INT180095

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Context Info
Confidence 0.55
First Reported 2005
Last Reported 2010
Negated 1
Speculated 1
Reported most in Body
Documents 22
Total Number 25
Disease Relevance 4.90
Pain Relevance 1.14

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

Golgi apparatus (Rock1) cytoskeleton (Rock1) cytoskeleton organization (Rock1)
kinase activity (Rock1) cytoplasm (Rock1)
Anatomy Link Frequency
neuronal 1
neurite 1
Rock1 (Mus musculus)
Pain Link Frequency Relevance Heat
Hippocampus 4 99.64 Very High Very High Very High
Inflammation 38 99.36 Very High Very High Very High
ischemia 12 98.30 Very High Very High Very High
cINOD 38 88.60 High High
Kinase C 160 84.08 Quite High
cva 21 80.96 Quite High
Central nervous system 130 57.60 Quite High
antagonist 1 51.44 Quite High
Spinal cord 76 45.00 Quite Low
adenocard 4 36.08 Quite Low
Disease Link Frequency Relevance Heat
Vasculitis 2 99.36 Very High Very High Very High
Death 42 98.96 Very High Very High Very High
Cv Unclassified Under Development 19 98.30 Very High Very High Very High
Stroke 62 97.76 Very High Very High Very High
Cardiovascular Disease 45 96.00 Very High Very High Very High
Apoptosis 128 95.52 Very High Very High Very High
Atherosclerosis 88 91.72 High High
INFLAMMATION 58 88.36 High High
Cancer 163 87.92 High High
Alzheimer's Dementia 190 86.56 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Since many isoprenoid-mediated Rho effects converge on ROCKs, we next transfected N2a cells with cDNAs encoding either green fluorescent protein (GFP) (control), CA ROCK1, or DN ROCK1 (Figure 5).
Gene_expression (transfected) of ROCK1
1) Confidence 0.55 Published 2005 Journal PLoS Medicine Section Body Doc Link PMC543463 Disease Relevance 0 Pain Relevance 0
Expression of ROCK-Related Molecules Modulates sAPP?
Gene_expression (Expression) of ROCK
2) Confidence 0.55 Published 2005 Journal PLoS Medicine Section Body Doc Link PMC543463 Disease Relevance 0 Pain Relevance 0
It will now be important to dissect pathways upstream of Rho/ROCK signaling in order to identify the intracellular and intercellular events that participate in Rho/ROCK regulation of ?
Gene_expression (participate) of ROCK
3) Confidence 0.48 Published 2005 Journal PLoS Medicine Section Body Doc Link PMC543463 Disease Relevance 0.05 Pain Relevance 0
For the detection of transfected ROCK1 proteins, samples were immunoprecipitated with 2 ?
Gene_expression (transfected) of ROCK1
4) Confidence 0.48 Published 2005 Journal PLoS Medicine Section Body Doc Link PMC543463 Disease Relevance 0 Pain Relevance 0
CA ROCK1 and DN ROCK1 molecules yielded direct and complementary evidence that ROCK1 was indeed a candidate for modulation of statin-activated ?
Gene_expression (molecules) of ROCK1
5) Confidence 0.48 Published 2005 Journal PLoS Medicine Section Body Doc Link PMC543463 Disease Relevance 0.09 Pain Relevance 0.14
Soon thereafter, ROCK1 was discovered by Zhou et al. [28] to modulate a downstream processing step in APP metabolism that involves presenilin/?
Gene_expression (discovered) of ROCK1
6) Confidence 0.48 Published 2005 Journal PLoS Medicine Section Body Doc Link PMC543463 Disease Relevance 0.14 Pain Relevance 0.16
Treatment of cells with a farnesyl transferase inhibitor or expression of a dominant negative (DN) ROCK1 molecule led to enhanced sAPP?
Gene_expression (molecule) of ROCK1
7) Confidence 0.48 Published 2005 Journal PLoS Medicine Section Body Doc Link PMC543463 Disease Relevance 0.07 Pain Relevance 0
CA ROCK1 and DN ROCK1 molecules yielded direct and complementary evidence that ROCK1 was indeed a candidate for modulation of statin-activated ?
Gene_expression (yielded) of ROCK1
8) Confidence 0.48 Published 2005 Journal PLoS Medicine Section Body Doc Link PMC543463 Disease Relevance 0.09 Pain Relevance 0.14
When CA ROCK1 was introduced, however, shedding of sAPP?
Gene_expression (introduced) of ROCK1
9) Confidence 0.48 Published 2005 Journal PLoS Medicine Section Body Doc Link PMC543463 Disease Relevance 0 Pain Relevance 0
Our results suggest that Rho/ROCK signaling provides modulation of basal and stimulated ?
Gene_expression (provides) of ROCK
10) Confidence 0.48 Published 2005 Journal PLoS Medicine Section Body Doc Link PMC543463 Disease Relevance 0 Pain Relevance 0
CA ROCK1 and DN ROCK1 molecules yielded direct and complementary evidence that ROCK1 was indeed a candidate for modulation of statin-activated ?
Gene_expression (molecules) of ROCK1
11) Confidence 0.48 Published 2005 Journal PLoS Medicine Section Body Doc Link PMC543463 Disease Relevance 0.09 Pain Relevance 0.14
For the detection of transfected ROCK1 proteins, samples were immunoprecipitated with 2 ?
Gene_expression (detection) of ROCK1
12) Confidence 0.48 Published 2005 Journal PLoS Medicine Section Body Doc Link PMC543463 Disease Relevance 0 Pain Relevance 0
Taken together, these results suggest the existence of a reciprocal relationship between isoprenoid-mediated Rho/ROCK signaling and sAPP?
Gene_expression (signaling) of ROCK
13) Confidence 0.48 Published 2005 Journal PLoS Medicine Section Body Doc Link PMC543463 Disease Relevance 0 Pain Relevance 0.04
Other ROCK substrates include the LIM (Lin11/Isl1/Mec3) kinases (Ohashi et al 2000; Sumi et al 2001) and collapsin response mediator protein-2 (CRMP-2) (Arimura et al 2000, 2004), all of which are involved in the regulation of cytoskeletal reorganization.
Gene_expression (include) of ROCK
14) Confidence 0.46 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2500253 Disease Relevance 0.65 Pain Relevance 0.06
In this case, the activation of myosin IIA, which is one of the downstream effectors of ROCK, is a key step for the exertion of the inhibitory effects of RGMa (Kubo et al in press).
Gene_expression (effectors) of ROCK
15) Confidence 0.46 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2500253 Disease Relevance 0 Pain Relevance 0
Most of the other documented neurite outgrowth inhibitors such as chondroitin sulfate proteoglycans (CSPGs) and members of the semaphorin and ephrin families are also reported to use the Rho-ROCK pathway for their inhibitory functions (Wahl et al 2000; Shamah et al 2001; Swiercz et al 2002; Monnier et al 2003; Lingor et al 2007).
Gene_expression (pathway) of ROCK in neurite
16) Confidence 0.46 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2500253 Disease Relevance 0 Pain Relevance 0.07
It is noteworthy that delayed treatment with fasudil also prevents ischemia-induced neuronal death in the CA1 region of the gerbil hippocampus, suggesting that ROCK inhibition has a wide therapeutic time window in the treatment of ischemic stroke (Satoh et al 2007).
Neg (inhibition) Gene_expression (inhibition) of ROCK in neuronal associated with stroke, ischemia, hippocampus and death
17) Confidence 0.46 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2500253 Disease Relevance 1.08 Pain Relevance 0.29
Transfection with the cDNA for a constitutively active (CA) ROCK1 molecule led to inhibition of statin-activated sAPP?
Gene_expression (Transfection) of ROCK1
18) Confidence 0.43 Published 2005 Journal PLoS Medicine Section Body Doc Link PMC543463 Disease Relevance 0.09 Pain Relevance 0
By microarray analysis and western blotting we did not observe any evident change in ROCK or RhoA expression in tumorigenic cen3tel cells (data not shown); however, microarray and western blot analyses revealed that the cellular inhibitor of ROCK-I, Rnd3 (Riento et al. 2003), was expressed at lower levels in tumorigenic cen3tel cells compared to non-tumorigenic ones (Fig. 5A, B), suggesting that Rnd3 downregulation might play a role in the transition to the ROCK dependent mode of invasion.
Gene_expression (expression) of ROCK
19) Confidence 0.31 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3014295 Disease Relevance 0 Pain Relevance 0
By microarray analysis and western blotting we did not observe any evident change in ROCK or RhoA expression in tumorigenic cen3tel cells (data not shown); however, microarray and western blot analyses revealed that the cellular inhibitor of ROCK-I, Rnd3 (Riento et al. 2003), was expressed at lower levels in tumorigenic cen3tel cells compared to non-tumorigenic ones (Fig. 5A, B), suggesting that Rnd3 downregulation might play a role in the transition to the ROCK dependent mode of invasion.
Gene_expression (expressed) of ROCK-I
20) Confidence 0.31 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3014295 Disease Relevance 0 Pain Relevance 0

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