INT77619

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Context Info
Confidence 0.75
First Reported 1998
Last Reported 2011
Negated 2
Speculated 0
Reported most in Body
Documents 43
Total Number 43
Disease Relevance 8.55
Pain Relevance 14.13

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

mitochondrion (Prkaca) Golgi apparatus (Prkaca) plasma membrane (Prkaca)
nucleus (Prkaca) protein complex (Prkaca) kinase activity (Prkaca)
Anatomy Link Frequency
tail 2
brain 2
neurons 2
Leydig cells 1
colon 1
Prkaca (Mus musculus)
Pain Link Frequency Relevance Heat
amygdala 207 100.00 Very High Very High Very High
Kinase C 127 100.00 Very High Very High Very High
nociceptor 10 100.00 Very High Very High Very High
dorsal root ganglion 65 99.96 Very High Very High Very High
Hyperalgesia 25 99.84 Very High Very High Very High
Glutamate 76 99.74 Very High Very High Very High
long-term potentiation 186 99.50 Very High Very High Very High
Dopamine 270 99.46 Very High Very High Very High
Versed 16 98.98 Very High Very High Very High
cytokine 43 98.92 Very High Very High Very High
Disease Link Frequency Relevance Heat
Hyperalgesia 62 99.84 Very High Very High Very High
Apoptosis 56 99.84 Very High Very High Very High
Ganglion Cysts 74 99.48 Very High Very High Very High
Shock 12 99.20 Very High Very High Very High
Colon Cancer 134 98.54 Very High Very High Very High
INFLAMMATION 185 98.52 Very High Very High Very High
Watson Syndrome 28 98.20 Very High Very High Very High
Neuropathic Pain 11 97.84 Very High Very High Very High
Neuroblastoma 8 97.84 Very High Very High Very High
Cognitive Disorder 27 97.36 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
GTS inhibited cAMP levels and protein expression of protein kinase A (PKA).
Gene_expression (expression) of PKA
1) Confidence 0.75 Published 2008 Journal Arch. Pharm. Res. Section Abstract Doc Link 18365685 Disease Relevance 0.08 Pain Relevance 0.64
This hypothesis was confirmed by pharmacological activations of adenylate cyclase (AC) by Forskolin (50 µM), a condition which we used previously in juvenile animals to demonstrate the role of the cAMP/PKA/Rim in the control of release probability at Cortico-LA synapses [38].
Gene_expression (synapses) of PKA in Rim associated with amygdala
2) Confidence 0.65 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2896423 Disease Relevance 0.21 Pain Relevance 0.21
Indeed, it is now well established that like its counterparts in other brain areas [32]–[36], LTP at Cortico-LA synapses is predominantly expressed by a presynaptic, cAMP/PKA-dependent increase in the probability of release [20], [21], [23], [37]–[38].
Gene_expression (expressed) of PKA in brain associated with amygdala
3) Confidence 0.65 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2896423 Disease Relevance 0.07 Pain Relevance 0.39
signaling, we focused on the genes encoding RGS4 and PKAC?
Gene_expression (encoding) of PKA
4) Confidence 0.65 Published 2010 Journal J Brachial Plex Peripher Nerve Inj Section Body Doc Link PMC3017042 Disease Relevance 0 Pain Relevance 0.38
It is even more striking that RGS4 and PKAC?
Gene_expression (striking) of PKA
5) Confidence 0.65 Published 2010 Journal J Brachial Plex Peripher Nerve Inj Section Body Doc Link PMC3017042 Disease Relevance 0.25 Pain Relevance 0.45
METHODS: Cellular changes of cAMP, PKA and c-Fos were detected by protein competitive conjunction, enzyme activity and isotope incorporation methods respectively.
Gene_expression (detected) of PKA
6) Confidence 0.58 Published 1999 Journal Zhongguo Yi Xue Ke Xue Yuan Xue Bao Section Body Doc Link 12567447 Disease Relevance 0.10 Pain Relevance 0
The increase in P(o) of these channels was also seen in an inside-out configuration and in the presence of PKA, ATP, and cAMP, but not with cAMP alone; phosphorylation did not influence single-channel conductance.
Gene_expression (presence) of PKA
7) Confidence 0.57 Published 2002 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 11820801 Disease Relevance 0 Pain Relevance 0.09
These results highly indicated that MDZ-induced steroidogenesis in mouse Leydig cells via PKA and PKC pathways, along with the expression of PBR and StAR proteins.
Gene_expression (pathways) of PKA in Leydig cells associated with versed
8) Confidence 0.53 Published 2010 Journal Toxicol. Lett. Section Abstract Doc Link 19857560 Disease Relevance 0.32 Pain Relevance 0.75
We demonstrate that PKA modulation of K(Na) channels does not happen at the level of channel gating but arises from the internal trafficking of Slack channels from DRG membranes.
Gene_expression (modulation) of PKA in DRG associated with dorsal root ganglion
9) Confidence 0.50 Published 2010 Journal J. Neurosci. Section Abstract Doc Link 20962237 Disease Relevance 0.62 Pain Relevance 0.55
PKA-induced internalization of slack KNa channels produces dorsal root ganglion neuron hyperexcitability.
Gene_expression (produces) of PKA in neuron associated with ganglion cysts, dorsal root ganglion, nociceptor and hyperexcitability
10) Confidence 0.50 Published 2010 Journal J. Neurosci. Section Title Doc Link 20962237 Disease Relevance 0.59 Pain Relevance 0.66
Using mice whose sperm express a mutant PKA catalytic subunit that is sensitive to the unique cell-permeant inhibitor 1NM-PP1, we found that acute application of the 1NM-PP1 to hyperactivated sperm did not remove waveform asymmetry.
Gene_expression (express) of PKA in sperm
11) Confidence 0.46 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2729922 Disease Relevance 0.08 Pain Relevance 0
The PKA activity seems to be regulated by the activity of PDE1 in the basal condition owing to the high affinity of PDE1 for Ca2+/CaM (Kd ?
Gene_expression (activity) of PKA
12) Confidence 0.38 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Compared with the results without GABABR stimulation, the reductions of the cAMP and active PKA levels during the conditioning stimulation were larger (Figure 2G and H), and the duration of the increase in active PP-1 was longer (Figure 2J).
Gene_expression (levels) of PKA
13) Confidence 0.38 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.04
The main findings from these simulations suggest that the presence of the PKA–PP2A–phosphoThr75 loop causes increased formation of free PKAc as well as phosphoThr34 if a dopamine input is paired with a transient calcium elevation.
Gene_expression (presence) of PKA associated with dopamine
14) Confidence 0.36 Published 2006 Journal PLoS Computational Biology Section Body Doc Link PMC1562452 Disease Relevance 0 Pain Relevance 0.07
We therefore studied the phosphorylation of GluR1 at two main sites, Ser845 (PKA site) and Ser831 (CaMKII/PKC site) (Fig. 4F).
Gene_expression (site) of PKA
15) Confidence 0.35 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2169299 Disease Relevance 0.54 Pain Relevance 0.12
More significantly, combined dopamine and glutamate stimulation produces a larger activation of PKA and inhibition of PP1 than dopamine alone (Figure 5).
Gene_expression (produces) of PKA associated with glutamate and dopamine
16) Confidence 0.32 Published 2006 Journal PLoS Computational Biology Section Body Doc Link PMC1562452 Disease Relevance 0 Pain Relevance 0.24
Given the widespread expression of PKA subunits, polymorphisms that drastically affect function may be expected to have widespread deleterious effects (Stergiopoulos and Stratakis 2003).
Gene_expression (expression) of PKA
17) Confidence 0.28 Published 2005 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2426818 Disease Relevance 0.14 Pain Relevance 0.31
Type II PKA is predominantly expressed in the brain.
Gene_expression (expressed) of PKA in brain
18) Confidence 0.28 Published 2005 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2426818 Disease Relevance 0.36 Pain Relevance 0.33
This release component was dependent on voltage-dependent Ca2+ channels that opened spontaneously after PKA and PKC activation and occurred in the absence of Na+ channel firing.
Gene_expression (opened) of PKA
19) Confidence 0.28 Published 2003 Journal J. Neurochem. Section Abstract Doc Link 14622090 Disease Relevance 0 Pain Relevance 0.46
This effect of dibutyryl cAMP is not dependent on activation of the PKA pathway, as the addition of forskolin does not result in a rebound in PrPSc levels (Fig. 4A).
Gene_expression (pathway) of PKA
20) Confidence 0.26 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2777304 Disease Relevance 0 Pain Relevance 0

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