INT26698

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.67
First Reported 1987
Last Reported 2011
Negated 1
Speculated 2
Reported most in Abstract
Documents 37
Total Number 56
Disease Relevance 26.33
Pain Relevance 39.10

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

transport (Cacna1a) DNA binding (Cacna1a) transmembrane transport (Cacna1a)
cytoplasm (Cacna1a) cell death (Cacna1a) nucleus (Cacna1a)
Anatomy Link Frequency
brain 5
pore 4
neurons 3
interneurons 2
plasma 1
Cacna1a (Mus musculus)
Pain Link Frequency Relevance Heat
amygdala 2363 100.00 Very High Very High Very High
qutenza 1429 100.00 Very High Very High Very High
long-term potentiation 1332 100.00 Very High Very High Very High
Migraine 368 100.00 Very High Very High Very High
Glutamate 105 100.00 Very High Very High Very High
gABA 96 100.00 Very High Very High Very High
depression 75 100.00 Very High Very High Very High
Neurotransmitter 45 100.00 Very High Very High Very High
isoflurane 198 99.52 Very High Very High Very High
GABAergic 164 99.38 Very High Very High Very High
Disease Link Frequency Relevance Heat
Headache 253 100.00 Very High Very High Very High
Migraine With Aura 179 100.00 Very High Very High Very High
Epilepsy 97 100.00 Very High Very High Very High
Depression 75 100.00 Very High Very High Very High
Malignant Neoplastic Disease 57 100.00 Very High Very High Very High
Ataxia 27 100.00 Very High Very High Very High
Urological Neuroanatomy 24 100.00 Very High Very High Very High
Spinocerebellar Ataxia Type 2 18 100.00 Very High Very High Very High
Paresis 5 99.92 Very High Very High Very High
Apoptosis 150 99.84 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Investigations of the signal pathways further supported that activation of alpha 1A -adrenoceptor is responsible for the stimulatory effect of caffeic acid on BER secretion from the adrenal medulla.
Positive_regulation (activation) of alpha 1A in adrenal medulla associated with medulla
1) Confidence 0.67 Published 2003 Journal Horm. Metab. Res. Section Abstract Doc Link 12778369 Disease Relevance 0.57 Pain Relevance 0.38
Therefore, beta-endorphin release from the adrenal gland appears to be responsible for the lowering of plasma glucose in STZ-diabetic rats induced by caffeic acid, through the activation of alpha 1A -adrenoceptors.
Positive_regulation (activation) of alpha 1A in adrenal gland associated with diabetes mellitus
2) Confidence 0.67 Published 2003 Journal Horm. Metab. Res. Section Abstract Doc Link 12778369 Disease Relevance 0.37 Pain Relevance 0.16
The endogenous catecholamines adrenaline and noradrenaline mediate their biological actions via activation of nine different adrenergic receptor subtypes, three alpha 1-receptors (alpha 1A, alpha 1B, alpha 1D), three alpha 2-receptors (alpha 2A, alpha 2B, alpha 2C) and three beta-receptors (beta 1, beta 2, beta 3).
Positive_regulation (activation) of alpha 1A associated with catecholamine and noradrenaline
3) Confidence 0.67 Published 2001 Journal Z Kardiol Section Abstract Doc Link 11677796 Disease Relevance 0.13 Pain Relevance 0.10
Expansion in a coding 3' CAG repeat causes spino-cerebellar ataxia type 6 (SCA6).
Positive_regulation (causes) of SCA6 associated with ataxia
4) Confidence 0.65 Published 1999 Journal Psychiatr. Genet. Section Abstract Doc Link 10412193 Disease Relevance 0.87 Pain Relevance 0.10
Familial hemiplegic migraine type 1 (FHM1) is caused by missense mutations in the CACNA1A gene that encodes the alpha1A pore-forming subunit of Ca(V)2.1 Ca(2+) channels.
Positive_regulation (caused) of FHM1 in pore associated with migraine with aura and migraine
5) Confidence 0.61 Published 2010 Journal Proteomics Section Abstract Doc Link 20391530 Disease Relevance 0.43 Pain Relevance 0.21
Here, we have used whole-cell recordings to determine whether the leaner mutation alters calcium channel currents in cerebellar Purkinje cells, both because these cells are profoundly affected in leaner mice and because they normally express high levels of alpha1A.
Positive_regulation (levels) of alpha1A in Purkinje cells associated with calcium channel
6) Confidence 0.50 Published 1998 Journal J. Neurosci. Section Abstract Doc Link 9614225 Disease Relevance 0.44 Pain Relevance 0.19
Mutations in the genes CACNA1A and SCNA1A, encoding the pore-forming alpha(1) subunits of the neuronal voltage-gated Ca2+ channels Ca(V)2.1 and Na+ channels Na(V)1.1, are responsible for FHM1 and FHM3, respectively, whereas mutations in ATP1A2, encoding the alpha2 subunit of the Na+, K+ adenosinetriphosphatase (ATPase), are responsible for FHM2.
Positive_regulation (responsible) of FHM2 in neuronal
7) Confidence 0.50 Published 2007 Journal Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics Section Abstract Doc Link 17395138 Disease Relevance 0.61 Pain Relevance 0.55
These findings are consistent with the hypothesis that FHM mutations share the ability of rendering the brain more susceptible to CSD by causing either excessive synaptic glutamate release (FHM1) or decreased removal of K+ and glutamate from the synaptic cleft (FHM2) or excessive extracellular K+ (FHM3).
Positive_regulation (causing) of FHM3 in brain associated with glutamate and migraine
8) Confidence 0.50 Published 2007 Journal Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics Section Abstract Doc Link 17395138 Disease Relevance 0.84 Pain Relevance 1.01
These findings are consistent with the hypothesis that FHM mutations share the ability of rendering the brain more susceptible to CSD by causing either excessive synaptic glutamate release (FHM1) or decreased removal of K+ and glutamate from the synaptic cleft (FHM2) or excessive extracellular K+ (FHM3).
Positive_regulation (causing) of FHM1 in brain associated with glutamate and migraine
9) Confidence 0.50 Published 2007 Journal Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics Section Abstract Doc Link 17395138 Disease Relevance 0.81 Pain Relevance 0.97
Mutations in the genes CACNA1A and SCNA1A, encoding the pore-forming alpha(1) subunits of the neuronal voltage-gated Ca2+ channels Ca(V)2.1 and Na+ channels Na(V)1.1, are responsible for FHM1 and FHM3, respectively, whereas mutations in ATP1A2, encoding the alpha2 subunit of the Na+, K+ adenosinetriphosphatase (ATPase), are responsible for FHM2.
Positive_regulation (responsible) of FHM1 in pore
10) Confidence 0.50 Published 2007 Journal Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics Section Abstract Doc Link 17395138 Disease Relevance 0.48 Pain Relevance 0.48
Mutations in the genes CACNA1A and SCNA1A, encoding the pore-forming alpha(1) subunits of the neuronal voltage-gated Ca2+ channels Ca(V)2.1 and Na+ channels Na(V)1.1, are responsible for FHM1 and FHM3, respectively, whereas mutations in ATP1A2, encoding the alpha2 subunit of the Na+, K+ adenosinetriphosphatase (ATPase), are responsible for FHM2.
Positive_regulation (responsible) of FHM3 in pore
11) Confidence 0.50 Published 2007 Journal Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics Section Abstract Doc Link 17395138 Disease Relevance 0.48 Pain Relevance 0.49
Thus, there is no current evidence that the genes causing FHM represent major susceptibility loci for the typical migraines.
Positive_regulation (causing) of FHM associated with cluster headache and migraine
12) Confidence 0.47 Published 2008 Journal J Headache Pain Section Body Doc Link PMC2276243 Disease Relevance 1.88 Pain Relevance 1.24
The 5-HT1B receptor appears to mediate the attenuating action of RU 24969; the exact mechanism of action of 8-OH-DPAT remains open but activation of an alpha 1-adrenoceptor is implicated.
Positive_regulation (activation) of alpha 1
13) Confidence 0.45 Published 1989 Journal Eur. J. Pharmacol. Section Abstract Doc Link 2566495 Disease Relevance 0 Pain Relevance 0.28
These studies show the following: (1) FHM1 mutations produce gain-of-function of the Ca(V)2.1 channel and, as a consequence, increased Ca(V)2.1-dependent neurotransmitter release from cortical neurons and facilitation of in vivo induction and propagation of cortical spreading depression (CSD: the phenomenon underlying migraine aura); (2) FHM2 mutations produce loss-of-function of the alpha2 Na+,K+-ATPase; and (3) the FHM3 mutation accelerates recovery from fast inactivation of Na(V)1.5 (and presumably Na(V)1.1) channels.
Positive_regulation (following) of FHM2 in neurons associated with epilepsy, neurotransmitter, depression and migraine
14) Confidence 0.44 Published 2007 Journal Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics Section Abstract Doc Link 17395138 Disease Relevance 0.90 Pain Relevance 0.89
Expansions of the CAG repeat in the CACNA1A gene on the short arm of the chromosome 19 induce SCA6, and point mutations in the same gene are responsible for EA2 and FHM.
Positive_regulation (induce) of SCA6 in arm associated with migraine and spinocerebellar ataxia type 2
15) Confidence 0.44 Published 2001 Journal J. Korean Med. Sci. Section Abstract Doc Link 11748369 Disease Relevance 1.09 Pain Relevance 0.33
Fig. 2B plots the changes in VOR gain induced by each training paradigm in leaner heterozygous mice (blue squares) and ?
Positive_regulation (induced) of leaner
16) Confidence 0.43 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2572847 Disease Relevance 0 Pain Relevance 0
CONCLUSIONS: The disease-causing mutation in this family was identified, showing that a unique mutation in the CACNA1A gene causes several phenotypes, including those of SCA6 and FHM, thus suggesting that SCA6 and FHM are not only allelic diseases but are the same disorder with a large phenotypic variability.


Positive_regulation (causes) of SCA6
17) Confidence 0.43 Published 2003 Journal Arch. Neurol. Section Body Doc Link 12707077 Disease Relevance 0.05 Pain Relevance 0
CONCLUSIONS: The disease-causing mutation in this family was identified, showing that a unique mutation in the CACNA1A gene causes several phenotypes, including those of SCA6 and FHM, thus suggesting that SCA6 and FHM are not only allelic diseases but are the same disorder with a large phenotypic variability.


Positive_regulation (causes) of FHM
18) Confidence 0.43 Published 2003 Journal Arch. Neurol. Section Body Doc Link 12707077 Disease Relevance 0.05 Pain Relevance 0
Thus, FHM 1, EA2 and SCA6 are all allelic channelopathies, with missense mutations mostly accounting for FHM, mutations disrupting the reading frame for EA2 and polyglutamine expansions in the COOH gene terminal for SCA6.
Positive_regulation (accounting) of FHM associated with migraine and channelopathies
19) Confidence 0.41 Published 2008 Journal J Headache Pain Section Body Doc Link PMC2276243 Disease Relevance 2.62 Pain Relevance 1.35
FHM is caused by a penetrant autosomal dominant genetic mutation; several mutations have been genotyped, involving brain-expressed ion channels.
Positive_regulation (caused) of FHM in brain associated with migraine
20) Confidence 0.40 Published 2003 Journal Neuroradiology Section Abstract Doc Link 12669159 Disease Relevance 0.71 Pain Relevance 0.46

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox