INT315020

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Context Info
Confidence 0.51
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 4
Disease Relevance 2.24
Pain Relevance 0.08

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

transport (Cacna1d) plasma membrane (Cacna1d) transmembrane transport (Cacna1d)
Anatomy Link Frequency
cerebellum 4
Cacna1d (Mus musculus)
Pain Link Frequency Relevance Heat
Intracerebroventricular 4 55.44 Quite High
addiction 12 24.08 Low Low
Neurotransmitter 28 20.92 Low Low
Glutamate 16 10.80 Low Low
Action potential 12 5.00 Very Low Very Low Very Low
long-term potentiation 8 5.00 Very Low Very Low Very Low
anesthesia 4 5.00 Very Low Very Low Very Low
adenocard 4 5.00 Very Low Very Low Very Low
amygdala 4 5.00 Very Low Very Low Very Low
halothane 4 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Channelopathies 68 99.92 Very High Very High Very High
Dystonia 40 99.68 Very High Very High Very High
Syndrome 24 98.20 Very High Very High Very High
Ataxia 8 58.36 Quite High
Stress 8 53.12 Quite High
Absence Epilepsy 4 39.68 Quite Low
Disease 56 33.00 Quite Low
Congenital Anomalies 4 25.20 Quite Low
Dyskinesias 4 21.52 Low Low
Anxiety Disorder 8 15.88 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The finding that enhanced LTCC expression and most likely activity in Purkinje cells contributes to the paroxysmal dystonia of the tottering phenotype is in good agreement with the observation that dystonic episodes lead to neuronal activation in the cerebellum and its relay nuclei in these mice [9], and that the dystonic phenotype is absent in tottering mice lacking Purkinje cells [11].
Positive_regulation (enhanced) of Gene_expression (expression) of LTCC in cerebellum associated with dystonia
1) Confidence 0.51 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0.67 Pain Relevance 0.03
Obviously, channelopathies in different LTCC ?
Positive_regulation (different) of Gene_expression (different) of LTCC associated with channelopathies
2) Confidence 0.37 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0.29 Pain Relevance 0
The finding that enhanced LTCC expression and most likely activity in Purkinje cells contributes to the paroxysmal dystonia of the tottering phenotype is in good agreement with the observation that dystonic episodes lead to neuronal activation in the cerebellum and its relay nuclei in these mice [9], and that the dystonic phenotype is absent in tottering mice lacking Purkinje cells [11].
Positive_regulation (contributes) of Gene_expression (expression) of LTCC in cerebellum associated with dystonia
3) Confidence 0.34 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0.63 Pain Relevance 0.03
Somehow, altered Cav2.1 channel signaling appears to activate pathways that enhance Cav1.2 (but not Cav1.3; [38]) LTCC expression.
Positive_regulation (enhance) of Gene_expression (expression) of LTCC
4) Confidence 0.34 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0.65 Pain Relevance 0.03

General Comments

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