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.

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.

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

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)

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).

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).

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

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

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

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

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).

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)

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).

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).

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).

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).

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).

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).

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).

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).

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).

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).

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.

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).

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).

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).

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.

PMID: 10534106, 10354505, 6092475, 1401905, 2548952 LPS has been shown previously to cause rapid down-regulation of CSF-1 binding to murine macrophages

PMID: 10534106, 10354505, 6092475, 1401905, 2548952 LPS has been shown previously to cause rapid down-regulation of CSF-1 binding to murine macrophages

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

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

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PMID: 10534106 The biological importance of the specific internalization of the CSF-1R in response to CpG DNA and LPS is not known.

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.

PMID: 10534106 The biological importance of the specific internalization of the CSF-1R in response to CpG DNA and LPS is not known.

PMID: 10534106, 7799956 More recently the same group claimed that activation of Raf in LPS-stimulated cells was ras-independent

PMID: 10534106 CSF-1 can activate Raf-1 in a ras-independent manner.

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

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