INT17962

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Context Info
Confidence 0.41
First Reported 1983
Last Reported 2010
Negated 25
Speculated 15
Reported most in Body
Documents 124
Total Number 141
Disease Relevance 33.98
Pain Relevance 22.71

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 11
cardiomyocyte 5
neuronal 4
brain 3
internal 3
Car2 (Mus musculus)
Pain Link Frequency Relevance Heat
Glutamate 434 100.00 Very High Very High Very High
antagonist 357 100.00 Very High Very High Very High
nMDA receptor 298 100.00 Very High Very High Very High
qutenza 263 100.00 Very High Very High Very High
Kinase C 116 100.00 Very High Very High Very High
Glutamate receptor 134 99.98 Very High Very High Very High
MU agonist 6 99.98 Very High Very High Very High
lidocaine 11 99.82 Very High Very High Very High
monoamine 34 99.80 Very High Very High Very High
Central nervous system 185 99.74 Very High Very High Very High
Disease Link Frequency Relevance Heat
Thiamine Deficiency 372 99.94 Very High Very High Very High
Pheochromocytoma 35 99.80 Very High Very High Very High
Death 524 99.76 Very High Very High Very High
Ganglion Cysts 139 99.68 Very High Very High Very High
Aging 233 99.66 Very High Very High Very High
Congenital Anomalies 84 99.60 Very High Very High Very High
Disease 1268 99.36 Very High Very High Very High
Obesity 182 99.20 Very High Very High Very High
Neurodegenerative Disease 116 99.12 Very High Very High Very High
Increased Venous Pressure Under Development 234 98.96 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Prediction of the model: role of PDE1 in the [Ca2+]i threshold regulation
Regulation (regulation) of Ca2
1) Confidence 0.41 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Our further study revealed the possible contribution of decreased adrenergic response, dysregulated intracellular Ca2+ homeostasis, protein damage and oxidative stress to impaired cardiomyocyte mechanical function in APP/PS1 mice.
Spec (possible) Regulation (dysregulated) of Ca2 in cardiomyocyte associated with stress
2) Confidence 0.40 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2696039 Disease Relevance 0.77 Pain Relevance 0
In this report we describe visualization and regulation of NO and calcium (Ca2+) in the myenteric nerve varicosities during neurotransmission using multiphoton microscopy.
Regulation (regulation) of Ca2 in nerve associated with increased venous pressure under development
3) Confidence 0.39 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2659787 Disease Relevance 0.18 Pain Relevance 0.32
CNQX and AP5 administration reduced the amplitude of the [Ca2+]i transients at the stimulus position (region b of Figure 3B) to 35.1±9.6% and 42.7±12.8% of the control condition in the cases of the 80 and 200 µA stimuli, respectively (n?
Regulation (amplitude) of Ca2
4) Confidence 0.38 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2966408 Disease Relevance 0 Pain Relevance 0.03
We measured the onset of the [Ca2+]i transients as the time when ?
Regulation (onset) of Ca2
5) Confidence 0.38 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2966408 Disease Relevance 0 Pain Relevance 0
In addition, Ca2+ oscillations of varying frequencies are important for gene expression and other rhythmic activities [1], [5].
Regulation (important) of Ca2
6) Confidence 0.37 Published 2007 Journal PLoS ONE Section Body Doc Link PMC1991622 Disease Relevance 0.47 Pain Relevance 0.19
Ca2+ pump activity is known to be reduced in muscular dystrophy and in Brody disease.22,25 However, little information is available on the role of Ca2+ pump in ocular disease, especially in oculomotor disease, although it was reported that Ca2+ pump activity changes in lens epithelial cells after treated with an oxidant or heat.26 In the present study, Ca2+ pump levels, which is one of the factors that impacts the Ca2+ uptake rate, were assayed by western blotting for SERCA 1, a fast twitch isoform of SERCA.
Regulation (impacts) of Ca2 in epithelial cells associated with frailty, disease and eye disease
7) Confidence 0.32 Published 2006 Journal Yonsei Medical Journal Section Body Doc Link PMC2687630 Disease Relevance 0.46 Pain Relevance 0.04
These include ryanodine receptor, a Ca2+ release channel which participates in Ca2+ release from sarcoplasmic reticulum into muscle cells, Ca2+-ATPase, which drives Ca2+ uptake, and calsequestrin that binds with Ca2+.8-11 Thus, since Ca2+ uptake by the sarcoplasmic reticulum and Ca2+ release from the sarcoplasmic reticulum play key roles in the regulation of Ca2+ concentrations in muscle cells, the above proteins are important elements in studies on the mechanisms of muscle contraction and relaxation.
Regulation (regulation) of Ca2 in muscle
8) Confidence 0.32 Published 2006 Journal Yonsei Medical Journal Section Body Doc Link PMC2687630 Disease Relevance 0.43 Pain Relevance 0
Several regulatory proteins present in the sarcoplasmic reticulum plays fundamental roles in regulating the intramuscular concentration of Ca2+.
Regulation (regulating) of Ca2 in reticulum
9) Confidence 0.32 Published 2006 Journal Yonsei Medical Journal Section Body Doc Link PMC2687630 Disease Relevance 0.22 Pain Relevance 0
In addition to the genes whose function is the regulation of intracellular Ca2+ levels, there were several genes whose expression was up-regulated and whose function is the modulation of intracellular signalling mediated by Ca2+, such as Camk2a, Camk2b, and Ppp3ca (Protein Phosphatase 3, Catalytic Subunit, Alpha Isoform).
Regulation (regulation) of Ca2
10) Confidence 0.32 Published 2010 Journal BMC Genomics Section Body Doc Link PMC2896956 Disease Relevance 0.05 Pain Relevance 0.24
These results support the idea that calcineurin-mediated feedforward inhibition is not significantly involved in the control of the [Ca2+]i threshold.
Regulation (control) of Ca2
11) Confidence 0.30 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Indeed, alteration of the affinity of CaMKII and Ca2+/CaM significantly affected the Ca2+-mediated CaMKII activation (see Supplementary information).
Regulation (affected) of Ca2
12) Confidence 0.30 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Surprisingly, alteration of the concentration of calcineurin had little effect on the [Ca2+]i threshold (Figure 6D–F).
Neg (little) Regulation (effect) of Ca2
13) Confidence 0.30 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
The predominant role of PDE1 in controlling the [Ca2+]i threshold was evident, even if the duration of [Ca2+]i stimulation was shortened (Supplementary Figure 5).
Regulation (controlling) of Ca2
14) Confidence 0.30 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
PDE1 inhibition did not significantly affect the [Ca2+]i increase triggered by each conditioning depolarization (Figure 7C) or the basal GABAAR responsiveness (Supplementary Table 1).
Neg (not) Regulation (affect) of Ca2
15) Confidence 0.30 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
In contrast, when the concentration of Ca2+-independent PDE4 was altered, the [Ca2+]i threshold required for sustained CaMKII activation was little affected (Figure 6C, E, and F).
Neg (little) Regulation (affected) of Ca2
16) Confidence 0.30 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
These pathways might regulate the [Ca2+]i threshold for RP induction.
Spec (might) Regulation (regulate) of Ca2
17) Confidence 0.30 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Thus, PDE4 has a marginal role in the regulation of the [Ca2+]i threshold for RP induction.
Regulation (regulation) of Ca2
18) Confidence 0.30 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Using these conditioning stimulations, we examined the [Ca2+]i threshold for RP induction.
Spec (examined) Regulation (threshold) of Ca2
19) Confidence 0.30 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.11
Taken together, the findings show that RP was induced in an all-or-none manner dependent on the [Ca2+]i increase (at least >0.45 ?
Regulation (dependent) of Ca2
20) Confidence 0.30 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.07

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