INT276079

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Context Info
Confidence 0.41
First Reported 2009
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 4
Disease Relevance 0
Pain Relevance 0.12

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

cytoplasm (Pde1b, Camk2a) signal transduction (Pde1b) plasma membrane (Camk2a)
nucleus (Pde1b) kinase activity (Camk2a)
Pde1b (Mus musculus)
Camk2a (Mus musculus)
Pain Link Frequency Relevance Heat
Central nervous system 8 97.84 Very High Very High Very High
long-term potentiation 16 85.44 High High
Dopamine 4 56.20 Quite High
interneuron 4 42.72 Quite Low
GABAergic 4 18.92 Low Low
depression 36 6.16 Low Low
gABA 44 5.00 Very Low Very Low Very Low
imagery 20 5.00 Very Low Very Low Very Low
Kinase C 4 5.00 Very Low Very Low Very Low
Serotonin 4 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Adhesions 8 26.48 Quite Low
Depression 36 6.16 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The simulation predicted that PDE1-mediated feedforward inhibition of CaMKII predominantly controls the Ca2+ threshold, which was confirmed by electrophysiological experiments in primary cerebellar cultures.
PDE1 Negative_regulation (inhibition) of CaMKII
1) Confidence 0.41 Published 2009 Journal Mol Syst Biol Section Abstract Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Thus, the PDE1-mediated feedforward inhibition of CaMKII and the positive-feedback loop consisting of CaMKII-mediated PDE1 inhibition might underlie regulation of the threshold and/or the maintenance of many forms of synaptic plasticity.
PDE1 Negative_regulation (inhibition) of CaMKII
2) Confidence 0.41 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.09
It also predicted that feedforward inhibition of CaMKII by a pathway including PDE1 predominantly determined the Ca2+ threshold for RP induction, which was confirmed by electrophysiological experiments.


PDE1 Negative_regulation (inhibition) of CaMKII
3) Confidence 0.41 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.03
Thus, the combined applications of computational simulation and cell biological experiments revealed a critical role of the feedforward inhibition of CaMKII by PDE1 in regulating the threshold for RP induction.
PDE1 Negative_regulation (inhibition) of CaMKII
4) Confidence 0.41 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0

General Comments

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