INT354078

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Context Info
Confidence 0.28
First Reported 2011
Last Reported 2011
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 2
Disease Relevance 2.71
Pain Relevance 0.08

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

signal transduction (Avpr1b, Pomc) cell-cell signaling (Pomc) cytoplasm (Pomc)
response to stress (Avpr1b) signal transducer activity (Avpr1b) extracellular space (Pomc)
Anatomy Link Frequency
corticotrophs 2
Avpr1b (Mus musculus)
Pomc (Mus musculus)
Pain Link Frequency Relevance Heat
antagonist 34 96.32 Very High Very High Very High
agonist 18 5.00 Very Low Very Low Very Low
depression 16 5.00 Very Low Very Low Very Low
medulla 12 5.00 Very Low Very Low Very Low
Hippocampus 8 5.00 Very Low Very Low Very Low
Catecholamine 6 5.00 Very Low Very Low Very Low
Potency 4 5.00 Very Low Very Low Very Low
ketamine 2 5.00 Very Low Very Low Very Low
Morphine 2 5.00 Very Low Very Low Very Low
amygdala 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Stress 160 98.92 Very High Very High Very High
Targeted Disruption 120 98.70 Very High Very High Very High
Attention Deficit Hyperactivity Disorder 4 94.44 High High
Aggression 34 5.00 Very Low Very Low Very Low
Sprains And Strains 24 5.00 Very Low Very Low Very Low
Depression 20 5.00 Very Low Very Low Very Low
Anxiety Disorder 16 5.00 Very Low Very Low Very Low
Obesity 6 5.00 Very Low Very Low Very Low
Hypersensitivity 6 5.00 Very Low Very Low Very Low
Hypoglycemia 6 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The studies in Avpr1b KO mice and Brattleboro rats highlight the discrepancy between Avp/Avpr1b-mediated ACTH and CORT secretion during acute and repeated stress—this may have implications on the potential use of Avpr1b antagonists to ameliorate symptoms of HPA axis hyperactivity in stress-related disorders.


Avpr1b Positive_regulation (mediated) of Localization (secretion) of ACTH associated with stress, targeted disruption, antagonist and attention deficit hyperactivity disorder
1) Confidence 0.28 Published 2011 Journal Stress (Amsterdam, Netherlands) Section Body Doc Link PMC3016603 Disease Relevance 1.84 Pain Relevance 0.05
As Oxt at high concentrations can elicit ACTH release via the Avpr1b, and the Oxtr may be expressed in corticotrophs, it has been suggested that increased expression of Oxtrs may be a compensatory mechanism through which Avpr1b KO mice and Brattleboro rats can, to some degree, make up for the lack of Avpr1b/Avp-mediated ACTH release (Nakamura et al. 2008).
Avpr1b Positive_regulation (elicit) of Localization (release) of ACTH in corticotrophs associated with targeted disruption
2) Confidence 0.28 Published 2011 Journal Stress (Amsterdam, Netherlands) Section Body Doc Link PMC3016603 Disease Relevance 0.87 Pain Relevance 0.03

General Comments

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