INT117621

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Context Info
Confidence 0.59
First Reported 2004
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 17
Total Number 18
Disease Relevance 13.26
Pain Relevance 6.06

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

unfolded protein binding (HSPA5) endoplasmic reticulum (HSPA5) ATPase activity (HSPA5)
nucleus (HSPA5) protein binding, bridging (HSPA5)
Anatomy Link Frequency
reticulum 3
band 1
HSPA5 (Homo sapiens)
Pain Link Frequency Relevance Heat
cINOD 40 99.98 Very High Very High Very High
qutenza 44 99.32 Very High Very High Very High
Osteoarthritis 54 99.04 Very High Very High Very High
tolerance 1 79.56 Quite High
Paracetamol 1 74.64 Quite High
Inflammation 24 53.84 Quite High
cytokine 16 52.80 Quite High
Arthritis 4 50.00 Quite Low
spondylitis 2 50.00 Quite Low
Pain 9 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Stress 51 100.00 Very High Very High Very High
Cancer 37 99.44 Very High Very High Very High
Apoptosis 89 99.32 Very High Very High Very High
Osteoarthritis 54 99.04 Very High Very High Very High
Stomach Cancer 5 98.84 Very High Very High Very High
Death 22 98.20 Very High Very High Very High
Toxicity 5 95.00 High High
INFLAMMATION 36 94.28 High High
Renal Cancer 8 86.00 High High
Disease 8 83.92 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Suppression of ATF4 expression by small interfering RNA (siRNA) partially inhibited the celecoxib-dependent upregulation of GRP78.
Positive_regulation (upregulation) of GRP78
1) Confidence 0.59 Published 2006 Journal Oncogene Section Abstract Doc Link 16205636 Disease Relevance 0.72 Pain Relevance 0.40
Celecoxib increased the intracellular Ca2+ concentration, while 1,2-bis(2-aminophenoxy)ethane-N,N,N'N'-tetraacetic acid, an intracellular Ca2+ chelator, inhibited the upregulation of GRP78 and ATF4.
Positive_regulation (upregulation) of GRP78
2) Confidence 0.59 Published 2006 Journal Oncogene Section Abstract Doc Link 16205636 Disease Relevance 0.74 Pain Relevance 0.35
Celecoxib also upregulated GRP78 in xenograft tumors, accompanying with the suppression of tumor growth in nude mice.
Positive_regulation (upregulated) of GRP78 associated with cancer
3) Confidence 0.59 Published 2006 Journal Oncogene Section Abstract Doc Link 16205636 Disease Relevance 0.78 Pain Relevance 0.50
Celecoxib, an NSAID, upregulated ER chaperones (GRP78 and its cochaperones ERdj3 and ERdj4) but also C/EBP homologous transcription factor (CHOP), a transcription factor involved in apoptosis.
Positive_regulation (upregulated) of GRP78 associated with cinod and apoptosis
4) Confidence 0.59 Published 2006 Journal Oncogene Section Abstract Doc Link 16205636 Disease Relevance 0.78 Pain Relevance 0.55
Induction of the endoplasmic reticulum stress proteins GRP78, GRP94, calreticulin and protein disulfide isomerase was assessed by immunoblotting.
Positive_regulation (Induction) of GRP78 in reticulum associated with stress
5) Confidence 0.49 Published 2004 Journal Basic Clin. Pharmacol. Toxicol. Section Abstract Doc Link 15049342 Disease Relevance 0.59 Pain Relevance 0.11
We show that DMC increases intracellular free calcium levels and potently triggers the ESR in various tumor cell lines, as indicated by transient inhibition of protein synthesis, activation of ER stress-associated proteins GRP78/BiP, CHOP/GADD153, and caspase-4, and subsequent tumor cell death.
Positive_regulation (activation) of BiP associated with stress, cancer and death
6) Confidence 0.49 Published 2007 Journal Mol. Cancer Ther. Section Abstract Doc Link 17431104 Disease Relevance 1.28 Pain Relevance 0.15
HLA-B27 assembly was assessed by pulse-chase analysis of B27 molecules, and UPR triggering was assessed by measuring BiP/Grp78 messenger RNA (mRNA) in splenic concanavalin A blasts.
Positive_regulation (measuring) of Grp78
7) Confidence 0.49 Published 2006 Journal Arthritis Rheum. Section Body Doc Link 16575857 Disease Relevance 0.08 Pain Relevance 0
HLA-B27 assembly was assessed by pulse-chase analysis of B27 molecules, and UPR triggering was assessed by measuring BiP/Grp78 messenger RNA (mRNA) in splenic concanavalin A blasts.
Positive_regulation (measuring) of BiP
8) Confidence 0.49 Published 2006 Journal Arthritis Rheum. Section Body Doc Link 16575857 Disease Relevance 0.08 Pain Relevance 0
Capsaicin treatment triggered ER stress by increasing levels of IRE1, GADD153/Chop, GRP78/Bip, and activated caspase-4.
Positive_regulation (activated) of GRP78 associated with stress and qutenza
9) Confidence 0.45 Published 2009 Journal Toxicology Section Abstract Doc Link 19699254 Disease Relevance 1.22 Pain Relevance 0.74
Capsaicin treatment triggered ER stress by increasing levels of IRE1, GADD153/Chop, GRP78/Bip, and activated caspase-4.
Positive_regulation (increasing) of GRP78 associated with stress and qutenza
10) Confidence 0.45 Published 2009 Journal Toxicology Section Abstract Doc Link 19699254 Disease Relevance 1.23 Pain Relevance 0.74
Capsaicin treatment triggered ER stress by increasing levels of IRE1, GADD153/Chop, GRP78/Bip, and activated caspase-4.
Positive_regulation (activated) of Bip associated with stress and qutenza
11) Confidence 0.45 Published 2009 Journal Toxicology Section Abstract Doc Link 19699254 Disease Relevance 1.22 Pain Relevance 0.73
Capsaicin treatment triggered ER stress by increasing levels of IRE1, GADD153/Chop, GRP78/Bip, and activated caspase-4.
Positive_regulation (increasing) of Bip associated with stress and qutenza
12) Confidence 0.45 Published 2009 Journal Toxicology Section Abstract Doc Link 19699254 Disease Relevance 1.23 Pain Relevance 0.74
We recently demonstrated that NSAIDs upregulate GRP78, an endoplasmic reticulum (ER) chaperone, in gastric mucosal cells in primary culture.
Positive_regulation (upregulate) of GRP78 in reticulum associated with cinod
13) Confidence 0.43 Published 2006 Journal Oncogene Section Abstract Doc Link 16205636 Disease Relevance 0.71 Pain Relevance 0.54
Selective inhibitors of ERK, p38 MAPK, and JNK suppressed the induction of GRP78, CHOP, and PPAR-beta, attenuated indomethacin-induced cytotoxicity and reduced increased caspase activity.
Positive_regulation (induction) of GRP78
14) Confidence 0.42 Published 2007 Journal Eur. J. Pharmacol. Section Abstract Doc Link 17341418 Disease Relevance 0.82 Pain Relevance 0.06
Densitometric analysis of the band intensities revealed an increase of GRP78 protein in GS- and GS + CS-treated samples that averaged 1.72-fold and 1.75-fold greater than control (P < 0.05) (Figure 4B).
Positive_regulation (increase) of GRP78 in band
15) Confidence 0.42 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2945029 Disease Relevance 0.31 Pain Relevance 0.11
As a proof of the act, in this work (and based on their previously described relationship with OA pathogenesis) we selected one protein that was increased (GRP78) by the drug treatment and one that was decreased (SOD2), and performed orthogonal studies on them to verify their alteration.
Positive_regulation (increased) of GRP78 associated with osteoarthritis
16) Confidence 0.39 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2945029 Disease Relevance 0.32 Pain Relevance 0.10
Indomethacin treatment was associated with increased expression of glucose-regulated protein 78 (GRP78) and C/EBP homologus protein (CHOP) and activation of ATF-6, characteristics of endoplasmic reticulum stress.
Positive_regulation (activation) of GRP78 in reticulum associated with stress
17) Confidence 0.28 Published 2007 Journal Eur. J. Pharmacol. Section Abstract Doc Link 17341418 Disease Relevance 1.14 Pain Relevance 0.22
These anti-Nuc-coated beads specifically immunoprecipitated structures which, in addition to containing Nuc, also contained COX-2 and GRP-78 (Fig. 5C), showing that the organelles containing Nuc also harbor COX-2 and Golgi/ER structures.
Positive_regulation (contained) of GRP-78
18) Confidence 0.24 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2373884 Disease Relevance 0 Pain Relevance 0

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