INT238431

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Context Info
Confidence 0.37
First Reported 2008
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 8
Total Number 8
Disease Relevance 2.53
Pain Relevance 0.25

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

cell differentiation (SRA1) cell proliferation (SRA1) nucleus (SRA1)
DNA binding (SRA1) cytoplasm (SRA1)
Anatomy Link Frequency
plasma 1
hip 1
SRA1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Arthritis 1 70.88 Quite High
Kinase C 1 67.92 Quite High
Pain 15 67.40 Quite High
addiction 6 31.12 Quite Low
Inflammatory response 12 14.48 Low Low
Inflammation 34 6.00 Low Low
cytokine 45 5.00 Very Low Very Low Very Low
Central nervous system 8 5.00 Very Low Very Low Very Low
dexamethasone 8 5.00 Very Low Very Low Very Low
antagonist 7 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
African Trypanosomiasis 66 96.32 Very High Very High Very High
Disorder Of Lipid Metabolism 38 96.04 Very High Very High Very High
Femoral Neck Fractures 10 93.60 High High
Targeted Disruption 9 93.48 High High
Trypanosomiasis 93 87.40 High High
Osteoporosis 2 84.56 Quite High
Dislocations 2 78.84 Quite High
Neuroblastoma 3 78.64 Quite High
Cyst 2 78.40 Quite High
Apoptosis 42 74.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Patient selection is greatly important when deciding between hip SRA and THA.
hip SRA Binding (deciding) of in hip
1) Confidence 0.37 Published 2010 Journal Patient Saf Surg Section Body Doc Link PMC2829516 Disease Relevance 0.89 Pain Relevance 0.21
In fact, removal of this C-terminal domain, by which the SRA can no longer interact, makes the APOL1 even lytic to NHS-resistant T. b. rhodesiense [98].
SRA Neg (no) Binding (interact) of
2) Confidence 0.22 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2826769 Disease Relevance 0.45 Pain Relevance 0
Furthermore, it has been shown that the full length baboon APOL1 (which does not interact with SRA) is protective against both the animal-infective and human-infective T. rhodesiense in an experimental mouse model, and, as such, it has been suggested to create transgenic livestock that would be resistant to animal and human-infective trypanosomes, which is envisaged to result in the reduction of the livestock trypanosomiasis and zoonotic transmission of human infective trypanosomes [119].
SRA Neg (not) Binding (interact) of associated with targeted disruption and trypanosomiasis
3) Confidence 0.16 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2826769 Disease Relevance 0.56 Pain Relevance 0
-helix which interacts with the SRA of T. b. rhodesiense and this interaction leads to a loss of trypanolytic capability of the APOL1.
SRA Binding (interacts) of
4) Confidence 0.15 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2826769 Disease Relevance 0.31 Pain Relevance 0
increase in Mad-1 binding complexes which could contribute to the switch from c-Myc/Max to Mad1/Max with repressor
complexes Binding (binding) of
5) Confidence 0.02 Published 2008 Journal PPAR Research Section Body Doc Link PMC2443425 Disease Relevance 0.20 Pain Relevance 0
In addition, calcitriol has rapid effects that are independent of gene transcription regulation, which are defined as non-genomic effects and not mediated directly through steroid receptor-ligand-DNA interaction.
steroid receptor-ligand-DNA Binding (interaction) of
6) Confidence 0.01 Published 2010 Journal Journal of Cancer Section Body Doc Link PMC2938072 Disease Relevance 0.11 Pain Relevance 0.03
Integral to the flow balances were the net mass transfers between the three soluble species: interstitially, the steady-state inflows for both free VEGF and sVEGFR1 outweighed their respective outflows, signifying a net tendency for them to associate and form sVEGFR1-VEGF complexes; in the plasma, the steady-state inflows for VEGF and sVEGFR1 were less than their respective outflows, indicative of an additional source from net dissociation of sVEGFR1-VEGF complexes.

2.

complexes Binding (associate) of in plasma
7) Confidence 0.01 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
The unconfirmed binding of VEGF-sVEGFR1 complexes directly onto unoccupied matrix sites was also neglected.


complexes Binding (binding) of
8) Confidence 0.01 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0

General Comments

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