INT75765

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Context Info
Confidence 0.70
First Reported 1998
Last Reported 2011
Negated 0
Speculated 1
Reported most in Body
Documents 17
Total Number 18
Disease Relevance 17.51
Pain Relevance 10.91

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
neurons 12
pore 4
synapses 4
juvenile 2
brain 2
Cacna1a (Mus musculus)
Pain Link Frequency Relevance Heat
amygdala 316 100.00 Very High Very High Very High
Migraine 149 100.00 Very High Very High Very High
qutenza 85 100.00 Very High Very High Very High
long-term potentiation 74 100.00 Very High Very High Very High
depression 17 100.00 Very High Very High Very High
Neurotransmitter 10 100.00 Very High Very High Very High
Calcium channel 6 97.40 Very High Very High Very High
headache 18 94.32 High High
medulla 30 86.80 High High
GABAergic 11 85.84 High High
Disease Link Frequency Relevance Heat
Cancer 801 100.00 Very High Very High Very High
Targeted Disruption 122 100.00 Very High Very High Very High
Headache 96 100.00 Very High Very High Very High
Malignant Neoplastic Disease 95 100.00 Very High Very High Very High
Migraine With Aura 65 100.00 Very High Very High Very High
Epilepsy 19 100.00 Very High Very High Very High
Depression 17 100.00 Very High Very High Very High
Apoptosis 251 99.84 Very High Very High Very High
Migraine Without Aura 6 99.52 Very High Very High Very High
Death 96 98.40 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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 Gene_expression (express) of alpha1A in Purkinje cells associated with calcium channel
1) Confidence 0.70 Published 1998 Journal J. Neurosci. Section Abstract Doc Link 9614225 Disease Relevance 0.44 Pain Relevance 0.19
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 (increased) of Gene_expression (produce) of FHM2 in neurons associated with epilepsy, neurotransmitter, depression and migraine
2) Confidence 0.44 Published 2007 Journal Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics Section Abstract Doc Link 17395138 Disease Relevance 0.94 Pain Relevance 0.94
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 (produce) of Gene_expression (produce) of FHM2 in neurons associated with epilepsy, neurotransmitter, depression and migraine
3) Confidence 0.44 Published 2007 Journal Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics Section Abstract Doc Link 17395138 Disease Relevance 0.95 Pain Relevance 0.95
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 (loss-of-function) of Gene_expression (produce) of FHM2 in neurons associated with epilepsy, neurotransmitter, depression and migraine
4) Confidence 0.44 Published 2007 Journal Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics Section Abstract Doc Link 17395138 Disease Relevance 0.91 Pain Relevance 0.91
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 (gain-of-function) of Gene_expression (produce) of FHM2 in neurons associated with epilepsy, neurotransmitter, depression and migraine
5) Confidence 0.44 Published 2007 Journal Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics Section Abstract Doc Link 17395138 Disease Relevance 0.95 Pain Relevance 0.95
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 (induction) of Gene_expression (produce) of FHM2 in neurons associated with epilepsy, neurotransmitter, depression and migraine
6) Confidence 0.44 Published 2007 Journal Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics Section Abstract Doc Link 17395138 Disease Relevance 0.92 Pain Relevance 0.92
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 (facilitation) of Gene_expression (produce) of FHM2 in neurons associated with epilepsy, neurotransmitter, depression and migraine
7) Confidence 0.44 Published 2007 Journal Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics Section Abstract Doc Link 17395138 Disease Relevance 0.92 Pain Relevance 0.92
Three genes for FHM have been identified: CACNA1A (FHM1), encoding the pore-forming ?
Positive_regulation (genes) of Gene_expression (identified) of FHM1 in pore associated with migraine
8) Confidence 0.35 Published 2010 Journal Mol Pain Section Body Doc Link PMC2974658 Disease Relevance 1.80 Pain Relevance 1.61
Three genes for FHM have been identified: CACNA1A (FHM1), encoding the pore-forming ?
Positive_regulation (genes) of Gene_expression (identified) of CACNA1A in pore associated with migraine
9) Confidence 0.35 Published 2010 Journal Mol Pain Section Body Doc Link PMC2974658 Disease Relevance 1.80 Pain Relevance 1.61
Indeed, as shown in Fig. 1B, Juvenile Thalamo-LA synapses typically behave as phasic synapses [31] with a small amount of PPR [1.23±0.07, n?
Positive_regulation (-) of Gene_expression (synapses) of LA in synapses associated with amygdala
10) Confidence 0.18 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2896423 Disease Relevance 0.05 Pain Relevance 0.35
Together with the strong decrease in Cortico-LA PPR in adult Mecp2308/Y mice (Fig. 2), we conclude that the prolonged absence of Mecp2 strongly increased release probability at Cortico-LA synapses, possibly compensating for the progressive synaptic elimination.


Spec (possibly) Positive_regulation (increased) of Gene_expression (synapses) of LA in synapses associated with amygdala
11) Confidence 0.18 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2896423 Disease Relevance 0 Pain Relevance 0.47
La overexpression in malignancy is consistent with the increased ribosomal biogenesis and protein synthesis that are invariant features of malignancy [44], and associated with overexpression of RNP in the nucleolus, the ribosome factory of the cell [45].
Positive_regulation (overexpression) of Gene_expression (overexpression) of La associated with malignant neoplastic disease
12) Confidence 0.16 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2645692 Disease Relevance 1.38 Pain Relevance 0
We discovered that La is overexpressed in malignancy and actively induced in apoptotic malignant cells in response to DNA-damaging treatment [29].
Positive_regulation (overexpressed) of Gene_expression (overexpressed) of La associated with malignant neoplastic disease and apoptosis
13) Confidence 0.16 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2645692 Disease Relevance 1.34 Pain Relevance 0
In contrast, chemotherapy not only markedly increased the frequency of dead tumor cells (Figure 2A) but also produced a cumulative increase in DAB4 binding to each dead tumor cell (Figure 2B), and suggested that DNA-damaging drugs induced tumor cell expression of La in vivo.
Positive_regulation (induced) of Gene_expression (expression) of La associated with cancer
14) Confidence 0.16 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2645692 Disease Relevance 1.45 Pain Relevance 0
La acts as a molecular chaperone for transfer and ribosomal RNA species generated by RNA polymerase III, which is overactive in malignancy [42].
Positive_regulation (transfer) of Gene_expression (transfer) of La associated with malignant neoplastic disease
15) Confidence 0.12 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2645692 Disease Relevance 1.27 Pain Relevance 0
We discovered that La is overexpressed in malignancy and actively induced in apoptotic malignant cells in response to DNA-damaging treatment [29].
Positive_regulation (induced) of Gene_expression (overexpressed) of La associated with malignant neoplastic disease and apoptosis
16) Confidence 0.11 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2645692 Disease Relevance 1.36 Pain Relevance 0
-syn was significantly increased in the brain of symptomatic A53T mice compared with nTg controls and asymptomatic mice (Fig. 8A).
Positive_regulation (increased) of Gene_expression (controls) of nTg in brain associated with targeted disruption
17) Confidence 0.05 Published 2010 Journal Mol Brain Section Body Doc Link PMC2873589 Disease Relevance 1.03 Pain Relevance 0.16
However, the suppressive effect of capsaicin on LA-LTP was also present in coronal slices derived from juvenile mice (control: 120.5±3.2% [n?
Positive_regulation (-) of Gene_expression (effect) of LA in juvenile associated with qutenza, long-term potentiation and amygdala
18) Confidence 0.05 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3020947 Disease Relevance 0 Pain Relevance 0.95

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