INT222089

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Context Info
Confidence 0.49
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 19
Total Number 21
Disease Relevance 8.73
Pain Relevance 1.58

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

enzyme binding (Esr1) DNA binding (Esr1) protein complex (Esr1)
cytoplasm (Esr1) lipid binding (Esr1) nucleus (Esr1)
Anatomy Link Frequency
astrocytes 4
thyroid 2
reticulum 2
Esr1 (Mus musculus)
Pain Link Frequency Relevance Heat
Neurotransmitter 10 99.64 Very High Very High Very High
agonist 38 99.34 Very High Very High Very High
Glutamate 112 97.74 Very High Very High Very High
Potency 5 91.60 High High
Glutamate receptor 63 89.36 High High
Inflammation 76 86.96 High High
Arthritis 82 81.36 Quite High
antagonist 46 81.04 Quite High
Action potential 8 78.08 Quite High
cINOD 148 70.96 Quite High
Disease Link Frequency Relevance Heat
Hypoxia 1022 99.98 Very High Very High Very High
Disease 184 99.10 Very High Very High Very High
Drug Induced Neurotoxicity 41 97.04 Very High Very High Very High
Death 171 96.40 Very High Very High Very High
Cancer 88 94.08 High High
Stress 25 93.52 High High
Increased Venous Pressure Under Development 15 92.32 High High
Scrapie 8 88.28 High High
Apoptosis 114 87.36 High High
INFLAMMATION 77 86.96 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In the present study, immunohistochemical localization of the truncated ER?
Positive_regulation (truncated) of Localization (localization) of ER
1) Confidence 0.49 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2978204 Disease Relevance 0.74 Pain Relevance 0
agonist displaying a more than 484-fold selectivity over ER?
Positive_regulation (over) of Localization (selectivity) of ER associated with agonist
2) Confidence 0.47 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2911889 Disease Relevance 0.42 Pain Relevance 0.46
Following rinsing in PBS, samples were blocked with normal goat serum (Vector Labs, Peterborough, UK) then incubated overnight at 4°C with the previously validated rabbit polyclonal ER?
Positive_regulation (Following) of Localization (validated) of ER
3) Confidence 0.34 Published 2008 Journal Reprod Biol Endocrinol Section Body Doc Link PMC2254628 Disease Relevance 0.07 Pain Relevance 0
is capable of activating other nuclear receptors such as thyroid receptor b, estrogen receptor and glucocorticoid receptor TR?
Positive_regulation (activating) of Localization (receptors) of estrogen receptor in thyroid
4) Confidence 0.11 Published 2010 Journal PPAR Research Section Body Doc Link PMC2943104 Disease Relevance 0.29 Pain Relevance 0
Activation of these channels allows extracellular Ca2+ to enter the cytosol, which subsequently induces further Ca2+ ion release from intracellular Ca2+ stores, such as the ER, by activating ryanodine receptors, the Ca2+ ion channels within the ER membrane.
Positive_regulation (induces) of Localization (release) of ER
5) Confidence 0.10 Published 2008 Journal PLoS Biology Section Body Doc Link PMC2225441 Disease Relevance 0.29 Pain Relevance 0.04
In the present study we show that an additional consequence of calcium release from the stressed ER is the hyperactivation in vitro and in vivo of a key protein, termed calcineurin (CaN).
Positive_regulation (hyperactivation) of Localization (release) of ER
6) Confidence 0.07 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2951383 Disease Relevance 0.73 Pain Relevance 0
The neural activity driven astrocytic Ca2+ surge is triggered by activation of metabotropic neurotransmitter receptors, which leads to production of inositol 1,4,5-triphosphate (IP3), and thereby to release of Ca2+ from the endoplasmic reticulum (ER) [3].
Positive_regulation (leads) of Localization (release) of ER in reticulum associated with neurotransmitter
7) Confidence 0.05 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2424136 Disease Relevance 0.07 Pain Relevance 0.33
Based on the crystal structure of the LBD [51], a series of point mutants around the glutamate binding pocket of the LBD of GluA2 subunit were examined to test if there is correlation between the ability to induce ligand-dependent conformational change of the LBD and the ER export of the receptor [148, 167].
Positive_regulation (induce) of Localization (export) of ER associated with glutamate
8) Confidence 0.03 Published 2010 Journal Mol Neurobiol Section Body Doc Link PMC2992128 Disease Relevance 0 Pain Relevance 0.19
Consistently, slowing the desensitization by introducing GluA2 L504A (equivalent to L483A) mutation accelerates ER export and tetramerization [148].
Positive_regulation (accelerates) of Localization (export) of ER
9) Confidence 0.03 Published 2010 Journal Mol Neurobiol Section Body Doc Link PMC2992128 Disease Relevance 0 Pain Relevance 0.04
In fact, the mutations that reduced glutamate affinity also impaired ER export, whereas a mutant that facilitated ligand-induced conformational change had an accelerated ER export.
Positive_regulation (accelerated) of Localization (export) of ER associated with glutamate
10) Confidence 0.03 Published 2010 Journal Mol Neurobiol Section Body Doc Link PMC2992128 Disease Relevance 0 Pain Relevance 0.24
For example, in familial AD, loss of function presenilin 1 mutants show exaggerated Ca2+ release from intracellular stores due to either defective Ca2+ leak from the ER or increased activity of Ca2+ release channels at ER [48–50, but see also 51 for alternative results].
Positive_regulation (increased) of Localization (release) of ER associated with disease
11) Confidence 0.03 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2447871 Disease Relevance 0.39 Pain Relevance 0.07
For example, in familial AD, loss of function presenilin 1 mutants show exaggerated Ca2+ release from intracellular stores due to either defective Ca2+ leak from the ER or increased activity of Ca2+ release channels at ER [48–50, but see also 51 for alternative results].
Positive_regulation (increased) of Localization (release) of ER associated with disease
12) Confidence 0.03 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2447871 Disease Relevance 0.29 Pain Relevance 0.07
For example, in familial AD, loss of function presenilin 1 mutants show exaggerated Ca2+ release from intracellular stores due to either defective Ca2+ leak from the ER or increased activity of Ca2+ release channels at ER [48–50, but see also 51 for alternative results].
Positive_regulation (exaggerated) of Localization (release) of ER associated with disease
13) Confidence 0.03 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2447871 Disease Relevance 0.29 Pain Relevance 0.07
For example, in familial AD, loss of function presenilin 1 mutants show exaggerated Ca2+ release from intracellular stores due to either defective Ca2+ leak from the ER or increased activity of Ca2+ release channels at ER [48–50, but see also 51 for alternative results].
Positive_regulation (exaggerated) of Localization (release) of ER associated with disease
14) Confidence 0.03 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2447871 Disease Relevance 0.39 Pain Relevance 0.07
Hypoxia-evoked ER Ca2+ release in astrocytes has also recently been attributed to cADPR-mediated activation of ryanodine receptors (Aley et al. 2006).
Positive_regulation (activation) of Localization (release) of ER in astrocytes associated with hypoxia
15) Confidence 0.03 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.78 Pain Relevance 0
Hypoxia-evoked ER Ca2+ release in astrocytes has also recently been attributed to cADPR-mediated activation of ryanodine receptors (Aley et al. 2006).
Positive_regulation (evoked) of Localization (release) of ER in astrocytes associated with hypoxia
16) Confidence 0.03 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.77 Pain Relevance 0
Moreover, the observation that ryanodine prevented anoxia-induced release of Ca2+ from the ER suggests that Ca2+ efflux via ryanodine receptors plays an important role in mediating this slow ER Ca2+ release.
Positive_regulation (mediating) of Localization (release) of ER associated with hypoxia
17) Confidence 0.03 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.63 Pain Relevance 0
Although we have not investigated possible links between anoxia and ER function in any detail, it is notable that the anoxia-induced ER Ca2+ release persists in the presence of FCCP.
Positive_regulation (induced) of Localization (release) of ER associated with hypoxia
18) Confidence 0.03 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.58 Pain Relevance 0
Moreover, the observation that ryanodine prevented anoxia-induced release of Ca2+ from the ER suggests that Ca2+ efflux via ryanodine receptors plays an important role in mediating this slow ER Ca2+ release.
Positive_regulation (induced) of Localization (release) of ER associated with hypoxia
19) Confidence 0.03 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.63 Pain Relevance 0
These observations suggest that inhibition of electron transport might be the key factor in promoting ER Ca2+ store release in response to anoxia and cyanide.
Positive_regulation (promoting) of Localization (release) of ER associated with hypoxia
20) Confidence 0.03 Published 2008 Journal Journal of Neurophysiology Section Body Doc Link PMC2493471 Disease Relevance 0.78 Pain Relevance 0

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