INT150853

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Context Info
Confidence 0.49
First Reported 2004
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 22
Total Number 22
Disease Relevance 12.61
Pain Relevance 5.72

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 (Cxcl1) extracellular region (Cxcl1)
Anatomy Link Frequency
macrophage 2
liver 2
lymph nodes 1
blood 1
Monocyte 1
Cxcl1 (Mus musculus)
Pain Link Frequency Relevance Heat
cytokine 532 100.00 Very High Very High Very High
Inflammation 513 100.00 Very High Very High Very High
chemokine 150 99.74 Very High Very High Very High
guanethidine 2 99.16 Very High Very High Very High
Morphine 61 98.68 Very High Very High Very High
Inflammatory response 85 98.24 Very High Very High Very High
tolerance 21 98.20 Very High Very High Very High
Paracetamol 6 95.20 Very High Very High Very High
agonist 17 94.84 High High
addiction 69 89.92 High High
Disease Link Frequency Relevance Heat
INFLAMMATION 611 100.00 Very High Very High Very High
Injury 425 99.68 Very High Very High Very High
Adhesions 129 99.44 Very High Very High Very High
Liver Failure 6 99.32 Very High Very High Very High
Infection 314 98.56 Very High Very High Very High
Pulmonary Disease 144 98.00 Very High Very High Very High
Sprains And Strains 6 95.92 Very High Very High Very High
Poisoning 3 93.84 High High
Urological Neuroanatomy 18 90.48 High High
Cancer 103 87.20 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
This effect complements the reported inhibition on KC and IL-1?
Negative_regulation (inhibition) of KC
1) Confidence 0.49 Published 2008 Journal FASEB J Section Body Doc Link PMC2700033 Disease Relevance 0.64 Pain Relevance 0.32
In view of the inhibition of CXCL1 production in the kidney by macrophage depletion and the documented protective effect of CXCL1 inhibition in ischemic AKI [64, 65], it is possible that part of the protective effect of macrophage depletion in ischemic AKI is mediated by inhibition of CXCL1.

6.

Negative_regulation (inhibition) of CXCL1 in macrophage associated with injury
2) Confidence 0.48 Published 2009 Journal Mediators of Inflammation Section Body Doc Link PMC2825552 Disease Relevance 1.35 Pain Relevance 0.14
In view of the inhibition of CXCL1 production in the kidney by macrophage depletion and the documented protective effect of CXCL1 inhibition in ischemic AKI [64, 65], it is possible that part of the protective effect of macrophage depletion in ischemic AKI is mediated by inhibition of CXCL1.

6.

Negative_regulation (inhibition) of CXCL1 in macrophage associated with injury
3) Confidence 0.35 Published 2009 Journal Mediators of Inflammation Section Body Doc Link PMC2825552 Disease Relevance 1.37 Pain Relevance 0.15
As demonstrated in Figure 2, the top networks identified by IPA at 6 hours after pneumonectomy are associated with cell-cell signaling (including up-regulation of Ceacam1 and ItgaV - Figure 2A), and inhibition of inflammatory cell migration (down-regulation of the pro-inflammatory cytokines Cxcl1 and Cxcl10, as well as Nf??
Negative_regulation (regulation) of Cxcl1 associated with inflammation and cytokine
4) Confidence 0.32 Published 2009 Journal Respir Res Section Body Doc Link PMC2770038 Disease Relevance 0.46 Pain Relevance 0.24
Following treatment with an MIP-2 polyclonal antibody, the corneal clinical scores and inflammatory responses decreased, the MIP-2 protein levels were downregulated significantly (p<0.01), and the KC protein levels decreased slightly (p>0.05).
Negative_regulation (decreased) of KC protein associated with inflammatory response
5) Confidence 0.29 Published 2009 Journal Molecular Vision Section Abstract Doc Link PMC2707360 Disease Relevance 0.80 Pain Relevance 0.35
The results showed that MIP-2 protein expression levels were reduced significantly (p=0.000) one, three, five, and seven days post-infection in the MIP-2 treated group compared to the infected group and that the KC protein expression levels decreased slightly (p>0.05).
Negative_regulation (decreased) of KC protein associated with infection
6) Confidence 0.29 Published 2009 Journal Molecular Vision Section Body Doc Link PMC2707360 Disease Relevance 0.63 Pain Relevance 0.33
The peak expression levels of MIP-2, KC, and IL-1?
Negative_regulation (levels) of KC
7) Confidence 0.29 Published 2009 Journal Molecular Vision Section Body Doc Link PMC2707360 Disease Relevance 0.90 Pain Relevance 0.36
Inhibition of CXCL8 or CXCL1 signaling or expression as a treatment target in COPD may hence inhibit inflammatory cell activation and tissue degradation, but may potentially delay wound repair in COPD.
Negative_regulation (Inhibition) of CXCL1 associated with pulmonary disease, inflammation and injury
8) Confidence 0.24 Published 2007 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2695202 Disease Relevance 0.96 Pain Relevance 0.15
Hypernociception induced by IL-1beta in immunized mice was inhibited by indomethacin, whereas KC/CXCL1-induced hypernociception was inhibited by indomethacin and guanethidine.
Negative_regulation (inhibited) of CXCL1 associated with guanethidine
9) Confidence 0.18 Published 2008 Journal Eur J Pain Section Abstract Doc Link 18372199 Disease Relevance 0.28 Pain Relevance 0.29
However, with the exception of KC levels, peri-incisional cytokine levels were reduced by the 100-fold lower 0.1 mg/kg morphine dose, a dose at which neutrophil infiltration was unaffected.
Negative_regulation (reduced) of KC in neutrophil associated with morphine and cytokine
10) Confidence 0.17 Published 2007 Journal Mol Pain Section Body Doc Link PMC2096620 Disease Relevance 0.87 Pain Relevance 1.23
Specific chemoattractants such as KC (Keratinocyte Chemoattractant), JE/MCP-1 (Monocyte Chemoattractant Protein 1), MCP-5 (Monocyte Chemoattractant Protein 5) and MIP-2 (Macrophage Inflammatory Protein 2) are also diminished in mice treated with hAFSC.
Negative_regulation (diminished) of KC in Monocyte associated with inflammation
11) Confidence 0.10 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2827539 Disease Relevance 1.10 Pain Relevance 0.48
A simultaneous reduction in KO and KC would also shift the macroscopic ATP doseĀ–response curves to higher ATP concentrations.
Negative_regulation (reduction) of KC
12) Confidence 0.07 Published 2008 Journal The Journal of General Physiology Section Body Doc Link PMC2442177 Disease Relevance 0 Pain Relevance 0.11
Following liver transplantation, donor KC not only migrate into the recipient lymph nodes, but also can be quickly replaced by recipient-derived monocytes [8,9].
Negative_regulation (replaced) of KC in lymph nodes
13) Confidence 0.07 Published 2004 Journal Comp Hepatol Section Body Doc Link PMC2410251 Disease Relevance 0.35 Pain Relevance 0.19
If KO and n in Scheme 2 are unaffected, it follows from the principle of microscopic reversibility that a decrease in m would simultaneously result in a decrease in KC and in the ratio KC/KO (since KC = KO*m/n).
Negative_regulation (decrease) of KC
14) Confidence 0.05 Published 2008 Journal The Journal of General Physiology Section Body Doc Link PMC2442177 Disease Relevance 0 Pain Relevance 0.06
A decrease in m will then have two effects on the ATP sensitivity of macroscopic KATP currents; it will shift the ATP doseĀ–response curves to higher ATP concentrations (due to the decrease in KC), and it will also increase the fraction of unblocked current at high ATP concentrations (via the increase in the KO/KC ratio).
Negative_regulation (decrease) of KC
15) Confidence 0.05 Published 2008 Journal The Journal of General Physiology Section Body Doc Link PMC2442177 Disease Relevance 0 Pain Relevance 0.03
This is predicted for a mutation that does not abolish ATP binding to the open state, but rather causes a defect in the mechanism by which ATP binding is transduced into channel closure (m in Scheme 2), and thus decreases the KC/KO ratio (see above).
Negative_regulation (decreases) of KC
16) Confidence 0.05 Published 2008 Journal The Journal of General Physiology Section Body Doc Link PMC2442177 Disease Relevance 0 Pain Relevance 0
In comparison, depletion of KC leaves the liver apparently fully intact. ii) A transplanted liver will be rejected if the SEC are damaged [71].
Negative_regulation (depletion) of KC in liver
17) Confidence 0.03 Published 2004 Journal Comp Hepatol Section Body Doc Link PMC2409441 Disease Relevance 0.30 Pain Relevance 0.16
On the other hand, if KC are depleted from the donor liver, it increases the chances that the transplanted liver will not be rejected. iii) The mechanism of acetaminophen (paracetamol) liver intoxication resides in the effect of this drug on LSEC [75]: Experiments in mice revealed that massive injury to SEC and thereby disrupted the microcirculation of liver preceded development of liver failure [76].
Negative_regulation (depleted) of KC in liver associated with liver failure, paracetamol, injury and poisoning
18) Confidence 0.02 Published 2004 Journal Comp Hepatol Section Body Doc Link PMC2409441 Disease Relevance 0.36 Pain Relevance 0.19
Although IgG immune complexes are removed from the blood predominantly by KC, it has been shown that following KC depletion these immune complexes become strongly associated with LSEC [57].
Negative_regulation (depletion) of KC in blood
19) Confidence 0.02 Published 2004 Journal Comp Hepatol Section Body Doc Link PMC2409441 Disease Relevance 0.07 Pain Relevance 0
The major angiogenic proteins downregulated by celecoxib treatment were VEGF, GRO, IL-6, IL-8, TIMP1, and TIMP2 (Figure 5).
Negative_regulation (downregulated) of GRO
20) Confidence 0.01 Published 2006 Journal Breast Cancer Res Section Body Doc Link PMC1797025 Disease Relevance 0.41 Pain Relevance 0.06

General Comments

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