INT215286

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Context Info
Confidence 0.00
First Reported 2007
Last Reported 2007
Negated 0
Speculated 1
Reported most in Body
Documents 1
Total Number 5
Disease Relevance 2.76
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.

plasma membrane (Siglec1, Ros1) cell differentiation (Ros1) cell proliferation (Ros1)
signal transduction (Ros1) extracellular region (Siglec1) cell adhesion (Siglec1)
Anatomy Link Frequency
DA neurons 2
Siglec1 (Mus musculus)
Ros1 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammatory mediators 35 92.56 High High
Inflammation 155 79.20 Quite High
midbrain 20 66.20 Quite High
narcan 10 45.52 Quite Low
opioid receptor 10 39.28 Quite Low
rheumatoid arthritis 10 5.00 Very Low Very Low Very Low
Inflammatory response 10 5.00 Very Low Very Low Very Low
imagery 10 5.00 Very Low Very Low Very Low
opiate 5 5.00 Very Low Very Low Very Low
Enkephalin 5 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Drug Induced Neurotoxicity 110 100.00 Very High Very High Very High
Toxicity 30 98.30 Very High Very High Very High
Death 30 96.68 Very High Very High Very High
INFLAMMATION 200 92.16 High High
Parkinson's Disease 20 91.56 High High
Stress 15 88.56 High High
Disease 85 82.80 Quite High
Neurodegenerative Disease 20 82.36 Quite High
Necrosis 10 76.72 Quite High
Cancer 10 76.36 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Taken together, these results demonstrated that SN can inhibit ROS production induced either directly by LPS stimulation or indirectly by MPP+-mediated reactive microgliosis, and lend further evidence to the idea that superoxide production, rather than TNF-?
SN Negative_regulation (inhibit) of Gene_expression (production) of ROS
1) Confidence 0.00 Published 2007 Journal J Neuroinflammation Section Body Doc Link PMC2064906 Disease Relevance 0.40 Pain Relevance 0.05
Our observation that MPP+-mediated neurotoxicity is significantly less in PHOX-/- animals [41], and that SN does not protect DA neurons from MPP+-mediated toxicity in neuron-enriched or neuron-astroglial cultures (Fig. 3), supports the notion that SN protects MPP+-induced neurotoxicity mainly through the inhibition of ROS production, which in turn slows down the self-propelling cycle and prevents further neuronal death.
SN Negative_regulation (inhibition) of Gene_expression (production) of ROS in DA neurons associated with toxicity, drug induced neurotoxicity and death
2) Confidence 0.00 Published 2007 Journal J Neuroinflammation Section Body Doc Link PMC2064906 Disease Relevance 1.31 Pain Relevance 0.07
Similarly, SN at 10-14 M significantly inhibited intracellular ROS production in PHOX+/+ mice, but not in PHOX-/- mice (Fig. 4C).
SN Negative_regulation (inhibited) of Gene_expression (production) of ROS
3) Confidence 0.00 Published 2007 Journal J Neuroinflammation Section Body Doc Link PMC2064906 Disease Relevance 0.06 Pain Relevance 0
Furthermore, we demonstrated that SN reduced LPS-induced extracellular ROS production through the inhibition of the PHOX cytosolic subunit p47phoxtranslocation to the cell membrane.


SN Negative_regulation (reduced) of Gene_expression (production) of ROS
4) Confidence 0.00 Published 2007 Journal J Neuroinflammation Section Abstract Doc Link PMC2064906 Disease Relevance 0.50 Pain Relevance 0.10
Therefore, we sought to determine whether SN is able to reduce MPP+-induced ROS production.
SN Spec (whether) Negative_regulation (reduce) of Gene_expression (production) of ROS
5) Confidence 0.00 Published 2007 Journal J Neuroinflammation Section Body Doc Link PMC2064906 Disease Relevance 0.48 Pain Relevance 0.03

General Comments

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