INT8801

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Context Info
Confidence 0.74
First Reported 1991
Last Reported 2010
Negated 2
Speculated 3
Reported most in Body
Documents 71
Total Number 74
Disease Relevance 45.60
Pain Relevance 10.83

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 (Csf3) extracellular region (Csf3) enzyme binding (Csf3)
Anatomy Link Frequency
motoneurons 12
granulocyte 7
macrophages 4
kidney 3
plasma 2
Csf3 (Mus musculus)
Pain Link Frequency Relevance Heat
cytokine 145 100.00 Very High Very High Very High
Angina 1 99.84 Very High Very High Very High
Central nervous system 175 99.82 Very High Very High Very High
Sciatic nerve 375 99.48 Very High Very High Very High
Inflammatory response 192 99.44 Very High Very High Very High
Spinal cord 350 98.84 Very High Very High Very High
rheumatoid arthritis 120 98.76 Very High Very High Very High
Inflammation 334 96.96 Very High Very High Very High
ischemia 25 96.44 Very High Very High Very High
abdominal pain 3 95.64 Very High Very High Very High
Disease Link Frequency Relevance Heat
Neutropenia 574 100.00 Very High Very High Very High
Coronary Artery Disease 4 100.00 Very High Very High Very High
Bladder Cancer 9 99.98 Very High Very High Very High
Cv General 3 Under Development 1 99.84 Very High Very High Very High
Targeted Disruption 436 99.78 Very High Very High Very High
Thrombophilia 1 99.64 Very High Very High Very High
Pancreatic Cancer 7 99.60 Very High Very High Very High
Motor Neuron Diseases 450 99.56 Very High Very High Very High
Infection 92 99.48 Very High Very High Very High
INFLAMMATION 557 99.44 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We therefore examined expression of the G-CSF receptor by quantitative PCR of whole spinal cords 4 days following neonatal axotomy of the right sciatic nerve (i.e. on postnatal day 9).
Spec (examined) Gene_expression (expression) of G-CSF in sciatic nerve associated with sciatic nerve
1) Confidence 0.74 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.35 Pain Relevance 0.27
In conclusion, the G-CSF receptor is expressed at the neonatal stage and its expression is increased in response to axotomy.


Gene_expression (expressed) of G-CSF
2) Confidence 0.74 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.75 Pain Relevance 0.31
The three groups are a.) mice not harbouring any transgene ("wt"), b.) mice harbouring only the BEG2 transgene (which do not express G-CSF), and c.) mice harbouring both the BEG2 transgene and the CaMKII-tTA driver, that do express G-CSF.
Gene_expression (express) of G-CSF
3) Confidence 0.74 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.43 Pain Relevance 0.20
CNS- targeted overexpression of G-CSF protects motoneurons against cell death in neonatal pups
Gene_expression (overexpression) of G-CSF in motoneurons associated with central nervous system and death
4) Confidence 0.74 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.79 Pain Relevance 0.28
We chose to use transgenic mice that overexpress G-CSF in the CNS as an endogenous "delivery system" to study effects of increased concentration of G-CSF on the lesioned motoneurons.
Gene_expression (overexpress) of G-CSF in motoneurons associated with targeted disruption and central nervous system
5) Confidence 0.74 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.74 Pain Relevance 0.26
Overexpression of G-CSF protects lumbar motoneurons to an extent that is comparable to many of the classic neurotrophic factors.
Gene_expression (Overexpression) of G-CSF in motoneurons
6) Confidence 0.74 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.28 Pain Relevance 0.04
This analysis revealed that only 50 - 60% of the motoneurons survived in the genotypes lacking the CaMK-tta driver transgene, whereas close to 90% of the motoneurons survived in the double transgenic mice (i.e. in animals overexpressing G-CSF) (BEG -/T CaMK-/T (88.76 ± 4.32%) vs.
Gene_expression (overexpressing) of G-CSF in motoneurons associated with targeted disruption
7) Confidence 0.74 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.40 Pain Relevance 0.09
On top of a relative increase of motoneuron numbers following overexpression of G-CSF, we also noted an increase of about 100 ?
Gene_expression (overexpression) of G-CSF in motoneuron
8) Confidence 0.74 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.38 Pain Relevance 0.03
The expression of G-CSF receptor is induced by neurons under neurodegenerative conditions such as after cerebral ischemia or in ALS, presumably as an endogenous protective response [6,7].
Gene_expression (expression) of G-CSF in neurons associated with cv general 4 under development, ischemia, neurodegenerative disease and motor neuron diseases
9) Confidence 0.74 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.41 Pain Relevance 0.24
 ;-promoter directed G-CSF overexpression in the forebrain leads to a strong elevation of G-CSF levels in the neonatal brain and spinal cord (P9; 28.00 ± 11.60 vs 0.24 ± 0.23 pg/mg tissue protein; p < 0.05) (Figure 3).
Gene_expression (overexpression) of G-CSF in forebrain associated with spinal cord
10) Confidence 0.74 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.25 Pain Relevance 0.25
Recombinant granulocyte colony-stimulating factor (rG-CSF) is a glycoprotein hormone which has been produced in mammalian cells and, in a nonglycosylated form, in the bacterium Escherichia coli through recombinant DNA technology.
Gene_expression (produced) of Recombinant granulocyte colony-stimulating factor in granulocyte
11) Confidence 0.66 Published 1991 Journal Drugs Section Abstract Doc Link 1717226 Disease Relevance 0.20 Pain Relevance 0.10
Interestingly, among the immune response genes induced by LPS treatment, expression of the Csf3 gene encoding G-CSF was significantly down-regulated in LNA-antimiR-treated cells compared to the untreated and LNA controls (P = 0.014 and P = 0.008, respectively, Student's t-test, two-sided), implying that the regulation of G-CSF expression is mediated by miR-155 (Figure 5A, Supplementary table S1).
Gene_expression (expression) of G-CSF
12) Confidence 0.65 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2761263 Disease Relevance 0.06 Pain Relevance 0.07
(B) Quantitative RT-PCR analysis of G-CSF expression normalized to GAPDH after LPS-stimulation of THP-1 cells.
Gene_expression (expression) of G-CSF in THP-1
13) Confidence 0.65 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2761263 Disease Relevance 0 Pain Relevance 0
Thus, it is possible that c/ebp Beta, which is modulated by miR-155, acts in part by fine-tuning G-CSF expression levels, consistent with a c/ebp Beta binding motif in the promoter of G-CSF (15,32).
Gene_expression (expression) of G-CSF
14) Confidence 0.65 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2761263 Disease Relevance 0.87 Pain Relevance 0.27
Interestingly, among the immune response genes induced by LPS treatment, expression of the Csf3 gene encoding G-CSF was significantly down-regulated in LNA-antimiR-treated cells compared to the untreated and LNA controls (P = 0.014 and P = 0.008, respectively, Student's t-test, two-sided), implying that the regulation of G-CSF expression is mediated by miR-155 (Figure 5A, Supplementary table S1).
Gene_expression (expression) of G-CSF
15) Confidence 0.65 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2761263 Disease Relevance 0.07 Pain Relevance 0.08
(A) Quantitative RT-PCR analysis of G-CSF expression normalized to ?
Gene_expression (expression) of G-CSF
16) Confidence 0.65 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2761263 Disease Relevance 0.06 Pain Relevance 0.06
Moreover, we report that miR-155 mediates regulation of G-CSF expression, thereby underscoring the role of miR-155 in fine-tuning important regulatory networks during inflammation.


Gene_expression (expression) of G-CSF associated with inflammation
17) Confidence 0.65 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2761263 Disease Relevance 0.79 Pain Relevance 0.36
Interestingly, among the immune response genes induced by LPS treatment, expression of the Csf3 gene encoding G-CSF was significantly down-regulated in LNA-antimiR-treated cells compared to the untreated and LNA controls (P = 0.014 and P = 0.008, respectively, Student's t-test, two-sided), implying that the regulation of G-CSF expression is mediated by miR-155 (Figure 5A, Supplementary table S1).
Gene_expression (expression) of Csf3 gene
18) Confidence 0.65 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2761263 Disease Relevance 0.07 Pain Relevance 0.08
The three groups are a.) mice not harbouring any transgene ("wt"), b.) mice harbouring only the BEG2 transgene (which do not express G-CSF), and c.) mice harbouring both the BEG2 transgene and the CaMKII-tTA driver, that do express G-CSF.
Neg (not) Gene_expression (express) of G-CSF
19) Confidence 0.64 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.44 Pain Relevance 0.19
Although we do not see significant effects on the number of contralateral motoneurons in the different transgenic crosses, there is an interesting trend (p = 0.1) towards more motoneurons contralaterally in the G-CSF overexpressors compared to littermates not transgenic for the CaMKII tta driver.
Gene_expression (overexpressors) of G-CSF in motoneurons associated with targeted disruption
20) Confidence 0.64 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2844381 Disease Relevance 0.89 Pain Relevance 0.03

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