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PMID: 10534106
To activate cells, CpG DNA probably needs to be internalized via the endosomes.
Although internalization of DNA appears to be essential for the biological response, the possibility that a co-stimulatory signal comes from a membrane receptor during the process of internalization should not be
discounted.</csml:comment>
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PMID: 10534106, 9245551, 10689778, 9464831
CpG DNA induces a range of cytokines in macrophages/
dendritic cells, including interleukin-12 (IL-12), tumor
necrosis factor a (TNF-a), IL-1b, and IL-6. </csml:comment>
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PMID: 10534106, 9245551, 10689778, 9464831
CpG DNA induces a range of cytokines in macrophages/
dendritic cells, including interleukin-12 (IL-12), tumor
necrosis factor a (TNF-a), IL-1b, and IL-6. </csml:comment>
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PMID: 10534106, 9245551, 10689778, 9464831
CpG DNA induces a range of cytokines in macrophages/
dendritic cells, including interleukin-12 (IL-12), tumor
necrosis factor a (TNF-a), IL-1b, and IL-6. </csml:comment>
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PMID: 10534106, 9245551, 10689778, 9464831
CpG DNA induces a range of cytokines in macrophages/
dendritic cells, including interleukin-12 (IL-12), tumor
necrosis factor a (TNF-a), IL-1b, and IL-6. </csml:comment>
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PMID: 10534106, 9568729, 8757335
In comparison to the response to LPS, CpG DNA was as effective
at increasing TNF-a mRNA in bone marrow-derived murine
macrophages, whereas it was a less effective inducer of IL-1b
and plasminogen activator inhibitor type-2 and did not, by
itself, lead to production of inducible nitric oxide synthase
(iNOS)</csml:comment>
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PMID: 10534106, 9245551, 8648098
In mixed spleen cell culture, CpG DNA-induced
macrophage IL-12 promotes interferon-g production by NK cells</csml:comment>
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PMID: 10534106, 9245551, 8648098
In mixed spleen cell culture, CpG DNA-induced
macrophage IL-12 promotes interferon-g production by NK cells</csml:comment>
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PMID: 10534106, 9568729, 8757335
In comparison to the response to LPS, CpG DNA was as effective
at increasing TNF-a mRNA in bone marrow-derived murine
macrophages, whereas it was a less effective inducer of IL-1b
and plasminogen activator inhibitor type-2 and did not, by
itself, lead to production of inducible nitric oxide synthase
(iNOS)
Interferon-g in turn primes murine macrophages to
respond to CpG DNA with expression of iNOS and nitric oxide
production as well as increasing a number of other responses,
creating a potential self-amplifying loop with NK cells</csml:comment>
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PMID: 10534106
Interferon-g in turn primes murine macrophages to
respond to CpG DNA with expression of iNOS and nitric oxide
production as well as increasing a number of other responses,
creating a potential self-amplifying loop with NK cells

PMID: 10534106, 1401905 
Baccarini et al reported an increase in serine phosphorylation
of the receptor in Bac1.2F5 cells treated with interferon-g
plus LPS.
</csml:comment>
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indirect</csml:comment>
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</csml:comment>
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<csml:comments>
<csml:comment type="text">



PMID: 10534106, 9568729, 8757335
In comparison to the response to LPS, CpG DNA was as effective
at increasing TNF-a mRNA in bone marrow-derived murine
macrophages, whereas it was a less effective inducer of IL-1b
and plasminogen activator inhibitor type-2 and did not, by
itself, lead to production of inducible nitric oxide synthase
(iNOS)
Interferon-g in turn primes murine macrophages to
respond to CpG DNA with expression of iNOS and nitric oxide
production as well as increasing a number of other responses,
creating a potential self-amplifying loop with NK cells</csml:comment>
</csml:comments>
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indirect</csml:comment>
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<csml:comments>
<csml:comment type="text">



PMID: 10534106, 9568729, 8757335
In comparison to the response to LPS, CpG DNA was as effective
at increasing TNF-a mRNA in bone marrow-derived murine
macrophages, whereas it was a less effective inducer of IL-1b
and plasminogen activator inhibitor type-2 and did not, by
itself, lead to production of inducible nitric oxide synthase
(iNOS)</csml:comment>
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</csml:comment>
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<csml:comments>
<csml:comment type="text">



PMID: 10534106, 10354505
LPS inhibits its own actions upstream of a
branching point in the signaling cascade for activation of
NF-kB and the MAP kinases (SAPK/JNK, p38, and ERK1/2).</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">



indirect</csml:comment>
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<csml:comments>
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</csml:comment>
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<csml:comment type="text">



PMID: 10534106, 9799232, 9568729
The latter (MAP kinases) are also activated by CpG DNA in myeloid cells</csml:comment>
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indirect</csml:comment>
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<csml:comments>
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</csml:comment>
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<csml:comments>
<csml:comment type="text">


PMID: 10534106, 9799232, 9568729
The latter (MAP kinases) are also activated by CpG DNA in myeloid cells</csml:comment>
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indirect</csml:comment>
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</csml:comment>
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<csml:comments>
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PMID: 10534106, 10334979
In the case of LPS signaling, it is now appreciated that such
upstream activators include members of the IL-1 receptor
signaling pathway, such as MyD88, IL-1 receptor-associated
kinases (IRAK) and TRAF 6

PMID: 10534106, 10354505
LPS inhibits its own actions upstream of a
branching point in the signaling cascade for activation of
NF-kB and the MAP kinases (SAPK/JNK, p38, and ERK1/2).</csml:comment>
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<csml:comments>
<csml:comment type="text">



indirect</csml:comment>
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<csml:comment type="text">



PMID: 10534106, 10334979
In the case of LPS signaling, it is now appreciated that such
upstream activators include members of the IL-1 receptor
signaling pathway, such as MyD88, IL-1 receptor-associated
kinases (IRAK) and TRAF 6

PMID: 10534106, 10354505
LPS inhibits its own actions upstream of a
branching point in the signaling cascade for activation of
NF-kB and the MAP kinases (SAPK/JNK, p38, and ERK1/2).</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">



indirect</csml:comment>
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</csml:comment>
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<csml:comments>
<csml:comment type="text">



PMID: 10534106, 10334979
In the case of LPS signaling, it is now appreciated that such
upstream activators include members of the IL-1 receptor
signaling pathway, such as MyD88, IL-1 receptor-associated
kinases (IRAK) and TRAF 6

PMID: 10534106, 10354505
LPS inhibits its own actions upstream of a
branching point in the signaling cascade for activation of
NF-kB and the MAP kinases (SAPK/JNK, p38, and ERK1/2).</csml:comment>
</csml:comments>
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indirect</csml:comment>
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</csml:comment>
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<csml:comments>
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PMID: 10534106, 10334979
In the case of LPS signaling, it is now appreciated that such
upstream activators include members of the IL-1 receptor
signaling pathway, such as MyD88, IL-1 receptor-associated
kinases (IRAK) and TRAF 6

PMID: 10534106, 10354505
LPS inhibits its own actions upstream of a
branching point in the signaling cascade for activation of
NF-kB and the MAP kinases (SAPK/JNK, p38, and ERK1/2).</csml:comment>
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indirect</csml:comment>
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<csml:comment type="text">



PMID: 10534106, 10334979
In the case of LPS signaling, it is now appreciated that such
upstream activators include members of the IL-1 receptor
signaling pathway, such as MyD88, IL-1 receptor-associated
kinases (IRAK) and TRAF 6

PMID: 10534106, 10354505
LPS inhibits its own actions upstream of a
branching point in the signaling cascade for activation of
NF-kB and the MAP kinases (SAPK/JNK, p38, and ERK1/2).</csml:comment>
</csml:comments>
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<csml:comment type="text">



indirect</csml:comment>
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</csml:comment>
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<csml:comment type="text">



PMID: 10534106, 10334979
In the case of LPS signaling, it is now appreciated that such
upstream activators include members of the IL-1 receptor
signaling pathway, such as MyD88, IL-1 receptor-associated
kinases (IRAK) and TRAF 6

PMID: 10534106, 10354505
LPS inhibits its own actions upstream of a
branching point in the signaling cascade for activation of
NF-kB and the MAP kinases (SAPK/JNK, p38, and ERK1/2).</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">


</csml:comment>
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PMID: 10534106, 10334979
In the case of LPS signaling, it is now appreciated that such
upstream activators include members of the IL-1 receptor
signaling pathway, such as MyD88, IL-1 receptor-associated
kinases (IRAK) and TRAF 6

PMID: 10534106, 10354505
LPS inhibits its own actions upstream of a
branching point in the signaling cascade for activation of
NF-kB and the MAP kinases (SAPK/JNK, p38, and ERK1/2).</csml:comment>
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indirect</csml:comment>
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PMID: 10534106, 10334979
In the case of LPS signaling, it is now appreciated that such
upstream activators include members of the IL-1 receptor
signaling pathway, such as MyD88, IL-1 receptor-associated
kinases (IRAK) and TRAF 6

PMID: 10534106, 10354505
LPS inhibits its own actions upstream of a
branching point in the signaling cascade for activation of
NF-kB and the MAP kinases (SAPK/JNK, p38, and ERK1/2).</csml:comment>
</csml:comments>
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indirect</csml:comment>
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PMID: 10534106, 10334979
In the case of LPS signaling, it is now appreciated that such
upstream activators include members of the IL-1 receptor
signaling pathway, such as MyD88, IL-1 receptor-associated
kinases (IRAK) and TRAF 6

PMID: 10534106, 10354505
LPS inhibits its own actions upstream of a
branching point in the signaling cascade for activation of
NF-kB and the MAP kinases (SAPK/JNK, p38, and ERK1/2).</csml:comment>
</csml:comments>
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<csml:comment type="text">



indirect</csml:comment>
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PMID: 10534106, 10334979
In the case of LPS signaling, it is now appreciated that such
upstream activators include members of the IL-1 receptor
signaling pathway, such as MyD88, IL-1 receptor-associated
kinases (IRAK) and TRAF 6

PMID: 10534106, 10354505
LPS inhibits its own actions upstream of a
branching point in the signaling cascade for activation of
NF-kB and the MAP kinases (SAPK/JNK, p38, and ERK1/2).


</csml:comment>
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indirect</csml:comment>
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</csml:comment>
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PMID: 10534106, 10334979
In the case of LPS signaling, it is now appreciated that such
upstream activators include members of the IL-1 receptor
signaling pathway, such as MyD88, IL-1 receptor-associated
kinases (IRAK) and TRAF 6

PMID: 10534106, 10354505
LPS inhibits its own actions upstream of a
branching point in the signaling cascade for activation of
NF-kB and the MAP kinases (SAPK/JNK, p38, and ERK1/2).</csml:comment>
</csml:comments>
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indirect</csml:comment>
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PMID: 10534106, 10334979
In the case of LPS signaling, it is now appreciated that such
upstream activators include members of the IL-1 receptor
signaling pathway, such as MyD88, IL-1 receptor-associated
kinases (IRAK) and TRAF 6

PMID: 10534106, 10354505
LPS inhibits its own actions upstream of a
branching point in the signaling cascade for activation of
NF-kB and the MAP kinases (SAPK/JNK, p38, and ERK1/2).</csml:comment>
</csml:comments>
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<csml:comment type="text">



indirect</csml:comment>
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<csml:comment type="text">



PMID: 10534106, 10334979
In the case of LPS signaling, it is now appreciated that such
upstream activators include members of the IL-1 receptor
signaling pathway, such as MyD88, IL-1 receptor-associated
kinases (IRAK) and TRAF 6

PMID: 10534106, 10354505
LPS inhibits its own actions upstream of a
branching point in the signaling cascade for activation of
NF-kB and the MAP kinases (SAPK/JNK, p38, and ERK1/2).</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">



indirect</csml:comment>
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PMID: 10534106, 10334979
In the case of LPS signaling, it is now appreciated that such
upstream activators include members of the IL-1 receptor
signaling pathway, such as MyD88, IL-1 receptor-associated
kinases (IRAK) and TRAF 6

PMID: 10534106, 10354505
LPS inhibits its own actions upstream of a
branching point in the signaling cascade for activation of
NF-kB and the MAP kinases (SAPK/JNK, p38, and ERK1/2).</csml:comment>
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indirect</csml:comment>
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PMID: 10534106, 10334979
In the case of LPS signaling, it is now appreciated that such
upstream activators include members of the IL-1 receptor
signaling pathway, such as MyD88, IL-1 receptor-associated
kinases (IRAK) and TRAF 6

PMID: 10534106, 10354505
LPS inhibits its own actions upstream of a
branching point in the signaling cascade for activation of
NF-kB and the MAP kinases (SAPK/JNK, p38, and ERK1/2).</csml:comment>
</csml:comments>
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</csml:comment>
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<csml:comments>
<csml:comment type="text">


PMID: 10534106, 9710599
We have demonstrated the constitutive activation of
this pathway in response to CSF-1, and its role in phosphorylation
of the transcription factor Ets2

PMID: 10534106
CSF-1 can activate Raf-1 in a ras-independent
manner.</csml:comment>
</csml:comments>
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</csml:comment>
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<csml:comments>
<csml:comment type="text">

</csml:comment>
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<csml:comments>
<csml:comment type="text">



PMID: 10534106, 10354505, 6092475, 1401905, 2548952
LPS has been shown previously to cause rapid down-regulation
of CSF-1 binding to murine macrophages </csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">


indirect</csml:comment>
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<csml:comments>
<csml:comment type="text">


</csml:comment>
</csml:comments>
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<csml:processSimulationProperty>
<csml:priority value="0"/>
<csml:firing firingStyle="csml-firingStyle:and" firingOnce="false" type="csml-variable:Boolean" value="true"/>
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<csml:viewProperty>
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<csml:comments>
<csml:comment type="text">


PMID: 10534106, 10354505, 6092475, 1401905, 2548952
LPS has been shown previously to cause rapid down-regulation
of CSF-1 binding to murine macrophages </csml:comment>
</csml:comments>
</csml:process>
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<csml:comments>
<csml:comment type="text">

</csml:comment>
</csml:comments>
</csml:connector>
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<csml:comments>
<csml:comment type="text">

</csml:comment>
</csml:comments>
</csml:connector>
<csml:processSimulationProperty>
<csml:priority value="0"/>
<csml:firing firingStyle="csml-firingStyle:and" firingOnce="false" type="csml-variable:Boolean" value="true"/>
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<csml:processKinetic calcStyle="csml-calcStyle:speed" kineticStyle="csml-kineticStyle:mass" fast="false">
<csml:parameter key="coefficient1" value="0.1"/>
<csml:parameter key="coefficient2" value="1.0"/>
</csml:processKinetic>
</csml:processSimulationProperty>
<csml:viewProperty>
<csml:position positionID="default" position="auto" x="412.0" y="788.0"/>
<csml:shape shapeID="default" visible="true">
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<csml:toolSpecificGraphics xmlns="http://www.csml.org/csml/cigraphics"/>
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<csml:comments>
<csml:comment type="text">


PMID: 10534106
Both LPS and bacterial DNA or
CpG oligonucleotides cause rapid down-modulation of the
CSF-1R from the cell surface.

PMID: 10534106, 8497248
Indeed, down-modulation of the
receptor from the cell surface is followed, at least in the case of
LPS, by specific repression of c-fms (CSF-1R) mRNA transcription and RAW264 macrophage cells treated with LPS or
CpG DNA for a prolonged period deplete both their cell surface and intracellular Golgi-associated pool of CSF-1R</csml:comment>
</csml:comments>
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<csml:connectorKinetic>
<csml:parameter key="stoichiometry" value="1"/>
</csml:connectorKinetic>
</csml:connectorSimulationProperty>
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</csml:shape>
</csml:viewProperty>
<csml:comments>
<csml:comment type="text">


indirect</csml:comment>
</csml:comments>
</csml:connector>
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<csml:connectorSimulationProperty>
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<csml:comments>
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</csml:comment>
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<csml:comments>
<csml:comment type="text">


PMID: 10534106
Both LPS and bacterial DNA or
CpG oligonucleotides cause rapid down-modulation of the
CSF-1R from the cell surface.</csml:comment>
</csml:comments>
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</csml:comment>
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<csml:comments>
<csml:comment type="text">


indirect</csml:comment>
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</csml:comment>
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</csml:processKinetic>
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<csml:comments>
<csml:comment type="text">


PMID: 10534106
The biological importance of the specific internalization of
the CSF-1R in response to CpG DNA and LPS is not known.</csml:comment>
</csml:comments>
</csml:process>
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<csml:comments>
<csml:comment type="text">


indirect</csml:comment>
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<csml:comments>
<csml:comment type="text">

</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">

</csml:comment>
</csml:comments>
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</csml:processSimulationProperty>
<csml:viewProperty>
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<csml:comments>
<csml:comment type="text">


PMID: 10534106
The biological importance of the specific internalization of
the CSF-1R in response to CpG DNA and LPS is not known.</csml:comment>
</csml:comments>
</csml:process>
<csml:process id="p41" name="p41" type="cso30:c:ProcessBiological">
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indirect</csml:comment>
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</csml:comment>
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<csml:comments>
<csml:comment type="text">


PMID: 10534106, 7799956
More recently the same group claimed that activation
of Raf in LPS-stimulated cells was ras-independent</csml:comment>
</csml:comments>
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</csml:comment>
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indirect</csml:comment>
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</csml:comment>
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<csml:comments>
<csml:comment type="text">


PMID: 10534106
CSF-1 can activate Raf-1 in a ras-independent
manner.</csml:comment>
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indirect</csml:comment>
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<csml:comment type="text">


PMID: 10534106, 9710599
We have demonstrated the constitutive activation of
this pathway in response to CSF-1, and its role in phosphorylation
of the transcription factor Ets2</csml:comment>
</csml:comments>
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indirect</csml:comment>
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<csml:comment type="text">

PMID: 10534106, 9710599
We have demonstrated the constitutive activation of
this pathway in response to CSF-1, and its role in phosphorylation
of the transcription factor Ets2</csml:comment>
</csml:comments>
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indirect</csml:comment>
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<csml:comments>
<csml:comment type="text">


PMID: 10534106
Both LPS and bacterial DNA or
CpG oligonucleotides cause rapid down-modulation of the
CSF-1R from the cell surface.

PMID: 10534106, 8497248
Indeed, down-modulation of the
receptor from the cell surface is followed, at least in the case of
LPS, by specific repression of c-fms (CSF-1R) mRNA transcription and RAW264 macrophage cells treated with LPS or
CpG DNA for a prolonged period deplete both their cell surface and intracellular Golgi-associated pool of CSF-1R</csml:comment>
</csml:comments>
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<csml:comments>
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</csml:comment>
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indirect</csml:comment>
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indirect</csml:comment>
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<csml:comments>
<csml:comment type="text">

</csml:comment>
</csml:comments>
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<csml:priority value="0"/>
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<csml:comments>
<csml:comment type="text">


PMID: 10534106, 1401905 
Baccarini et al reported an increase in serine phosphorylation
of the receptor in Bac1.2F5 cells treated with interferon-g
plus LPS.</csml:comment>
</csml:comments>
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</csml:comment>
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indirect</csml:comment>
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<csml:comments>
<csml:comment type="text">


PMID: 10534106, 9799232, 9568729
The latter (MAP kinases) are also activated by CpG DNA in myeloid cells

PMID: 10534106, 10586047
More recently, we
confirmed that CpG DNA can mimic the ability of CSF-1 to
activate phosphorylation of the MAP kinases ERK-1 and
ERK-2 in macrophages</csml:comment>
</csml:comments>
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indirect</csml:comment>
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<csml:comment type="text">


PMID: 10534106, 9799232, 9568729
The latter (MAP kinases) are also activated by CpG DNA in myeloid cells

PMID: 10534106, 10586047
More recently, we
confirmed that CpG DNA can mimic the ability of CSF-1 to
activate phosphorylation of the MAP kinases ERK-1 and
ERK-2 in macrophages</csml:comment>
</csml:comments>
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<csml:comments>
<csml:comment type="text">


indirect</csml:comment>
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<csml:processKinetic calcStyle="csml-calcStyle:speed" kineticStyle="csml-kineticStyle:mass" fast="false">
<csml:parameter key="coefficient1" value="0.1"/>
<csml:parameter key="coefficient2" value="1.0"/>
</csml:processKinetic>
</csml:processSimulationProperty>
<csml:viewProperty>
<csml:position positionID="default" position="auto" x="355.0" y="1219.0"/>
<csml:shape shapeID="default" visible="true">
<csml:image width="25.0" height="25.0" filePath="" fileType="resourceFile" fileFormat="svg" resourceID="10003" outlineColor="0 0 0 0"></csml:image>
<csml:toolSpecificGraphics xmlns="http://www.csml.org/csml/cigraphics"/>
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<csml:biologicalProperty refBiologicalEventID="cso30:i:ME_UnknownActivation" refCellComponentID="cso30:i:CC_Cytosol">
<csml:property key="edgeScore" value="1.0"/>
<csml:property key="relationType" value="Type 0"/>
</csml:biologicalProperty>
<csml:comments>
<csml:comment type="text">


PMID:10534106
One possibility is that after internalization the receptor provides
a CSF-1-independent signal to the ras-raf-MAP kinase
pathway.</csml:comment>
</csml:comments>
</csml:process>
<csml:process id="p50" name="p49" type="cso30:c:ProcessBiological">
<csml:connector id="c156" name="c156" refID="e31" type="cso30:c:InputAssociation">
<csml:connectorSimulationProperty>
<csml:connectorFiring connectorFiringStyle="csml-connectorFiringStyle:threshold" value="0"/>
<csml:connectorKinetic>
<csml:parameter key="stoichiometry" value="1"/>
</csml:connectorKinetic>
</csml:connectorSimulationProperty>
<csml:viewProperty>
<csml:position positionID="default" position="auto" x="434.0" y="1188.0"/>
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<csml:comments>
<csml:comment type="text">

</csml:comment>
</csml:comments>
</csml:connector>
<csml:connector id="c157" name="c157" refID="MO000000009" type="cso30:c:InputProcess">
<csml:connectorSimulationProperty>
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<csml:connectorKinetic>
<csml:parameter key="stoichiometry" value="1"/>
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</csml:connectorSimulationProperty>
<csml:viewProperty>
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<csml:shape shapeID="default" visible="true">
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</csml:viewProperty>
<csml:comments>
<csml:comment type="text">

</csml:comment>
</csml:comments>
</csml:connector>
<csml:connector id="c158" name="c158" refID="e27" type="cso30:c:OutputProcess">
<csml:connectorSimulationProperty>
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<csml:comments>
<csml:comment type="text">

</csml:comment>
</csml:comments>
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<csml:firing firingStyle="csml-firingStyle:and" firingOnce="false" type="csml-variable:Boolean" value="true"/>
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</csml:biologicalProperty>
<csml:comments>
<csml:comment type="text">


PMID:10534106
One possibility is that after internalization the receptor provides
a CSF-1-independent signal to the ras-raf-MAP kinase
pathway.</csml:comment>
</csml:comments>
</csml:process>
<csml:process id="p51" name="p49" type="cso30:c:ProcessBiological">
<csml:connector id="c159" name="c159" refID="e27" type="cso30:c:InputAssociation">
<csml:connectorSimulationProperty>
<csml:connectorFiring connectorFiringStyle="csml-connectorFiringStyle:threshold" value="0"/>
<csml:connectorKinetic>
<csml:parameter key="stoichiometry" value="1"/>
</csml:connectorKinetic>
</csml:connectorSimulationProperty>
<csml:viewProperty>
<csml:position positionID="default" position="auto" x="685.0" y="1260.0"/>
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<csml:toolSpecificGraphics xmlns="http://www.csml.org/csml/cigraphics">
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<csml:comments>
<csml:comment type="text">


indirect</csml:comment>
</csml:comments>
</csml:connector>
<csml:connector id="c160" name="c160" refID="MO000000077" type="cso30:c:InputProcess">
<csml:connectorSimulationProperty>
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<csml:connectorKinetic>
<csml:parameter key="stoichiometry" value="1"/>
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<csml:viewProperty>
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<csml:comments>
<csml:comment type="text">

</csml:comment>
</csml:comments>
</csml:connector>
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<csml:connectorSimulationProperty>
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<csml:connectorKinetic>
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<csml:comments>
<csml:comment type="text">

</csml:comment>
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<csml:comments>
<csml:comment type="text">


PMID:10534106
One possibility is that after internalization the receptor provides
a CSF-1-independent signal to the ras-raf-MAP kinase
pathway.</csml:comment>
</csml:comments>
</csml:process>
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