INT62786

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Context Info
Confidence 0.29
First Reported 1996
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 2
Total Number 6
Disease Relevance 0.52
Pain Relevance 0.70

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

signal transduction (Chrm1) plasma membrane (Chrm1) signal transducer activity (Chrm1)
Chrm1 (Mus musculus)
Pain Link Frequency Relevance Heat
Hippocampus 50 96.92 Very High Very High Very High
agonist 110 90.40 High High
noradrenaline 5 89.48 High High
long-term potentiation 315 83.36 Quite High
lidocaine 1 73.84 Quite High
antagonist 35 65.96 Quite High
nMDA receptor 10 45.20 Quite Low
Pyramidal cell 75 37.56 Quite Low
Action potential 25 24.72 Low Low
potassium channel 30 19.44 Low Low
Disease Link Frequency Relevance Heat
Targeted Disruption 5 99.96 Very High Very High Very High
Cognitive Disorder 35 92.48 High High
Convulsion 1 85.28 High High
Depression 15 5.00 Very Low Very Low Very Low
Disease 15 5.00 Very Low Very Low Very Low
Camurati-engelmann Disease 5 5.00 Very Low Very Low Very Low
Schizophrenia 5 5.00 Very Low Very Low Very Low
Ganglion Cysts 5 5.00 Very Low Very Low Very Low
Spontaneous Rupture 5 5.00 Very Low Very Low Very Low
Disseminated Intravascular Coagulation 5 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Therefore, we also tested whether the CK2 inhibitors 4,5,6,7-tetrabromobenzotriazole (TBB) or 2-(4,5,6,7-tetrabromo-2-(dimethylamino)-1H-benzo[d]imidazol-1-yl) acetic acid (TMCB) (Pagano et al., 2008) could block the M1 receptor-induced inhibition of IAHP.
Negative_regulation (inhibition) of M1 receptor
1) Confidence 0.29 Published 2010 Journal Neuron Section Body Doc Link PMC3003154 Disease Relevance 0 Pain Relevance 0.04
Bath application of the PKC inhibitor Go6976 (200 nM) significantly reduced the M1 receptor-induced inhibition of IAHP (Figure 7A; 87% ± 2% of control, n = 6, p < 0.05 compared to 77-LH-28-1), indicating that activation of PKC by M1 receptors is necessary for the inhibition of SK channels.
Negative_regulation (reduced) of M1 receptor
2) Confidence 0.29 Published 2010 Journal Neuron Section Body Doc Link PMC3003154 Disease Relevance 0 Pain Relevance 0
We next investigated the mechanism for the M1 receptor-mediated inhibition of SK channels.
Spec (investigated) Negative_regulation (inhibition) of M1 receptor
3) Confidence 0.29 Published 2010 Journal Neuron Section Body Doc Link PMC3003154 Disease Relevance 0 Pain Relevance 0.03
Therefore, we tested whether PKC inhibitors could block the M1 receptor-mediated prolongation of EPSPs and inhibition of IAHP.
Negative_regulation (inhibition) of M1 receptor
4) Confidence 0.29 Published 2010 Journal Neuron Section Body Doc Link PMC3003154 Disease Relevance 0 Pain Relevance 0.03
Learning, working memory, and the induction of synaptic plasticity are all impaired in M1 receptor knockout mice (Anagnostaras et al., 2003; Shinoe et al., 2005; Wess, 2004).
Negative_regulation (impaired) of M1 receptor associated with targeted disruption
5) Confidence 0.25 Published 2010 Journal Neuron Section Body Doc Link PMC3003154 Disease Relevance 0.43 Pain Relevance 0.52
At micromolar concentrations, compounds 1, 12, and 13 inhibited the binding of [3H]-pirenzepine and of [3H]-di-o-tolylguanidine respectively on M1 and sigma receptors; in the last case comp. 13 was more active (IC50 = 0.3 microM) than the epimeric 1.
Negative_regulation (inhibited) of M1
6) Confidence 0.19 Published 1996 Journal Farmaco Section Abstract Doc Link 8688138 Disease Relevance 0.09 Pain Relevance 0.07

General Comments

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