INT106719

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Context Info
Confidence 0.77
First Reported 2002
Last Reported 2010
Negated 4
Speculated 0
Reported most in Body
Documents 18
Total Number 20
Disease Relevance 12.18
Pain Relevance 8.42

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

lyase activity (Adcy1) plasma membrane (Adcy1) nucleus (Adcy1)
Anatomy Link Frequency
body 4
neurons 2
insular cortex 1
cingulate cortex 1
hippocampus 1
Adcy1 (Mus musculus)
Pain Link Frequency Relevance Heat
nMDA receptor 104 100.00 Very High Very High Very High
Anterior cingulate cortex 333 99.96 Very High Very High Very High
Pain 309 99.80 Very High Very High Very High
Pyramidal cell 35 99.58 Very High Very High Very High
allodynia 172 99.36 Very High Very High Very High
Inflammation 123 99.32 Very High Very High Very High
Hippocampus 96 98.96 Very High Very High Very High
long-term potentiation 151 98.44 Very High Very High Very High
Inflammatory stimuli 3 96.48 Very High Very High Very High
amygdala 76 96.40 Very High Very High Very High
Disease Link Frequency Relevance Heat
Targeted Disruption 609 99.80 Very High Very High Very High
Myalgia 145 99.80 Very High Very High Very High
Nervous System Injury 16 99.60 Very High Very High Very High
Neuropathic Pain 208 99.36 Very High Very High Very High
INFLAMMATION 126 99.32 Very High Very High Very High
Pain 277 99.08 Very High Very High Very High
Nociception 94 98.38 Very High Very High Very High
Injury 86 97.52 Very High Very High Very High
Body Weight 25 97.40 Very High Very High Very High
Anxiety Disorder 217 95.04 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
AC1 and AC8 are highly expressed in the anterior cingulate cortex (ACC), and contribute to inflammation-induced activation of CREB.
Gene_expression (expressed) of AC1 in cingulate cortex associated with inflammation and anterior cingulate cortex
1) Confidence 0.77 Published 2002 Journal Neuron Section Abstract Doc Link 12441059 Disease Relevance 0.74 Pain Relevance 0.62
The contribution of AC1 and AC8 to the behavioral responses to acute muscle pain induced by intramuscular injection of 10 ?
Gene_expression (contribution) of AC1 in acute muscle associated with pain and myalgia
2) Confidence 0.67 Published 2006 Journal Mol Pain Section Body Doc Link PMC1395303 Disease Relevance 1.47 Pain Relevance 0.44
The novel AC1 inhibitor NB001 was dissolved in 1% DMSO in normal saline and injected into the peritoneal cavity in doses varying from 0.1 to 5 mg/kg body weight in a volume of 10 ?
Gene_expression (The) of AC1 in body associated with body weight
3) Confidence 0.67 Published 2006 Journal Mol Pain Section Body Doc Link PMC1395303 Disease Relevance 0.48 Pain Relevance 0.45
The novel AC1 inhibitor NB001 was dissolved in 1% DMSO in normal saline and injected into the peritoneal cavity in doses varying from 0.1 to 5 mg/kg body weight in a volume of 10 ?
Gene_expression (dissolved) of AC1 in body associated with body weight
4) Confidence 0.67 Published 2006 Journal Mol Pain Section Body Doc Link PMC1395303 Disease Relevance 0.48 Pain Relevance 0.45
The novel AC1 inhibitor NB001 was dissolved in 1% DMSO in normal saline and injected into the peritoneal cavity in doses varying from 0.1 to 5 mg/kg body weight in a volume of 10 ?
Gene_expression (injected) of AC1 in body associated with body weight
5) Confidence 0.67 Published 2006 Journal Mol Pain Section Body Doc Link PMC1395303 Disease Relevance 0.49 Pain Relevance 0.45
The novel AC1 inhibitor NB001 was dissolved in 1% DMSO in normal saline and injected into the peritoneal cavity in doses varying from 0.1 to 5 mg/kg body weight in a volume of 10 ?
Gene_expression (novel) of AC1 in body associated with body weight
6) Confidence 0.67 Published 2006 Journal Mol Pain Section Body Doc Link PMC1395303 Disease Relevance 0.48 Pain Relevance 0.45
4.06 fc) of DKO mice compared to those of WT mice; however, AC1 only met the FDR threshold in the hippocampus (?
Gene_expression (met) of AC1 in hippocampus associated with targeted disruption and hippocampus
7) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 0.88 Pain Relevance 0.34
At the cellular level, AC1 and AC8 are localized to the synapse, specifically the postsynaptic region for AC1 and presynaptic region for AC8 [11].
Gene_expression (presynaptic) of AC1 in synapse
8) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 0.75 Pain Relevance 0.16
Cortical lesions induced by NMDA were significantly reduced in AC1 but not in AC8 knock-out mice.
Neg (not) Gene_expression (reduced) of AC1 associated with targeted disruption
9) Confidence 0.59 Published 2007 Journal J. Biol. Chem. Section Abstract Doc Link 17121841 Disease Relevance 0.34 Pain Relevance 0.36
In Purkinje neurons, unlike hippocampal CA1 pyramidal neurons, Ca2+/CaM-activated adenylyl cyclases such as type-1 and type-8 are not expressed (Cooper et al, 1995).
Neg (not) Gene_expression (expressed) of adenylyl cyclase in neurons associated with pyramidal cell
10) Confidence 0.58 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0.43 Pain Relevance 0.39
Behavioral nociceptive responses to subcutaneous formalin injection or nerve injury were significantly reduced in mice lacking AC1 or AC8, and more profoundly compromised in AC1&8 DKO mice.
Neg (lacking) Gene_expression (reduced) of AC1 in nerve associated with targeted disruption, nociception and nervous system injury
11) Confidence 0.52 Published 2010 Journal Current Genomics Section Body Doc Link PMC2851120 Disease Relevance 1.63 Pain Relevance 0.83
We found that AC1 and AC8 were both expressed at high levels in two pain-related forebrain areas, the ACC and the insular cortex.
Gene_expression (expressed) of AC1 in insular cortex associated with pain and anterior cingulate cortex
12) Confidence 0.52 Published 2010 Journal Current Genomics Section Body Doc Link PMC2851120 Disease Relevance 1.60 Pain Relevance 0.85
As the downstream target of AC1, cAMP-dependent protein kinase (PKA) may activate MEK and ERK/MAPK.
Gene_expression (target) of AC1
13) Confidence 0.44 Published 2009 Journal Mol Pain Section Body Doc Link PMC2734546 Disease Relevance 0 Pain Relevance 0.62
Three different Stealth siRNA duplex oligoribonucleotides (Invitrogen, Paisley, UK) were used to abolish the expression and function of AC1 and AC3.
Gene_expression (expression) of AC1
14) Confidence 0.28 Published 2010 Journal Cell Signal Section Body Doc Link PMC2791881 Disease Relevance 0 Pain Relevance 0
Additional RT-PCR analysis of these genes with single knockout animals (AC1KO, AC8KO) suggests that these genes are not targeted by one specific Ca2+-stimulated AC as both single knockouts show similar reduction in expression levels.
Gene_expression (expression) of AC1KO associated with targeted disruption
15) Confidence 0.25 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 1.04 Pain Relevance 0.33
We found that Ishikawa cells express mRNA for AC1, AC3, AC4, AC5, AC6, AC7, AC9 and the soluble AC (SAC), but not AC2 or AC8 isoforms (data not shown).
Neg (not) Gene_expression (express) of AC1 in AC2
16) Confidence 0.24 Published 2010 Journal Cell Signal Section Body Doc Link PMC2791881 Disease Relevance 0 Pain Relevance 0.10
As shown in Fig. 3C, transfection with AC3 siRNA completely abolished the potentiation of Butaprost-stimulated cAMP by PGF significantly (P < 0.001) while AC1 siRNA transfection had no effect on cAMP accumulation.
Gene_expression (transfection) of AC1
17) Confidence 0.24 Published 2010 Journal Cell Signal Section Body Doc Link PMC2791881 Disease Relevance 0 Pain Relevance 0
Transfection studies using siRNA to abolish expression of AC1 or AC3 in FPEP2 cells revealed that the calcium sensitive AC3 (but not AC1) isoform is responsible for PGF-mediated potentiation of Butaprost-stimulated cAMP.
Gene_expression (expression) of AC1
18) Confidence 0.24 Published 2010 Journal Cell Signal Section Body Doc Link PMC2791881 Disease Relevance 0 Pain Relevance 0.03
Studies using AC1&AC8 double knockout or NR2B overexpression mice show that NMDA receptors, AC1 and AC8 contribute to activation of immediate early genes by injury [49,57] (see fig 4).


Gene_expression (receptors) of AC1 associated with targeted disruption, nmda receptor and injury
19) Confidence 0.22 Published 2007 Journal Mol Pain Section Body Doc Link PMC1904186 Disease Relevance 1.38 Pain Relevance 0.71
In the ACC, AC1 is highly expressed in cingulate neurons located in most of layers [49].
Gene_expression (expressed) of AC1 in neurons associated with anterior cingulate cortex
20) Confidence 0.19 Published 2007 Journal Mol Pain Section Body Doc Link PMC1904186 Disease Relevance 0 Pain Relevance 0.82

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