INT170507

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Context Info
Confidence 0.43
First Reported 2001
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 27
Total Number 27
Disease Relevance 6.25
Pain Relevance 1.31

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 8
reticulum 2
muscle 1
pore 1
skeletal muscle 1
Tmie (Mus musculus)
Pain Link Frequency Relevance Heat
addiction 179 99.92 Very High Very High Very High
anesthesia 14 97.20 Very High Very High Very High
adenocard 8 94.00 High High
agonist 78 92.72 High High
halothane 30 92.12 High High
amygdala 8 72.68 Quite High
long-term potentiation 16 72.04 Quite High
Hippocampus 8 70.24 Quite High
cva 7 66.96 Quite High
TRP channel 1 46.00 Quite Low
Disease Link Frequency Relevance Heat
Osteoporosis 17 99.20 Very High Very High Very High
Disease 238 99.00 Very High Very High Very High
Malignant Hyperthermia 229 98.72 Very High Very High Very High
Renal Failure 8 96.84 Very High Very High Very High
Contracture 30 95.44 Very High Very High Very High
Myoglobinuria 8 95.32 Very High Very High Very High
Hyperkalemia 8 93.88 High High
Rhabdomyolysis 8 91.36 High High
Adverse Drug Reaction 8 90.48 High High
Acidosis 8 89.24 High 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
Localization (molecule) of SR in osteoclasts associated with osteoporosis
1) Confidence 0.43 Published 2010 Journal International Journal of Women's Health Section Body Doc Link PMC2971725 Disease Relevance 0.47 Pain Relevance 0
IP3 induces the release of Ca2+ from the sarcoplasmatic reticulum (SR), which is thought to trigger the influx of extracellular Ca2+ by a mechanism known as store-operated Ca2+ entry (SOCE) (5, 6).
Localization (release) of SR in reticulum
2) Confidence 0.14 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2442636 Disease Relevance 0.68 Pain Relevance 0.08
The degree of decrease was more pronounced in APP/PS1 mice at frequencies greater than 1 Hz (Fig. 4A), indicating existence of compromised SR storage and release of intracellular Ca2+ in APP/PS1 mouse hearts.


Localization (release) of SR in hearts
3) Confidence 0.13 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2696039 Disease Relevance 0.19 Pain Relevance 0
In addition, our data revealed exaggerated decline in the steady-state myocyte peak shortening in response to increased stimulating frequency in APP/PS1 mice, suggesting a possibly reduced capacity in SR Ca2+ storage and release in this murine model of AD.
Localization (release) of SR in myocyte associated with disease
4) Confidence 0.13 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2696039 Disease Relevance 0.20 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].
Localization (release) of SR
5) Confidence 0.11 Published 2001 Journal BMC Physiol Section Body Doc Link PMC37314 Disease Relevance 0.08 Pain Relevance 0.12
A recent report indicates that the SR Ca2+ release rate is slightly higher in ?
Localization (release) of SR
6) Confidence 0.10 Published 2001 Journal BMC Physiol Section Body Doc Link PMC37314 Disease Relevance 0 Pain Relevance 0.08
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].
Localization (release) of SR
7) Confidence 0.07 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0.26 Pain Relevance 0.06
Treatment of a crisis by early administration of dantrolene, an inhibitor of SR Ca2+ release, substantially reduces mortality.
Localization (release) of SR
8) Confidence 0.07 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 1.17 Pain Relevance 0.18
In R163C Het myotubes, there was a small hyperpolarizing shift in SR Ca2+ release and a slight reduction in maximal release ([?
Localization (release) of SR in myotubes
9) Confidence 0.06 Published 2010 Journal The Journal of General Physiology Section Body Doc Link PMC2888063 Disease Relevance 0.05 Pain Relevance 0.18
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).
Localization (release) of SR in foot
10) Confidence 0.06 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 (?
Localization (release) of SR in myotubes
11) Confidence 0.06 Published 2010 Journal The Journal of General Physiology Section Abstract Doc Link PMC2888063 Disease Relevance 0.34 Pain Relevance 0.03
This retrograde effect of RYR1 is independent of SR Ca2+ release (Grabner et al., 1999; Hurne et al., 2005) and affects not only the magnitude of the current, but also activation kinetics (Avila and Dirksen, 2000; Ahern et al., 2003; Sheridan et al., 2006).
Localization (release) of SR
12) Confidence 0.06 Published 2010 Journal The Journal of General Physiology Section Body Doc Link PMC2888063 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.
Localization (release) of SR
13) Confidence 0.06 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0.19 Pain Relevance 0
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.
Localization (release) of SR
14) Confidence 0.06 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0.06 Pain Relevance 0
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.
Localization (release) of SR
15) Confidence 0.06 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0.06 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.
Localization (release) of SR in pore
16) Confidence 0.06 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0.18 Pain Relevance 0.14
Intramembrane charge movements of both Hom and heterozygous (Het) myotubes displayed hyperpolarizing shifts similar to that observed in voltage-gated SR Ca2+ release.
Localization (release) of SR in myotubes
17) Confidence 0.06 Published 2010 Journal The Journal of General Physiology Section Abstract Doc Link PMC2888063 Disease Relevance 0.30 Pain Relevance 0.04
In R163C Hom myotubes, the voltage dependence of SR Ca2+ release shifted to a greater extent and maximal release was substantially reduced (Fig. 1 and Table I).
Localization (release) of SR in myotubes associated with addiction
18) Confidence 0.06 Published 2010 Journal The Journal of General Physiology Section Body Doc Link PMC2888063 Disease Relevance 0.07 Pain Relevance 0.19
A malignant hyperthermia–inducing mutation in RYR1 (R163C): consequent alterations in the functional properties of DHPR channels

Bidirectional communication between the 1,4-dihydropyridine receptor (DHPR) in the plasma membrane and the type 1 ryanodine receptor (RYR1) in the sarcoplasmic reticulum (SR) is responsible for both skeletal-type excitation–contraction coupling (voltage-gated Ca2+ release from the SR) and increased amplitude of L-type Ca2+ current via the DHPR.

Localization (release) of SR in reticulum associated with malignant hyperthermia
19) Confidence 0.06 Published 2010 Journal The Journal of General Physiology Section Title Doc Link PMC2888063 Disease Relevance 0.37 Pain Relevance 0.03
Thus, intact R163C Het or Hom myotubes may have enhanced Ca2+-induced Ca2+ release, which can compensate for a reduction in SR Ca2+ release that is directly voltage gated.
Localization (release) of SR in myotubes
20) Confidence 0.06 Published 2010 Journal The Journal of General Physiology Section Body Doc Link PMC2888063 Disease Relevance 0 Pain Relevance 0

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