 0.27 Published 2010 Journal Frontiers in Behavioral Neuroscience Section Abstract Doc Link PMC2972729 Disease Relevance 0.17 Pain Relevance 0.12

GAD65, an isoform of glutamic acid decarboxylase, is localized to GABAergic presynaptic terminals and physically coupled to synaptic vesicles ([29]).

glutamic acid decarboxylase Binding (coupled) of in synaptic vesicles associated with gabaergic

5) Confidence 0.25 Published 2008 Journal PLoS Biology Section Body Doc Link PMC2689695 Disease Relevance 0 Pain Relevance 0.15

We recently reported that acute (days) elevation of superoxide production in brain by ketamine caused the loss of phenotype of PV-interneurons, as demonstrated by reduced PV and GAD67 immunoreactivity, which recovered over a few days.

GAD67 Binding (recovered) of in brain associated with ketamine

6) Confidence 0.24 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2678193 Disease Relevance 0.49 Pain Relevance 0.13

500, Sigma, T8660), polyclonal anti-GAD1(GAD67) (rabbit, 1?

GAD67 Binding (rabbit) of

7) Confidence 0.21 Published 2010 Journal PLoS Biology Section Body Doc Link PMC2872647 Disease Relevance 0 Pain Relevance 0.04

General Comments

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