ArticleMolecular and cellular biology1995
Ras-dependent and -independent pathways target the mitogen-activated protein kinase network in macrophages.
Article in Molecular and cellular biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 179 citations in OpenAlex.
- The use of moderate hypothermia during cardiac surgery is associated with repression of tumour necrosis factor-alpha via inhibition of activating protein-1: an experimental study.Critical care (London, England) · 2006Trial
- Review
- MEK2 Negatively Regulates Lipopolysaccharide-Mediated IL-1β Production through HIF-1α Expression.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Method for Studying the Effect of Gene Silencing on Bacterial Infection-induced ERK1/2 Signaling in Bone-marrow Derived Macrophages.Bio-protocol · 2018Article
- Arp2/3 Complex Is Required for Macrophage Integrin Functions but Is Dispensable for FcR Phagocytosis and In Vivo Motility.Developmental cell · 2017Article
- Role of MEK1 in TLR4 Mediated Signaling.Journal of cell signaling · 2017Article
- Neurofibromin is a novel regulator of Ras-induced reactive oxygen species production in mice and humans.Free radical biology & medicine · 2016Article
- Innate immune regulation by STAT-mediated transcriptional mechanisms.Immunological reviews · 2014Review
- Caveosomal oxidative stress causes Src-p21ras activation and lysine 63 TRAF6 protein polyubiquitination in iron-induced M1 hepatic macrophage activation.The Journal of biological chemistry · 2012Article
- The role of atypical protein kinase C in CSF-1-dependent Erk activation and proliferation in myeloid progenitors and macrophages.PloS one · 2011Article
- Consequences and utility of the zinc-dependent metalloprotease activity of anthrax lethal toxin.Toxins · 2010Review
- TNFR1 promotes tumor necrosis factor-mediated mouse colon epithelial cell survival through RAF activation of NF-kappaB.The Journal of biological chemistry · 2008Article
- Pathway crosstalk between Ras/Raf and PI3K in promotion of M-CSF-induced MEK/ERK-mediated osteoclast survival.Journal of cellular biochemistry · 2008Article
- Signalling mechanisms underlying subversion of the immune response by the filarial nematode secreted product ES-62.Immunology · 2005Review
- Activation of protein kinase A (PKA) by 8-Cl-cAMP as a novel approach for antileukaemic therapy.British journal of cancer · 2004Article
- Imbalanced gp130-dependent signaling in macrophages alters macrophage colony-stimulating factor responsiveness via regulation of c-fms expression.Molecular and cellular biology · 2004Article
- Differential regulation of the mitogen-activated protein kinases by pathogenic and nonpathogenic mycobacteria.Infection and immunity · 2002Article
- Opposite effects of different doses of MCSF on ERK phosphorylation and cell proliferation in macrophages.Oncogene · 2002Article
- Protective role of Raf-1 in Salmonella-induced macrophage apoptosis.The Journal of experimental medicine · 2001Article
- Growth factor-independent proliferation of erythroid cells infected with Friend spleen focus-forming virus is protein kinase C dependent but does not require Ras-GTP.Journal of virology · 2000Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitogen-activated protein kinases (MAPKs) are activated upon a variety of extracellular stimuli in different cells. In macrophages, colony-stimulating factor 1 (CSF-1) stimulates proliferation, while bacterial lipopolysaccharide (LPS) inhibits cell growth and causes differentiation and activation. Both CSF-1 and LPS rapidly activate the MAPK network and induce the phosphorylation of two distinct ternary complex factors (TCFs), TCF/Elk and TCF/SAP. CSF-1, but not LPS, stimulated the formation of p21ras. GTP complexes. Expression of a dominant negative ras mutant reduced, but did not abolish, CSF-1-mediated stimulation of MEK and MAPK. In contrast, activation of the MEK kinase Raf-1 was Ras independent. Treatment with the phosphatidylcholine-specific phospholipase C inhibitor D609 suppressed LPS-mediated, but not CSF-1-mediated, activation of Raf-1, MEK, and MAPK. Similarly, down-regulation or inhibition of protein kinase C blocked MEK and MAPK induction by LPS but not that by CSF-1. Phorbol 12-myristate 13-acetate pretreatment led to the sustained activation of the Raf-1 kinase but not that of MEK and MAPK. Thus, activated Raf-1 alone does not support MEK/MAPK activation in macrophages. Phosphorylation of TCF/Elk but not that of TCF/SAP was blocked by all treatments that interfered with MAPK activation, implying that TCF/SAP was targeted by a MAPK-independent pathway. Therefore, CSF-1 and LPS target the MAPK network by two alternative pathways, both of which induce Raf-1 activation. The mitogenic pathway depends on Ras activity, while the differentiation signal relies on protein kinase C and phosphatidylcholine-specific phospholipase C activation.
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