INT180250

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Context Info
Confidence 0.29
First Reported 2004
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 23
Total Number 23
Disease Relevance 7.57
Pain Relevance 3.23

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

mitochondrion (GLUL) small molecule metabolic process (GLUL) lyase activity (GLUL)
Golgi apparatus (GLUL) intracellular (GLUL) ligase activity (GLUL)
Anatomy Link Frequency
chondrocytes 2
band 1
platelet 1
urine 1
frontal cortex 1
GLUL (Homo sapiens)
Pain Link Frequency Relevance Heat
Glutamate 35 100.00 Very High Very High Very High
gABA 59 99.96 Very High Very High Very High
agonist 326 96.50 Very High Very High Very High
Osteoarthritis 85 94.52 High High
Serotonin 117 94.08 High High
cytokine 25 90.84 High High
Inflammation 37 90.56 High High
adenocard 1 90.08 High High
antagonist 82 88.68 High High
GABA receptor 2 68.12 Quite High
Disease Link Frequency Relevance Heat
Convulsion 7 99.36 Very High Very High Very High
Syndrome 54 99.22 Very High Very High Very High
Acromegaly 166 98.80 Very High Very High Very High
Urological Neuroanatomy 2 98.52 Very High Very High Very High
Stress 28 97.44 Very High Very High Very High
Cystitis 20 96.12 Very High Very High Very High
Pituitary Cancer 36 95.96 Very High Very High Very High
Hypercalcemia 2 95.68 Very High Very High Very High
Precocious Puberty 2 95.56 Very High Very High Very High
Adenoma 60 95.36 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
This platelet activation process is enhanced when Gi is activated and inhibited when Gs is activated both by modulating the intracellular cAMP level.
Positive_regulation (activated) of Gs in platelet
1) Confidence 0.29 Published 2007 Journal Eur J Pediatr Section Body Doc Link PMC2042511 Disease Relevance 0.18 Pain Relevance 0.05
A number of previous reports have described the positive modulation of GS on ER proteins, including GRP78 expression [52], but this is the first time that such modulation was found to arise from GS treatment in chondrocytes; thus interestingly suggesting an specific mechanism of action for the putative anti-inflammatory effect of GS in OA.
Positive_regulation (modulation) of GS in chondrocytes associated with inflammation and osteoarthritis
2) Confidence 0.20 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2945029 Disease Relevance 0.62 Pain Relevance 0.27
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 GS in band
3) Confidence 0.20 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2945029 Disease Relevance 0.31 Pain Relevance 0.11
Real-time PCR assays demonstrated the GS-dependent upregulation of GRP78 gene expression, showing remarkable increases of almost 30-fold in GS-treated chondrocytes (P < 0.05, n = 6, age range: 55 to 63 years), and even slightly higher with combined GS and CS treatment (Figure 4A).
Positive_regulation (upregulation) of GS in chondrocytes
4) Confidence 0.18 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2945029 Disease Relevance 0.28 Pain Relevance 0.11
Unfortunately, the efficacy of the ligand-induced Gs response was also significantly compromised, diminishing the utility of these receptors.


Positive_regulation (induced) of Gs
5) Confidence 0.17 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2267039 Disease Relevance 0.07 Pain Relevance 0.04
Therefore, we could use drugs with distinct chemical structures (Figure S1) to activate Gs or Gs/Gq signaling of Rs1.
Positive_regulation (activate) of Gs
6) Confidence 0.17 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2267039 Disease Relevance 0 Pain Relevance 0.04
Since the same agonists can be used to activate all of the RASSLs within this series and therefore+ engage different G-protein signaling pathways (Table 1), we can more easily compare the effect of activating the Gs, Gs/q, or Gi pathway.
Positive_regulation (activating) of Gs associated with agonist
7) Confidence 0.12 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2267039 Disease Relevance 0.17 Pain Relevance 0.24
Constitutive and ligand-induced Gs signaling were also largely preserved (Figures S3A, S3B).
Positive_regulation (induced) of Gs
8) Confidence 0.12 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2267039 Disease Relevance 0 Pain Relevance 0.03
These are the same ligands used to selectively activate the Gs signaling of Rs1 without activating the Gs signaling of the wildtype 5-HT4 receptor (Figure 2).
Neg (without) Positive_regulation (activating) of Gs
9) Confidence 0.12 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2267039 Disease Relevance 0 Pain Relevance 0.03
These are the same ligands used to selectively activate the Gs signaling of Rs1 without activating the Gs signaling of the wildtype 5-HT4 receptor (Figure 2).
Positive_regulation (activate) of Gs
10) Confidence 0.12 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2267039 Disease Relevance 0 Pain Relevance 0.03
In addition, GR113808, GR125487, and RO110-0235 potently activated Gs signaling of 5-HT4-D100A without stimulating the wildtype receptor (Figures 3B–E).
Positive_regulation (activated) of Gs
11) Confidence 0.12 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2267039 Disease Relevance 0 Pain Relevance 0.34
Since the same agonists can be used to activate all of the RASSLs within this series and therefore+ engage different G-protein signaling pathways (Table 1), we can more easily compare the effect of activating the Gs, Gs/q, or Gi pathway.
Positive_regulation (activating) of Gs associated with agonist
12) Confidence 0.12 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2267039 Disease Relevance 0.17 Pain Relevance 0.24
Therefore, we could use drugs with distinct chemical structures (Figure S1) to activate Gs or Gs/Gq signaling of Rs1.
Positive_regulation (activate) of Gs
13) Confidence 0.10 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2267039 Disease Relevance 0 Pain Relevance 0.04
This syndrome is related to a somatic mutation that activates the alpha subunit of Gs protein [48].
Positive_regulation (activates) of Gs associated with syndrome
14) Confidence 0.10 Published 2008 Journal Orphanet J Rare Dis Section Body Doc Link PMC2459162 Disease Relevance 2.19 Pain Relevance 0
These RASSLs are based on the human 5-HT4b receptor, a GPCR with high constitutive Gs signaling and strong ligand-induced G-protein activation of the Gs and Gs/q pathways.
Positive_regulation (activation) of Gs
15) Confidence 0.10 Published 2007 Journal PLoS ONE Section Abstract Doc Link PMC2267039 Disease Relevance 0 Pain Relevance 0.18
These modified GPCRs will help us better study the effect of constitutive Gs signaling and ligand-induced Gs, Gs/Gq, and Gi signaling in vivo.


Positive_regulation (induced) of Gs
16) Confidence 0.10 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2267039 Disease Relevance 0 Pain Relevance 0.15
A mutated Gs?
Positive_regulation (mutated) of Gs
17) Confidence 0.10 Published 2008 Journal Orphanet J Rare Dis Section Body Doc Link PMC2459162 Disease Relevance 1.21 Pain Relevance 0
These RASSLs are based on the human 5-HT4b receptor, a GPCR with high constitutive Gs signaling and strong ligand-induced G-protein activation of the Gs and Gs/q pathways.
Positive_regulation (activation) of Gs
18) Confidence 0.05 Published 2007 Journal PLoS ONE Section Abstract Doc Link PMC2267039 Disease Relevance 0 Pain Relevance 0.18
These modified GPCRs will help us better study the effect of constitutive Gs signaling and ligand-induced Gs, Gs/Gq, and Gi signaling in vivo.


Positive_regulation (induced) of Gs
19) Confidence 0.05 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2267039 Disease Relevance 0 Pain Relevance 0.15
Glutamine synthetase (glnA), which assimilates ammonia with high affinity in an energy-dependent manner and is transcriptionally induced by nitrogen-limited growth [44], was among the most highly expressed genes in urine from 5 of 8 cystitis patients (Table 1).
Positive_regulation (induced) of Glutamine synthetase in urine associated with cystitis
20) Confidence 0.03 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2978726 Disease Relevance 0.42 Pain Relevance 0.04

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