INT29967

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Context Info
Confidence 0.40
First Reported 1988
Last Reported 2010
Negated 1
Speculated 3
Reported most in Body
Documents 40
Total Number 44
Disease Relevance 8.03
Pain Relevance 10.13

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

cytosol (Car2) extracellular space (Car2) lyase activity (Car2)
cytoplasm (Car2)
Anatomy Link Frequency
neurons 10
internal 4
spine 4
erythrocytes 2
smooth muscle 2
Car2 (Mus musculus)
Pain Link Frequency Relevance Heat
Glutamate 286 99.98 Very High Very High Very High
qutenza 47 99.98 Very High Very High Very High
Neurotransmitter 89 99.90 Very High Very High Very High
Eae 40 99.80 Very High Very High Very High
dorsal root ganglion 61 99.76 Very High Very High Very High
nMDA receptor 96 99.68 Very High Very High Very High
excitatory amino acid 5 99.54 Very High Very High Very High
GABAergic 58 99.52 Very High Very High Very High
Hyperalgesia 38 99.16 Very High Very High Very High
Dorsal horn neuron 24 99.16 Very High Very High Very High
Disease Link Frequency Relevance Heat
Apoptosis 201 100.00 Very High Very High Very High
Anaerobic Bacterial Infections 12 100.00 Very High Very High Very High
Inflammatory Pain 41 99.80 Very High Very High Very High
Alzheimer's Dementia 61 99.78 Very High Very High Very High
Ganglion Cysts 80 99.76 Very High Very High Very High
Hyperalgesia 46 99.16 Very High Very High Very High
INFLAMMATION 114 99.04 Very High Very High Very High
Anxiety Disorder 106 96.88 Very High Very High Very High
Repression 1 96.40 Very High Very High Very High
Increased Venous Pressure Under Development 52 91.28 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Local application of acetylcholine (ACh; 0.3 mM, 20 microl) elicited bi-phasic elevation of intracellular Ca2+ concentrations (contractile fast and non-contractile slow Ca2- signal measured as aequorin luminescence) in diaphragm muscle preparation.
Positive_regulation (elicited) of Positive_regulation (elevation) of Ca2 in muscle
1) Confidence 0.40 Published 1999 Journal Neurosci. Res. Section Abstract Doc Link 10096467 Disease Relevance 0 Pain Relevance 0.11
Induction of RP requires a postsynaptic [Ca2+]i increase and the subsequent activation of Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII) (Kano et al, 1992, 1996).
Positive_regulation (requires) of Positive_regulation (activation) of Ca2
2) Confidence 0.39 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0.15 Pain Relevance 0.27
To examine this issue, we investigated how large an increase in [Ca2+]i is required to induce sustained CaMKII activation by systematically altering the amplitude of transient [Ca2+]i increase (from 0.1 to 1 ?
Positive_regulation (induce) of Spec (investigated) Positive_regulation (increase) of Ca2
3) Confidence 0.34 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
On the other hand, a PDE1 increase of >30% made it impossible for any increase of [Ca2+]i (up to 10 ?
Positive_regulation (impossible) of Positive_regulation (increase) of Ca2
4) Confidence 0.34 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
In the absence of PDE1, the [Ca2+]i increase required for triggering sustained CaMKII activation (>1 ?
Positive_regulation (required) of Positive_regulation (increase) of Ca2
5) Confidence 0.34 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Therefore, the amount of active PP-1 transiently increased in response to the [Ca2+]i increase and subsequently showed a long-term decrease (Figure 2J).
Positive_regulation (increased) of Positive_regulation (response) of Ca2
6) Confidence 0.34 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.03
When the duration of conditioning stimulation was shorter, a slightly larger [Ca2+]i increase was required for triggering sustained CaMKII activation (0.6 ?
Positive_regulation (required) of Positive_regulation (increase) of Ca2
7) Confidence 0.34 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Since increased release of synaptic Glu would likely lead to hyper-activation of its receptors and increased accumulation of intracellular Ca2+, it might be expected that neurons of the Glud1 mice would adapt to over-stimulation of Glu receptors by increasing systems that either pump Ca2+ out of cells or sequester Ca2+ into organelles.
Positive_regulation (increased) of Positive_regulation (accumulation) of Ca2 in neurons associated with glutamate
8) Confidence 0.33 Published 2010 Journal BMC Genomics Section Body Doc Link PMC2896956 Disease Relevance 0 Pain Relevance 0.18
Stimulation of Ca2+ waves in astrocytes can increase both excitatory and inhibitory postsynaptic currents in hippocampal cultures [6].
Positive_regulation (increase) of Positive_regulation (Stimulation) of Ca2 in astrocytes
9) Confidence 0.33 Published 2005 Journal Purinergic Signal Section Body Doc Link PMC2096541 Disease Relevance 0.09 Pain Relevance 0.11
These results indicated that the exposure of ELF-MF might cause Ca2+ -dependent NOS activation, which then induces hyperalgesia with the increase in NO synthesis.
Spec (might) Positive_regulation (cause) of Spec (might) Positive_regulation (activation) of Ca2 associated with hyperalgesia
10) Confidence 0.32 Published 2006 Journal Life Sci. Section Abstract Doc Link 16457856 Disease Relevance 0.63 Pain Relevance 0.76
Pretreatment of tissues with calmodulin (CaM) inhibitor W7 did not affect Ca2+ increase, but markedly suppressed NO production by EFS , suggesting that increase in internal Ca2+ stimulates nNOS via a Ca2+-CaM mediated process to produce NO.
Positive_regulation (stimulates) of Positive_regulation (increase) of Ca2 in internal
11) Confidence 0.32 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2659787 Disease Relevance 0.24 Pain Relevance 0.35
This progressive decline occurred regardless of the extent of intraneuronal Ca2+ buffering, indicating that it was not due to accumulation of cytosolic Ca2+.
Neg (not) Positive_regulation (due) of Positive_regulation (accumulation) of Ca2
12) Confidence 0.28 Published 1988 Journal Neurosci. Lett. Section Abstract Doc Link 2850518 Disease Relevance 0 Pain Relevance 0.22
Activation of mGluRs may downregulate K+ currents, but this downregulation is not sufficient to explain a voltage-dependent ADP as indicated by the ramp current experiments (Figure 7), which show that upregulation of R-type Ca2+ current is required to produce the ADP.
Positive_regulation (required) of Positive_regulation (upregulation) of Ca2
13) Confidence 0.24 Published 2010 Journal PLoS Biology Section Body Doc Link PMC2982802 Disease Relevance 0.07 Pain Relevance 0.07
Superfusion of myocytes with Ang II (10 nM) induced acute increases of free systolic Ca2+i levels in both genotypes.
Positive_regulation (induced) of Positive_regulation (increases) of Ca2 in myocytes
14) Confidence 0.23 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC2916114 Disease Relevance 0 Pain Relevance 0
Increase in cytosolic Ca2+ started at the onset of the depolarization and peaked ?
Positive_regulation (peaked) of Positive_regulation (Increase) of Ca2
15) Confidence 0.23 Published 2001 Journal BMC Physiol Section Body Doc Link PMC37314 Disease Relevance 0 Pain Relevance 0.14
While this subunit is clearly non-essential for activation of the L-type Ca2+ channel and for triggering skeletal-type EC coupling, ?
Positive_regulation (essential) of Positive_regulation (activation) of Ca2
16) Confidence 0.23 Published 2001 Journal BMC Physiol Section Body Doc Link PMC37314 Disease Relevance 0.09 Pain Relevance 0.05
25–35 induced a [Ca2+]mit increase in 67±3% of the cells (mean±SEM, 1008±250 µM, 37 cells, 3 experiments) whereas 62±10% of the neurons responded to A?
Positive_regulation (induced) of Positive_regulation (increase) of Ca2 in neurons
17) Confidence 0.22 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2447871 Disease Relevance 0 Pain Relevance 0.03
Segal et al., proposed a unifying hypothesis relating intracellular calcium concentration with spine plasticity: moderate increase of Ca2+ would increase size and number of spines; low or high concentration of Ca2+ would lead to shrinkage and repression (Segal et al., 2000).
Positive_regulation (increase) of Positive_regulation (increase) of Ca2 in spine associated with repression
18) Confidence 0.21 Published 2010 Journal Anatomy & Cell Biology Section Body Doc Link PMC3015039 Disease Relevance 0.10 Pain Relevance 0
25–35 induced a similar large increase in both [Ca2+]cyt and [Ca2+]mit in GT1 neural cells (data not shown).
Positive_regulation (induced) of Positive_regulation (increase) of Ca2 in neural
19) Confidence 0.20 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2447871 Disease Relevance 0 Pain Relevance 0
An increased level of Ca2+ via activation of Ca2+ signaling pathways by inflammatory mediators would serve to increase the sensitivity of TRPA1 to its agonists [19].
Positive_regulation (increased) of Positive_regulation (activation) of Ca2 associated with inflammatory mediators and agonist
20) Confidence 0.17 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2753652 Disease Relevance 1.15 Pain Relevance 0.63

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