The DOI matches its Crossref record; 67 of the 69 references it cites were found in a registry or an index.
The JNK Are Important for Development and Survival of Macrophages
Abstract
We report in this study that activation of the JNK by the growth factor, CSF-1 is critical for macrophage development, proliferation, and survival. Inhibition of JNK with two distinct classes of inhibitors, the pharmacological agent SP600125, or the peptide D-JNKI1 resulted in cell cycle inhibition with an arrest at the G2/M transition and subsequent apoptosis. JNK inhibition resulted in decreased expression of CSF-1R (c-fms) and Bcl-xL mRNA in mature macrophages and repressed CSF-1-dependent differentiation of bone marrow cells to macrophages. Macrophage sensitivity to JNK inhibitors may be linked to phosphorylation of the PU.1 transcription factor. Inhibition of JNK disrupted PU.1 binding to an element in the c-fms gene promoter and decreased promoter activity. Promoter activity could be restored by overexpression of PU.1. A comparison of expression profiles of macrophages with 22 other tissue types showed that genes that signal JNK activation downstream of tyrosine kinase receptors, such as focal adhesion kinase, Nck-interacting kinase, and Rac1 and scaffold proteins are highly expressed in macrophages relative to other tissues. This pattern of expression may underlie the novel role of JNK in macrophages.
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“The JNK inhibitor SP600125 reduces the number of macrophages developing from murine marrow cells cultured in the presence of M-CSF (Himes et al., 2006).”
BackgroundMajor pathways involved in macrophage polarization in cancer
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Metadata
- Authors
- Himes, S. R., Sester, D. P., Ravasi, T., Cronau, S. L., Sasmono, T., & Hume, D. A.
- Affiliations
- The University of Queensland (AU)
- Cooperative Research Centre for Chronic Inflammatory Disease, Institute for Molecular Biosciences, University of Queensland , Brisbane ,
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2006-02
- Volume
- 176
- Issue
- 4
- Pages
- 2219-2228
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1582648966
- Cited by
- 117
- References
- 69
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 4 · 2023: 3 · 2022: 5 · 2021: 4 · 2020: 7 · 2019: 10 · 2018: 1 · 2017: 5 · 2016: 6 · 2015: 6 · 2014: 11 · 2013: 9 · 2012: 5
- FWCI
- 3.24
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Keywords
- JNK, macrophage development, macrophage survival, CSF-1, CSF-1 receptor, c-fms, Bcl-xL, apoptosis, cell cycle arrest, G2/M cell cycle arrest, PU.1, transcriptional regulation, macrophage differentiation, bone marrow, JNK inhibitor, SP600125, tyrosine kinase signaling, focal adhesion kinase, Rac1, scaffold proteins
- MeSH terms
- Proto-Oncogene Protein Spi-1, Animals, Bone Marrow Cells, Cell Differentiation, Cell Survival, Cells, Cultured, DNA, Gene Expression Regulation, Macrophages, Phosphorylation, Promoter Regions, Genetic, Protein Binding, Proto-Oncogene Proteins, RNA, Messenger, Signal Transduction, Trans-Activators, Macrophage Colony-Stimulating Factor, Receptor, Macrophage Colony-Stimulating Factor, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, JNK Mitogen-Activated Protein Kinases, Mice
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