INT69952

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Context Info
Confidence 0.32
First Reported 1997
Last Reported 2010
Negated 4
Speculated 0
Reported most in Abstract
Documents 45
Total Number 52
Disease Relevance 16.08
Pain Relevance 14.59

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

extracellular space (IK) nucleus (IK) cell-cell signaling (IK)
Anatomy Link Frequency
striatum 2
DRG 2
synovial fluids 1
visceral 1
cardiomyocyte 1
IK (Homo sapiens)
Pain Link Frequency Relevance Heat
cytokine 554 100.00 Very High Very High Very High
Inflammation 323 100.00 Very High Very High Very High
Sumatriptan 81 99.84 Very High Very High Very High
Enkephalin 18 99.58 Very High Very High Very High
adenocard 21 99.38 Very High Very High Very High
Action potential 326 99.12 Very High Very High Very High
agonist 107 98.76 Very High Very High Very High
fibrosis 10 98.66 Very High Very High Very High
psoriasis 88 98.56 Very High Very High Very High
antagonist 18 98.56 Very High Very High Very High
Disease Link Frequency Relevance Heat
INFLAMMATION 334 100.00 Very High Very High Very High
Primary Sclerosing Cholangitis 2 100.00 Very High Very High Very High
Apoptosis 46 99.72 Very High Very High Very High
Fibrosis 10 98.66 Very High Very High Very High
Herpes Simplex Virus 238 98.64 Very High Very High Very High
Psoriasis 96 98.56 Very High Very High Very High
Heart Rate Under Development 21 98.46 Very High Very High Very High
Depression 194 98.44 Very High Very High Very High
Cardiovascular Disease 6 98.40 Very High Very High Very High
Disease 141 98.20 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In C6 glioma cells expressing either recombinant h 5-HT1B or h 5-HT1D receptors, sumatriptan similarly increased IK in a concentration-dependent manner (maximum increase 19.4+/-7.2%, n=8, P<0.05 and 25.1+/-3.9%, n=6, P<0.001, respectively) with EC50 values (geometric mean with 95% confidence intervals in parentheses) of 56.3 nM (7.9-140 nM) and 68.7 nM (16-120 nM), respectively.
Positive_regulation (increased) of IK associated with sumatriptan and glioma
1) Confidence 0.32 Published 1998 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 9879718 Disease Relevance 0.35 Pain Relevance 0.27
In C6 cells expressing cloned h 5-HT1B receptors, sumatriptan (1 microM) similarly failed to significantly increase IK in the presence of dibutyryl cAMP (10 microM) or when a nominally Ca2+-free medium was included in the patch pipette (-19.4+/-5.1%, n=5 and -5.2+/-4.3%, n=5, respectively, P=NS in each case).
Neg (failed) Positive_regulation (increase) of IK associated with sumatriptan
2) Confidence 0.28 Published 1998 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 9879718 Disease Relevance 0.07 Pain Relevance 0.63
In addition, the Ca2+-dependent K+ channel blockers iberiotoxin (0.1 microM) and tetraethylammonium (TEA, 1 mM) abolished sumatriptan-induced increases in IK (-0.5+/-1.0%, n=4 and -3.9+/-3.1%, n=4, respectively, P=NS in each case) in C6 cells expressing h 5-HT1B receptors, confirming the involvement of Ca2+-dependent K+ channels.
Positive_regulation (increases) of IK associated with sumatriptan
3) Confidence 0.28 Published 1998 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 9879718 Disease Relevance 0.13 Pain Relevance 0.55
In C6 cells expressing either cloned h 5-HT1B or h 5-HT1D receptors, sumatriptan-induced increases in IK were prevented by the calcium chelator EGTA (5 mM) when included in the patch pipette (maximum increase 0.57+/-0.6%, n=3, P=NS and -2.8+/-1.6%, n=5, P=NS, respectively).
Positive_regulation (increases) of IK associated with sumatriptan
4) Confidence 0.28 Published 1998 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 9879718 Disease Relevance 0.13 Pain Relevance 0.66
In the presence of the mixed 5-HT1B/D receptor antagonist GR 127935 (0.1 microM), sumatriptan (1 microM) failed to significantly increase IK in C6 cells expressing h 5-HT1B receptors (-7.5+/-3.5%, P=NS, n=6), although a higher concentration of GR 127935 (1 microM) was required to significantly inhibit sumatriptan-evoked increases in IK in C6 cells expressing h 5-HT1D receptors (-1.8+/-3.5%, P=NS, n=6), confirming that sumatriptan-evoked responses were indeed mediated by h 5-HT1B and h 5-HT1D receptors, respectively.
Neg (failed) Positive_regulation (increase) of IK associated with sumatriptan and antagonist
5) Confidence 0.28 Published 1998 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 9879718 Disease Relevance 0.27 Pain Relevance 0.56
Sumatriptan failed to elicit increases in IK in non-transfected cells, confirming a specific involvement of the respective membrane h 5-HT1B and h 5-HT1D receptors in transfected C6 cells.
Positive_regulation (increases) of IK associated with sumatriptan
6) Confidence 0.19 Published 1998 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 9879718 Disease Relevance 0.31 Pain Relevance 0.43
In C6 cells expressing cloned h 5-HT1B receptors, sumatriptan (1 microM) similarly failed to significantly increase IK after 30-min incubation with thapsigargin (1 microM) or when heparin (2 mg/ml) was included in the patch pipette (1.1+/-0.4%, n=5 and 1.2+/-2.4%, n=5, respectively, P=NS).
Neg (failed) Positive_regulation (increase) of IK associated with sumatriptan
7) Confidence 0.19 Published 1998 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 9879718 Disease Relevance 0.15 Pain Relevance 0.43
In the presence of the mixed 5-HT1B/D receptor antagonist GR 127935 (0.1 microM), sumatriptan (1 microM) failed to significantly increase IK in C6 cells expressing h 5-HT1B receptors (-7.5+/-3.5%, P=NS, n=6), although a higher concentration of GR 127935 (1 microM) was required to significantly inhibit sumatriptan-evoked increases in IK in C6 cells expressing h 5-HT1D receptors (-1.8+/-3.5%, P=NS, n=6), confirming that sumatriptan-evoked responses were indeed mediated by h 5-HT1B and h 5-HT1D receptors, respectively.
Positive_regulation (increases) of IK associated with sumatriptan and antagonist
8) Confidence 0.19 Published 1998 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 9879718 Disease Relevance 0.25 Pain Relevance 0.63
IK was elicited by a depolarizing step from a holding potential of -60 mV.
Positive_regulation (elicited) of IK
9) Confidence 0.19 Published 1998 Journal Naunyn Schmiedebergs Arch. Pharmacol. Section Abstract Doc Link 9879718 Disease Relevance 0.36 Pain Relevance 0.15
During our search for transcription factors that control the developmental expression of the enkephalin (ENK) gene we found that Ik-1 and Ik-2 isoforms are specifically expressed in the embryonic striatum and bind the Ik-like cis-regulatory DNA element present on the ENK gene.
Positive_regulation (bind) of Ik in striatum associated with enkephalin
10) Confidence 0.15 Published 2007 Journal J. Neurochem. Section Abstract Doc Link 17504264 Disease Relevance 0 Pain Relevance 0.54
During our search for transcription factors that control the developmental expression of the enkephalin (ENK) gene we found that Ik-1 and Ik-2 isoforms are specifically expressed in the embryonic striatum and bind the Ik-like cis-regulatory DNA element present on the ENK gene.
Positive_regulation (bind) of Ik in striatum associated with enkephalin
11) Confidence 0.15 Published 2007 Journal J. Neurochem. Section Abstract Doc Link 17504264 Disease Relevance 0 Pain Relevance 0.54
The used Oil Red O staining protocol was as follows; aspirate all the media off the cells, wash once with 2 ml of PBS, replace the PBS with 2 ml of 10% formalin for 30 min at room temperature to fixate the cells, replace the formalin with 2 ml of sterile water for a few minutes, replace water with 60% isopropanol for 5 minutes, replace isopropanol with 2 ml of Oil Red O working solution made up as described by Cambrex, after 5 minutes the Oil red O solution was washed of indirectly with tap water.
Positive_regulation (used) of Red
12) Confidence 0.13 Published 2007 Journal BMC Biotechnol Section Body Doc Link PMC1904213 Disease Relevance 0 Pain Relevance 0
The A1 receptor agonist R-N6-phenylisopropyl-adenosine (R-PIA; 50 microM) reversibly increased IK.
Positive_regulation (increased) of IK associated with adenocard and agonist
13) Confidence 0.12 Published 1998 Journal Brain Res. Section Abstract Doc Link 9630670 Disease Relevance 0.09 Pain Relevance 0.27
The present study demonstrates that in frog melanotrophs adenosine inhibits the electrical activity by activating IK through an A1 receptor subtype coupled to a pertussis toxin-sensitive pathway independent of the cAMP/PKA system.
Positive_regulation (activating) of IK in melanotrophs associated with adenocard and bordatella infection
14) Confidence 0.12 Published 1998 Journal Brain Res. Section Abstract Doc Link 9630670 Disease Relevance 0.18 Pain Relevance 0.28
Perfusion of dibutyryl-cAMP (1 mM) in the external solution did not modify the R-PIA-induced enhancement of IK.
Positive_regulation (enhancement) of IK in external
15) Confidence 0.10 Published 1998 Journal Brain Res. Section Abstract Doc Link 9630670 Disease Relevance 0.15 Pain Relevance 0.27
This is plausible because INa is 20 to 50 times larger than either the maximum outward current due to IK1 or the fully activated IK in this tissue.
Positive_regulation (activated) of IK
16) Confidence 0.10 Published 1997 Journal Can J Cardiol Section Abstract Doc Link 9413245 Disease Relevance 0 Pain Relevance 0.25
The second hypothesis is that residual activation of the delayed rectifier potassium ion current (IK) causes the stimulus to become subthreshold as the rate of stimulation increases.
Positive_regulation (activation) of IK
17) Confidence 0.08 Published 1997 Journal Can J Cardiol Section Abstract Doc Link 9413245 Disease Relevance 0 Pain Relevance 0.08
In cells with preloaded intracellular Ca2+ stores, oxytocin (10(-12) mol/l to 10(-9) mol/l) caused a dose-dependent activation of the charybdotoxin-blockable non-inactivating component of IK (IK(sl)) of single voltage-clamped cells, which was accompanied by hyperpolarization of the cell membranes. 8Lys-vasopressin and 8arg-vasopressin failed to mimic the effects of oxytocin on both contraction and K+ currents.
Positive_regulation (activation) of IK
18) Confidence 0.07 Published 1997 Journal Eur. J. Endocrinol. Section Abstract Doc Link 9186274 Disease Relevance 0 Pain Relevance 0.09
In cells with preloaded intracellular Ca2+ stores, oxytocin (10(-12) mol/l to 10(-9) mol/l) caused a dose-dependent activation of the charybdotoxin-blockable non-inactivating component of IK (IK(sl)) of single voltage-clamped cells, which was accompanied by hyperpolarization of the cell membranes. 8Lys-vasopressin and 8arg-vasopressin failed to mimic the effects of oxytocin on both contraction and K+ currents.
Positive_regulation (activation) of IK
19) Confidence 0.07 Published 1997 Journal Eur. J. Endocrinol. Section Abstract Doc Link 9186274 Disease Relevance 0 Pain Relevance 0.09
The present experiments on isolated atrial cardiomyocyte show that IK,CCh is induced and ICa inhibited by CCh.
Positive_regulation (induced) of IK in cardiomyocyte
20) Confidence 0.06 Published 2010 Journal BMC Physiol Section Body Doc Link PMC2894799 Disease Relevance 0 Pain Relevance 0.18

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