INT107771

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Context Info
Confidence 0.78
First Reported 2003
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 10
Total Number 11
Disease Relevance 8.47
Pain Relevance 4.30

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

extracellular space (HSPG2) small molecule metabolic process (HSPG2) extracellular region (HSPG2)
plasma membrane (HSPG2) extracellular matrix organization (HSPG2) lipid metabolic process (HSPG2)
Anatomy Link Frequency
anatomical site 1
HSPG2 (Homo sapiens)
Pain Link Frequency Relevance Heat
Kinase C 32 99.50 Very High Very High Very High
Opioid 17 98.56 Very High Very High Very High
qutenza 13 98.52 Very High Very High Very High
cINOD 11 97.52 Very High Very High Very High
dorsal root ganglion 4 95.68 Very High Very High Very High
analgesia 3 94.84 High High
Pain 10 93.80 High High
bradykinin 22 92.72 High High
agonist 60 91.48 High High
antagonist 10 91.32 High High
Disease Link Frequency Relevance Heat
Staphylococcus Infection 257 100.00 Very High Very High Very High
Bullous Skin Disease 212 100.00 Very High Very High Very High
Syndrome 55 100.00 Very High Very High Very High
Apoptosis 23 98.88 Very High Very High Very High
INFLAMMATION 22 98.48 Very High Very High Very High
Drug Eruptions 10 96.64 Very High Very High Very High
Ganglion Cysts 4 95.68 Very High Very High Very High
Hepatocellular Cancer 3 95.56 Very High Very High Very High
Neurological Disease 2 95.12 Very High Very High Very High
Pain 12 93.80 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Another and more relevant mechanism of long-term opioid binding is that of subsequent protein kinase C (PKC), phospholipase C (PLC) translocation and activation of nitric oxide synthetase (NOS).
Localization (translocation) of PLC associated with kinase c and opioid
1) Confidence 0.78 Published 2003 Journal Anasthesiol Intensivmed Notfallmed Schmerzther Section Abstract Doc Link 12522725 Disease Relevance 0.07 Pain Relevance 1.25
Intracellular effects of B2 stimulation were the following: (a) the increase of free intracellular Ca(2+) concentration by a mechanism dependent upon the phospholipase C (PLC) activity; (b) the cytosol-to-membrane translocation of conventional (PKC)-alpha and -beta isozymes, novel PKC-delta, -epsilon, and -eta isozymes; (c) the phosphorylation of the extracellular-regulated kinase 1 and 2 (ERK1/2); and (d) the stimulation of the expression of c-Fos protein.
Localization (translocation) of PLC
2) Confidence 0.73 Published 2004 Journal J. Cell. Physiol. Section Abstract Doc Link 15281091 Disease Relevance 0.41 Pain Relevance 0.50
While types 1A and 1B are caused by mutations in Perlecan at 1p36.1, type 2 shows no linkage to the SJS locus on chromosome 1. [7] Type 2 is now identified as Stüve-Wiedemann syndrome, a genetically distinct, and highly lethal disorder. [4]
Localization (locus) of SJS associated with syndrome
3) Confidence 0.64 Published 2003 Journal BMC Neurol Section Body Doc Link PMC166146 Disease Relevance 1.20 Pain Relevance 0.07
Perlecan mutations characterized thus far in patients with SJS were missense mutations, splicing mutations with exon skipping, and deletions.[3,4] In these patients, mutant Perlecan molecules or reduced amounts of wild-type Perlecan are secreted in the tissue matrix.
Localization (secreted) of Perlecan associated with syndrome
4) Confidence 0.60 Published 2003 Journal BMC Neurol Section Body Doc Link PMC166146 Disease Relevance 0.93 Pain Relevance 0.03
The reported ability or likelihood of a drug be the cause of SJS/TEN can be found in Pubmed/Medline or other appropriate sources such as the Litt's drug eruption reference manual [63].


Localization (cause) of SJS associated with staphylococcus infection, drug eruptions and bullous skin disease
5) Confidence 0.39 Published 2010 Journal Orphanet J Rare Dis Section Body Doc Link PMC3018455 Disease Relevance 1.59 Pain Relevance 0.07
In a case control study of patients hospitalized for SJS/TEN in selected hospitals in France, Germany, Italy and Portugal between 1989 and 1993, Roujeau et al. reported that the following drugs are at increased risk of inducing SJS/TEN when used over a short period of time: trimetroprim-sulfamethoxazole and other sulfonamide-antibiotics, aminopenicillins, cephalosporins, quinolones and chlormezanone.
Localization (hospitalized) of SJS associated with staphylococcus infection and bullous skin disease
6) Confidence 0.39 Published 2010 Journal Orphanet J Rare Dis Section Body Doc Link PMC3018455 Disease Relevance 1.85 Pain Relevance 0.06
Integration of information from all mRNA-seq read classes including SJs led to genome reannotations specifically relevant for the species used (rat), the anatomical site studied (DRG), and the neurological disease considered (pain); for example, a 64-exon coreceptor for the nociceptive transmitter substance P was identified, and 21.9% of newly discovered exons were shown to be dysregulated.
Localization (classes) of SJs in anatomical site associated with nociception, pain, dorsal root ganglion, neurological disease and substance p
7) Confidence 0.34 Published 2010 Journal Genome Res. Section Abstract Doc Link 20452967 Disease Relevance 0.85 Pain Relevance 0.71
PURPOSE: Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) associated with the use of nonsteroidal antiinflammatory drugs (NSAIDs) are described.
Localization (necrolysis) of SJS associated with staphylococcus infection, inflammation, syndrome and cinod
8) Confidence 0.19 Published 2010 Journal Am J Health Syst Pharm Section Abstract Doc Link 20101062 Disease Relevance 0.37 Pain Relevance 0.10
Collectively, these results suggest that the capsaicin-induced apoptosis in the HepG2 cells may result from the activation of a PLC-dependent intracellular Ca2+ release pathway, and it is further suggested that capsaicin may be valuable for the therapeutic intervention of human hepatomas.
Localization (release) of PLC-dependent associated with qutenza, hepatocellular cancer and apoptosis
9) Confidence 0.09 Published 2005 Journal Arch. Pharm. Res. Section Abstract Doc Link 15742812 Disease Relevance 0.86 Pain Relevance 0.85
Localization of PLC isoforms to the membrane appears to be regulated by interaction of pleckstrin homology domains in PLC with specific phosphoinositides and G??
Localization (Localization) of PLC
10) Confidence 0.08 Published 2003 Journal Respir Res Section Body Doc Link PMC152647 Disease Relevance 0 Pain Relevance 0.08
Downstream to this receptor activation, the PLC-pathway (4.) leads to the release of Ca2+ from intracellular stores (5.) as well as to activation of PKC (6.).
Localization (release) of PLC-pathway associated with kinase c
11) Confidence 0.07 Published 2008 Journal Mol Pain Section Body Doc Link PMC2424039 Disease Relevance 0.27 Pain Relevance 0.58

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