INT114715

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Context Info
Confidence 0.36
First Reported 2003
Last Reported 2010
Negated 1
Speculated 1
Reported most in Body
Documents 8
Total Number 9
Disease Relevance 4.26
Pain Relevance 1.32

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

mitochondrion (SRC) cytoplasm (SRC) cytosol (SRC)
signal transduction (SRC) cell adhesion (SRC) nucleus (SRC)
Anatomy Link Frequency
cardiomyocytes 1
pore 1
upper 1
SRC (Homo sapiens)
Pain Link Frequency Relevance Heat
Stimulus evoked pain 3 97.76 Very High Very High Very High
Nicotine 2 92.76 High High
Pain 6 87.84 High High
Kinase C 3 87.20 High High
nMDA receptor 2 87.04 High High
cytokine 12 79.00 Quite High
Peripheral nerve injury 1 75.52 Quite High
Enkephalin 1 75.28 Quite High
Inflammation 5 75.00 Quite High
Neuropathic pain 2 75.00 Quite High
Disease Link Frequency Relevance Heat
Pancreatic Cancer 2 98.80 Very High Very High Very High
Hypersensitivity 3 97.76 Very High Very High Very High
Pain 6 97.42 Very High Very High Very High
Cancer 23 97.32 Very High Very High Very High
Adenocarcinoma 4 95.60 Very High Very High Very High
Snake Bites 10 95.28 Very High Very High Very High
Emergencies 3 92.80 High High
Fever 1 92.28 High High
Acquired Immune Deficiency Syndrome Or Hiv Infection 1 91.04 High High
Anaphylaxis 1 91.00 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
To further study the interaction between c-Src and IGF-1R proteins in human pancreatic cancer, we examined their coexpression in 47 human pancreatic ductal adenocarcinomas (PDA).
c-Src Spec (examined) Binding (interaction) of associated with adenocarcinoma and pancreatic cancer
1) Confidence 0.36 Published 2003 Journal Dig. Dis. Sci. Section Abstract Doc Link 14627343 Disease Relevance 0.60 Pain Relevance 0
The structure also implies that a Src homology domain 3 may interact with the left-handed proline-rich helix at the dimer interface and regulate LTB(4) 12-HD/PGR activity by disruption of the substrate binding pore to accommodate the omega-chain.
Src Binding (interact) of in pore
2) Confidence 0.36 Published 2004 Journal J. Biol. Chem. Section Abstract Doc Link 15007077 Disease Relevance 0.05 Pain Relevance 0.20
Inhibition of c-Src and Janus kinase 2 and 3 activities abolished STAT3 activation induced by Galpha14QL, but no physical association between Galpha14QL and c-Src could be detected by coimmunoprecipitation.
c-Src Neg (no) Binding (association) of
3) Confidence 0.36 Published 2004 Journal Mol. Pharmacol. Section Abstract Doc Link 15155836 Disease Relevance 0.13 Pain Relevance 0.27
In 48 h PO tissue samples, c-Src was active in all detergent-lysed subfractions, as indicated by its Tyr416 phosphorylation (Figure 3a, lower panel) and in addition, c-Src recruitment to the CSK (upper panel).
c-Src Binding (recruitment) of in upper
4) Confidence 0.36 Published 2008 Journal International Journal of Biological Sciences Section Body Doc Link PMC2443357 Disease Relevance 0 Pain Relevance 0
Although our previous work both in 48 h PO myocardium and in RGD-stimulated adult cardiomyocytes3, 4 demonstrates c-Src recruitment and activation, expression of DNSrc in cardiomyocytes in the 3D environment did not affect the RGD-stimulated STAT3 phosphorylation.
c-Src Binding (recruitment) of in cardiomyocytes
5) Confidence 0.36 Published 2008 Journal International Journal of Biological Sciences Section Body Doc Link PMC2443357 Disease Relevance 0 Pain Relevance 0.04
Whereas our previous studies show c-Src and FAK recruitment to the CSK fraction, we observe in the present study BMX recruitment to the MSK fraction similar to STAT3.
c-Src Binding (recruitment) of
6) Confidence 0.36 Published 2008 Journal International Journal of Biological Sciences Section Body Doc Link PMC2443357 Disease Relevance 0.06 Pain Relevance 0
The median time of recovery from envenomation was 8 hours (range 6-120 hours) after initiating ASV.
ASV Binding (initiating) of
7) Confidence 0.32 Published 2008 Journal Journal of Emergencies, Trauma and Shock Section Body Doc Link PMC2700611 Disease Relevance 1.60 Pain Relevance 0.15
In these experiments inhibition of Src kinases in originally cetuximab-resistant cell lines resulted in a regaining of sensitivity against cetuximab, indicating a close interaction between Src and EGF-R regarding the processes causing cetuximab resistance in tumour cells [27].
Src Binding (interaction) of associated with cancer
8) Confidence 0.14 Published 2010 Journal Head Neck Oncol Section Body Doc Link PMC2868849 Disease Relevance 0.64 Pain Relevance 0
Here we report a means to suppress pain hypersensitivity without blocking NMDARs, but rather by inhibiting the binding of a key enhancer of NMDAR function, the protein tyrosine kinase Src.
Src Binding (tyrosine) of associated with hypersensitivity and stimulus evoked pain
9) Confidence 0.04 Published 2008 Journal Nat. Med. Section Abstract Doc Link 19011637 Disease Relevance 1.18 Pain Relevance 0.67

General Comments

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