INT170503

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Context Info
Confidence 0.29
First Reported 2001
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 11
Total Number 11
Disease Relevance 3.27
Pain Relevance 0.61

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

Anatomy Link Frequency
myotubes 6
pore 2
skeletal muscle 2
osteoclasts 2
foot 2
Tmie (Mus musculus)
Pain Link Frequency Relevance Heat
addiction 76 94.48 High High
halothane 13 94.28 High High
adenocard 5 94.00 High High
agonist 20 78.08 Quite High
amygdala 5 73.16 Quite High
long-term potentiation 10 72.52 Quite High
Hippocampus 5 70.72 Quite High
anesthesia 5 57.20 Quite High
Neurotransmitter 35 5.00 Very Low Very Low Very Low
Glutamate 21 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Osteoporosis 17 99.80 Very High Very High Very High
Contracture 13 95.44 Very High Very High Very High
Adverse Drug Reaction 5 92.64 High High
Malignant Hyperthermia 100 91.76 High High
Hypercapnia 5 86.48 High High
Hypokalemic Periodic Paralysis 145 83.96 Quite High
Acidosis 5 83.36 Quite High
Targeted Disruption 22 80.96 Quite High
Rhabdomyolysis 5 79.60 Quite High
Disease 76 78.44 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
SR is composed of two atoms of stable strontium and one molecule of ranelic acid.4 SR is a treatment for osteoporosis and unlike other drugs, has a dual effect on bone remodeling, being able to stimulate bone formation by osteoblasts, a property shared with bone-forming agents, and to inhibit bone resumption by osteoclasts, as antiresumptive agents.5,6
Positive_regulation (treatment) of Localization (molecule) of SR in osteoclasts associated with osteoporosis
1) Confidence 0.29 Published 2010 Journal International Journal of Women's Health Section Body Doc Link PMC2971725 Disease Relevance 0.47 Pain Relevance 0
1 subunit is unlikely to play a critical role in the activation of SR Ca2+ release, in agreement with a recent report [32].
Positive_regulation (activation) of Localization (release) of SR
2) Confidence 0.07 Published 2001 Journal BMC Physiol Section Body Doc Link PMC37314 Disease Relevance 0.08 Pain Relevance 0.12
In a porcine model of MHS (RyR1 point mutation), the typical increased sensitivity to a broad range of pharmacological stimuli was accompanied by a lower threshold for SR Ca2+ release and contraction [24].
Positive_regulation (threshold) of Localization (release) of SR
3) Confidence 0.04 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0.26 Pain Relevance 0.06
1 R1086H mutation lowers the half-maximal voltage required for the induction of SR Ca2+ release by about 5 mV and enhances the sensitivity of SR release to caffeine [24], a drug that is used as a primary diagnostic measure for MHS.
Positive_regulation (induction) of Localization (release) of SR
4) Confidence 0.04 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0.06 Pain Relevance 0
This finding is compatible with a mutation-induced facilitation of SR Ca2+ release by both pharmacologic (caffeine) and endogenous (voltage sensor) activators.
Positive_regulation (facilitation) of Localization (release) of SR
5) Confidence 0.04 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0.19 Pain Relevance 0
Although the fast conformational changes of their voltage-sensing domains induce pore opening very slowly, they are quickly transmitted to the sarcoplasmic reticulum (SR) ryanodine receptors (RyR1), thus serving as fast voltage sensors for SR Ca2+ release.
Positive_regulation (sensors) of Localization (release) of SR in pore
6) Confidence 0.04 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0.18 Pain Relevance 0.14
In myotubes homozygous (Hom) for the R163C mutation, voltage-gated Ca2+ release from the SR was substantially reduced and shifted (?
Positive_regulation (gated) of Localization (release) of SR in myotubes
7) Confidence 0.04 Published 2010 Journal The Journal of General Physiology Section Abstract Doc Link PMC2888063 Disease Relevance 0.34 Pain Relevance 0.03
Because the inactivation of ECC leads to a cessation of SR Ca2+ release via RYR1, it seems reasonable to hypothesize that cytoplasmic domains of the DHPR, and the foot of RYR1, assume a different conformation than in the ECC-activated state (Fig. 6).
Positive_regulation (cessation) of Localization (release) of SR in foot
8) Confidence 0.04 Published 2010 Journal The Journal of General Physiology Section Body Doc Link PMC2888063 Disease Relevance 0 Pain Relevance 0.04
In myotubes homozygous (Hom) for the R163C mutation, voltage-gated Ca2+ release from the SR was substantially reduced and shifted (?
Positive_regulation (shifted) of Localization (release) of SR in myotubes
9) Confidence 0.04 Published 2010 Journal The Journal of General Physiology Section Abstract Doc Link PMC2888063 Disease Relevance 0.34 Pain Relevance 0.03
Intramembrane charge movements of both Hom and heterozygous (Het) myotubes displayed hyperpolarizing shifts similar to that observed in voltage-gated SR Ca2+ release.
Positive_regulation (gated) of Localization (release) of SR in myotubes
10) Confidence 0.04 Published 2010 Journal The Journal of General Physiology Section Abstract Doc Link PMC2888063 Disease Relevance 0.30 Pain Relevance 0.04
Exposure to these drugs can quickly lead to skeletal muscle hypermetabolism resulting from an uncontrolled increase in the concentration of free myoplasmic Ca2+ released from the SR Ca2+ stores [40].
Positive_regulation (increase) of Localization (released) of SR in skeletal muscle
11) Confidence 0.04 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 1.05 Pain Relevance 0.15

General Comments

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