INT180418

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Context Info
Confidence 0.32
First Reported 2005
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 16
Total Number 16
Disease Relevance 7.05
Pain Relevance 0.20

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 (Rhoa) mitochondrion (Rhoa) cell morphogenesis (Rhoa)
intracellular (Rhoa) GTPase activity (Rhoa) cytoplasm (Rhoa)
Anatomy Link Frequency
brain 1
neurite 1
neural 1
Rhoa (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 54 100.00 Very High Very High Very High
agonist 10 72.64 Quite High
cytokine 7 62.72 Quite High
cerebral cortex 12 52.48 Quite High
adenocard 1 50.96 Quite High
Spinal cord 19 29.92 Quite Low
Thalamus 10 25.76 Quite Low
Hippocampus 23 24.96 Low Low
interneuron 2 22.84 Low Low
Kinase C 5 19.20 Low Low
Disease Link Frequency Relevance Heat
INFLAMMATION 56 100.00 Very High Very High Very High
Stress 14 100.00 Very High Very High Very High
Mevalonate Kinase Deficiency 580 99.16 Very High Very High Very High
Apoptosis 56 97.40 Very High Very High Very High
Adhesions 32 85.20 High High
Atherosclerosis 35 78.56 Quite High
Aging 49 69.28 Quite High
Disease 34 61.84 Quite High
Cancer 7 42.00 Quite Low
Necrosis 2 41.52 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Collectively, these findings firstly demonstrated a participation of RhoA-mediated Ca2+ sensitization in ACh-induced BSM contraction in mice.
RhoA Binding (participation) of
1) Confidence 0.32 Published 2005 Journal Respir Res Section Body Doc Link PMC545934 Disease Relevance 0 Pain Relevance 0.07
Effect of simvastatin on activation of soluble and membrane-bound RhoA and Rac1
RhoA Binding (bound) of
2) Confidence 0.27 Published 2010 Journal J Inherit Metab Dis Section Body Doc Link PMC2946549 Disease Relevance 0.43 Pain Relevance 0
Again, MKD cells were more sensitive to treatment with simvastatin, with markedly increased levels of active soluble RhoA and decreased levels of active membrane-bound RhoA already observed after incubation with low concentrations of simvastatin.
RhoA Binding (bound) of associated with mevalonate kinase deficiency
3) Confidence 0.27 Published 2010 Journal J Inherit Metab Dis Section Body Doc Link PMC2946549 Disease Relevance 0.57 Pain Relevance 0
Incubation with simvastatin led to an increase of active soluble RhoA and a decrease of active membrane-bound RhoA in a concentration-dependent manner in both control and MKD cells.
RhoA Binding (bound) of associated with mevalonate kinase deficiency
4) Confidence 0.27 Published 2010 Journal J Inherit Metab Dis Section Body Doc Link PMC2946549 Disease Relevance 0.65 Pain Relevance 0
Incubation with simvastatin led to an increase in the total levels of active, GTP-bound RhoA and Rac1 in both control and MKD cells.
RhoA Binding (bound) of associated with mevalonate kinase deficiency
5) Confidence 0.27 Published 2010 Journal J Inherit Metab Dis Section Body Doc Link PMC2946549 Disease Relevance 0.24 Pain Relevance 0
To determine whether the observed increase of active GTP-bound RhoA and Rac1 during the different culturing conditions was due to activation of soluble or membrane-bound RhoA and Rac1, we studied separately the effect of simvastatin.
RhoA Binding (bound) of
6) Confidence 0.27 Published 2010 Journal J Inherit Metab Dis Section Body Doc Link PMC2946549 Disease Relevance 0.53 Pain Relevance 0
Incubation with GGTI led to a reduction in membrane-bound RhoA and Rac1 that was similar for both control and MKD cells (Fig. 2b, g) and, in parallel, an increase in the levels of soluble RhoA and Rac1 (Fig. 2c and 2h).
RhoA Binding (bound) of associated with mevalonate kinase deficiency
7) Confidence 0.27 Published 2010 Journal J Inherit Metab Dis Section Body Doc Link PMC2946549 Disease Relevance 0.30 Pain Relevance 0
When MKD and control cells were cultured in the absence of simvastatin, levels of active RhoA protein in the soluble fraction were markedly higher in MKD cells, whereas levels of active membrane-bound RhoA were similar in both control and MKD cells (Fig. 3b, c).
RhoA Binding (bound) of associated with mevalonate kinase deficiency
8) Confidence 0.27 Published 2010 Journal J Inherit Metab Dis Section Body Doc Link PMC2946549 Disease Relevance 0.59 Pain Relevance 0
However, MKD cells were more sensitive to treatment with simvastatin, already resulting in decreased levels of membrane-bound RhoA after incubation with 0.02 ?
RhoA Binding (bound) of associated with mevalonate kinase deficiency
9) Confidence 0.27 Published 2010 Journal J Inherit Metab Dis Section Body Doc Link PMC2946549 Disease Relevance 0.93 Pain Relevance 0
Fig. 3Effect of simvastatin on activation of membrane-bound and soluble RhoA (a–c) and Rac1 (d–f).
RhoA Binding (bound) of
10) Confidence 0.27 Published 2010 Journal J Inherit Metab Dis Section Body Doc Link PMC2946549 Disease Relevance 0.50 Pain Relevance 0
To determine whether the observed increase of active GTP-bound RhoA and Rac1 during the different culturing conditions was due to activation of soluble or membrane-bound RhoA and Rac1, we studied separately the effect of simvastatin.
RhoA Binding (bound) of
11) Confidence 0.27 Published 2010 Journal J Inherit Metab Dis Section Body Doc Link PMC2946549 Disease Relevance 0.50 Pain Relevance 0
Furthermore, these results can be similarly reproduced using RhoA/ROCK inhibitors (by DN-RhoA transfection, C3 pretreatment or ROCK inhibition with Y-27632), but not inhibiting other geranylated GTPases such as Rac1 or Cdc42.
RhoA Binding (using) of
12) Confidence 0.15 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2597201 Disease Relevance 0.83 Pain Relevance 0
Co-immunoprecipation analyses in brain lysates revealed that neural PC also interacts with RhoA and with the related small GTPase RhoG (Fig. 2h,i).
RhoA Binding (interacts) of in neural
13) Confidence 0.13 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2919383 Disease Relevance 0 Pain Relevance 0
In the present study, we found that brain PC interacts with the Ezrin/NHERF1-2/RhoA-G complex, thereby suggesting that activation of this protein complex is responsible for the reduction in neurite growth and branching observed in PC loss-of-function models.
RhoA Binding (interacts) of in brain
14) Confidence 0.12 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2919383 Disease Relevance 0.17 Pain Relevance 0.06
The following gene products emerged as hubs: Fos, a transcription factor involved in stress response; glucocorticoid receptor (encoded by Nr3c1), involved in stress response and inflammation; RhoA, an important signaling molecule associated with cytoskeletal remodeling; and Cdkn1b, which maintains cell cycle arrest.
RhoA Binding (emerged) of associated with stress and inflammation
15) Confidence 0.12 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2975639 Disease Relevance 0.82 Pain Relevance 0.05
It has also been demonstrated that RhoA mediates the actions of myelin-associated neurite outgrowth inhibitors through direct binding to CRMP-4 (Alabed et al 2007).
RhoA Binding (binding) of in neurite
16) Confidence 0.10 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2500253 Disease Relevance 0 Pain Relevance 0.03

General Comments

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