INT128178

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.68
First Reported 2000
Last Reported 2010
Negated 1
Speculated 2
Reported most in Body
Documents 59
Total Number 61
Disease Relevance 9.30
Pain Relevance 4.70

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
d cell 2
neuronal 1
monocytes 1
endothelial cells 1
MDCK 1
RHOA (Homo sapiens)
Pain Link Frequency Relevance Heat
Kinase C 2 100.00 Very High Very High Very High
agonist 560 99.98 Very High Very High Very High
antagonist 52 99.62 Very High Very High Very High
Morphine 17 99.50 Very High Very High Very High
fluoxetine 2 97.72 Very High Very High Very High
cytokine 542 97.68 Very High Very High Very High
Serotonin 7 97.50 Very High Very High Very High
Opioid 6 97.32 Very High Very High Very High
cINOD 31 90.64 High High
addiction 1 90.08 High High
Disease Link Frequency Relevance Heat
Adhesions 300 99.00 Very High Very High Very High
Stress 135 98.50 Very High Very High Very High
Sprains And Strains 2 97.60 Very High Very High Very High
Herpes Simplex Virus 1666 97.52 Very High Very High Very High
Breast Cancer 28 94.96 High High
Infection 728 94.88 High High
Hypersensitivity 14 91.88 High High
Leukemia 44 91.76 High High
Injury 4 90.56 High High
INFLAMMATION 394 90.40 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Thus, 5-HT has a potent enhancing action on migration of HAECs through activating the RhoA and ERK pathways following 5-HT1 receptor stimulation.
Positive_regulation (activating) of RhoA
1) Confidence 0.68 Published 2005 Journal FEBS Lett. Section Abstract Doc Link 16310780 Disease Relevance 0.10 Pain Relevance 0.20
The purpose of the present study was to investigate whether 5-hydroxytryptamine (5-HT, serotonin) affects migration of vascular endothelial cells. 5-HT significantly enhanced migration of human aortic endothelial cells (HAECs), and this enhancement was completely inhibited by GR 55562, a 5-HT1 receptor antagonist, and fluoxetine, a 5-HT transporter inhibitor, but was not affected by ketanserin, a 5-HT2 receptor antagonist. 5-HT stimulation increased RhoA and ERK activity of HAECs, and inhibitors of RhoA (Y-27632 and H-1152) and inhibitors of MEK (U0126 and PD98059) abolished the 5-HT-induced increase in migration velocity.
Positive_regulation (increased) of RhoA in endothelial cells associated with antagonist, serotonin and fluoxetine
2) Confidence 0.68 Published 2005 Journal FEBS Lett. Section Abstract Doc Link 16310780 Disease Relevance 0.08 Pain Relevance 0.24
For instance, NO reportedly inhibits calcium sensitization by PKG-mediated inhibition of RhoA [34]–[35] and telokin [36], as well as by inhibition of RhoA activation through protein kinase A (PKA)-dependent phosphorylation of G?
Positive_regulation (activation) of RhoA
3) Confidence 0.67 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3013104 Disease Relevance 0 Pain Relevance 0
Using pomalidomide and primary human monocytes, we report that pomalidomide rapidly and selectively activated RhoA and Rac1, but not Cdc42 or Ras, in the absence of any costimulation.
Positive_regulation (activated) of RhoA in monocytes
4) Confidence 0.59 Published 2009 Journal Blood Section Abstract Doc Link 19417207 Disease Relevance 0.16 Pain Relevance 0.09
Finally, we demonstrated that pomalidomide was able to regulate the activity of Rho GTPases and the formation of F-actin in primary human T cells as it did in monocytes and showed that the activation of RhoA was essential for pomalidomide-induced interleukin-2 expression in T cells.
Positive_regulation (activation) of RhoA in T cells
5) Confidence 0.59 Published 2009 Journal Blood Section Abstract Doc Link 19417207 Disease Relevance 0.15 Pain Relevance 0.06
Further, we showed that in Swiss 3T3 cells, pomalidomide only activated RhoA, not Rac1 or Cdc42, and potently induced stress fiber formation.
Neg (not) Positive_regulation (activated) of RhoA associated with stress
6) Confidence 0.59 Published 2009 Journal Blood Section Abstract Doc Link 19417207 Disease Relevance 0.17 Pain Relevance 0.08
Moreover, both SIN-1 and the alternative NO-donor FK409 also specifically impaired U46619-induced RhoA activation by TP?
Positive_regulation (activation) of RhoA
7) Confidence 0.49 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.04
expressed in HEK 293 cells readily induced RhoA activation, F-actin polymerization and cofilin phosphorylation in response to U46619.
Positive_regulation (activation) of RhoA
8) Confidence 0.49 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0.07 Pain Relevance 0.04
activation, both the NO and prostacyclin analogues SIN-1 and Cicaprost impair TP-mediated cytoskeletal changes involving RhoA activation and cofilin phosphorylation in 1° h.AoSMCs and that they do so, at least in part, by specifically and directly targeting TP?
Positive_regulation (activation) of RhoA
9) Confidence 0.49 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0.06 Pain Relevance 0
also mediated rapid RhoA activation in HEK.TP?
Positive_regulation (activation) of RhoA
10) Confidence 0.49 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0
We next examined the effect of the inhibitory vasodilatory agents SIN-1 and Cicaprost on U46619-mediated RhoA activation and signaling in 1° h.AoSMCs in the presence of the respective TP-isoform specific siRNA reagents.
Positive_regulation (activation) of RhoA
11) Confidence 0.49 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0
Consistent with this, the specific PGD2 receptor (DP) agonist BW245C also significantly impaired RhoA activation (Fig. 7C) and cofilin phosphorylation in 1° h.AoSMCs.
Positive_regulation (activation) of RhoA associated with agonist
12) Confidence 0.49 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.09
Similarly, while the NO donors SIN-1 and FK409 alone did not induce substantial RhoA signaling relative to the drug vehicle per se, they each significantly impaired U46619-induced RhoA activation and cofilin phosphorylation following their pre-incubation in 1° h.AoSMCs (Fig. 7B and D).
Positive_regulation (activation) of RhoA
13) Confidence 0.49 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.08
From their studies, they proposed that Ser188 phosphorylation of RhoA may act as a ‘secondary molecular switch’ capable of overriding GTP-elicited activation of certain RhoA effectors, such as ROCK, but directing it to signal with (an)other subset of Rho effectors, perhaps in a cell specific manner.
Positive_regulation (activation) of RhoA
14) Confidence 0.49 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0
RhoA activation through GPCRs predominantly occurs by coupling to G12 (G?
Positive_regulation (activation) of RhoA
15) Confidence 0.49 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0.06 Pain Relevance 0
On the other hand, pre-stimulation with Cicaprost impaired U46619-induced [Ca2+]i mobilization and RhoA activation by TP?
Positive_regulation (activation) of RhoA
16) Confidence 0.49 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.09
The functional implications of these interactions are best understood for mammalian Sema4D and mammalian PlexB1: activation of PlexB1 by Sema4D enhances the activity of RhoGEFs, activating the small GTPase RhoA, and leads to cytoskeletal rearrangement and repulsive axon guidance.
Positive_regulation (activating) of RhoA
17) Confidence 0.49 Published 2006 Journal Genome Biol Section Body Doc Link PMC1557745 Disease Relevance 0 Pain Relevance 0
are coupled to downstream signaling pathways via interaction with predominantly Gq11, and exhibit complex interactions, including activation of protein kinase C, RhoA [6] and AMP-activated protein kinase [7] and can stimulate release of intracellular calcium stores.
Positive_regulation (activation) of RhoA associated with kinase c
18) Confidence 0.45 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2939892 Disease Relevance 0.66 Pain Relevance 0.17
Furthermore, MS, DAMGO and VEGF induced RhoA activation which was inhibited by MNTX or VEGF receptor tyrosine kinase inhibition.
Positive_regulation (activation) of RhoA
19) Confidence 0.41 Published 2006 Journal Microvasc. Res. Section Abstract Doc Link 16820176 Disease Relevance 0.05 Pain Relevance 0.65
Taken together, these results indicate that MNTX inhibits opioid-induced EC proliferation and migration via inhibition of VEGF receptor phosphorylation/transactivation with subsequent inhibition of RhoA activation.
Positive_regulation (activation) of RhoA associated with opioid
20) Confidence 0.38 Published 2006 Journal Microvasc. Res. Section Abstract Doc Link 16820176 Disease Relevance 0 Pain Relevance 0.49

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox