CSF-1 signal transduction
Abstract
Colony-stimulating factor-1 (CSF-1) or macrophage-CSF (M-CSF) is a growth factor involved in the proliferation, differentiation, and activation of cells of the monocyte/macrophage lineage. Its receptor is the homodimeric, tyrosine kinase product of the c-fms proto-oncogene, which contains a so-called kinase insert domain. This review focuses mainly on recent studies of signal transduction events that are initiated on interaction of CSF-1 and its receptor. A summary is given of the tyrosine autophosphorylation sites on c-Fms identified to date, including their interaction with various substrates and their possible significance for signal transduction and cellular function. In addition, the signal transduction pathways that have been identified to lie downstream of activated c-Fms are reviewed. Although it is apparent that there have been many recent significant developments in our understanding of CSF-1 signaling, a number of examples are mentioned of significant discrepancies in the literature, some possible reasons for which can sometimes be offered. It is also apparent that any particular biochemical response or signal transduction pathway, even though widespread in other ligand receptor/cellular systems, including those with similar receptor structures to c-Fms, may not be relevant to CSF-1 signaling. The relevance of any potentially important molecular signaling pathway activated by CSF-1 in cells in vitro will ultimately have to be related to the functions of monocytes/m…
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The inflammatory phenotype observed in HDLS has been reported in other studies investigating consequences of loss of CSF-1 signaling.
“In addition, the inflammatory phenotype we observe in HDLS has been reported in other studies investigating consequences of loss of CSF-1 signaling [16, 43].”
From Loss of homeostatic microglial phenotype in CSF1R-related Leukoencephalopathy (2020) · cites this paper as [16]
CSF-2 promotes migration of blood-borne monocytes across the blood-brain barrier, which then differentiate into macrophages in the presence of CSF-1 and CSF-2.
“CSF-2 promotes migration of blood-borne monocytes across the blood-brain barrier, which then differentiate into macrophages in the presence of CSF-1 and CSF-2 [16, 17, 26, 52].”
From Loss of homeostatic microglial phenotype in CSF1R-related Leukoencephalopathy (2020) · cites this paper as [16]
Cited by
Sorted by citations
Dai, X.-M., Ryan, G. R., Hapel, A. J., Dominguez, M. G., Russell, R. G., Kapp, S., Sylvestre, V., & Stanley, E. R. (2002) · Blood · doi:10.1182/blood.v99.1.111 · Cited by 1,184 · see citing works
Estrogens and androgens in skeletal physiology and pathophysiology
Almeida, M., Laurent, M. R., Dubois, V., Claessens, F., O'Brien, C. A., Bouillon, R., Vanderschueren, D., & Manolagas, S. C. (2017) · Physiological Reviews · doi:10.1152/physrev.00033.2015 · Cited by 860 · see citing works
CSF-1 regulation of the wandering macrophage: complexity in action
Pixley, F. J., & Stanley, E. R. (2004) · Trends in Cell Biology · doi:10.1016/j.tcb.2004.09.016 · Cited by 807 · see citing works
Rademakers, R., Baker, M., Nicholson, A. M., Rutherford, N. J., Finch, N., Soto-Ortolaza, A., Lash, J., Wider, C., Wojtas, A., DeJesus-Hernandez, M., et al. (2012) · Nature Genetics · doi:10.1038/ng.1027 · Cited by 571 · see citing works
Lue, L.-F., Walker, D. G., Brachova, L., Beach, T. G., Rogers, J., Schmidt, A. M., Stern, D. M., & Yan, S. D. (2001) · Experimental Neurology · doi:10.1006/exnr.2001.7732 · Cited by 439 · see citing works
Otero, K., Turnbull, I. R., Poliani, P. L., Vermi, W., Cerutti, E., Aoshi, T., Tassi, I., Takai, T., Stanley, S. L., Miller, M., et al. (2009) · Nature Immunology · doi:10.1038/ni.1744 · Cited by 315 · see citing works
Luo, J., Elwood, F., Britschgi, M., Villeda, S., Zhang, H., Ding, Z., Zhu, L., Alabsi, H., Getachew, R., Narasimhan, R., et al. (2013) · Journal of Experimental Medicine · doi:10.1084/jem.20120412 · Cited by 262 · see citing works
Colony stimulating factors and myeloid cell biology in health and disease
Hamilton, J. A., & Achuthan, A. (2013) · Trends in Immunology · doi:10.1016/j.it.2012.08.006 · Cited by 285 · see citing works
Self-citationLoss of homeostatic microglial phenotype in CSF1R-related Leukoencephalopathy
Kempthorne, L., Yoon, H., Madore, C., Smith, S., Wszolek, Z. K., Rademakers, R., Kim, J., Butovsky, O., & Dickson, D. W. (2020) · Acta Neuropathologica Communications · doi:10.1186/s40478-020-00947-0 · Cited by 77 · see citing works
“Thus, it might be interesting to further investigate whether alteration in CSF-2 or IL-34 mediated pathways account for, or compensate, the phenotypic changes in brain regions less vulnerable to pathology in HDLS.”
BackgroundInfluentialGiricz, O., Mo, Y., Dahlman, K. B., Cotto-Rios, X. M., Vardabasso, C., Nguyen, H., Matusow, B., Bartenstein, M., Polishchuk, V., Johnson, D. B., et al. (2018) · JCI Insight · doi:10.1172/jci.insight.120422 · Cited by 40 · see citing works
- Authors
- Hamilton, J. A.
- Affiliations
- The Royal Melbourne Hospital (AU)
- Corresponding author
- Hamilton, John A
- ORCID
- Hamilton, John A
- Venue
- Journal of Leukocyte Biology
- Publisher
- Oxford University Press (OUP)
- Published
- 1997-08-01
- Volume
- 62
- Issue
- 2
- Pages
- 145-155
- ISSN
- 0741-5400 (ISSN-L)
- 1938-3673
- OpenAlex
- W2115790755
- Cited by
- 206
- References
- 0
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 6 · 2023: 4 · 2022: 6 · 2021: 2 · 2020: 3 · 2019: 5 · 2018: 2 · 2017: 8 · 2016: 4 · 2015: 6 · 2014: 12 · 2013: 13 · 2012: 12
- FWCI
- 3.92
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Leukocyte Biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Keywords
- colony-stimulating factor 1, macrophage colony-stimulating factor, c-fms, signal transduction, receptor tyrosine kinase, monocyte/macrophage lineage, downstream signaling pathways
- MeSH terms
- Src Homology 2 Domain-Containing, Transforming Protein 1, Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases, Proto-Oncogene Mas, Cyclic AMP, Animals, DNA-Binding Proteins, Endocytosis, Phospholipases, Phosphoric Monoester Hydrolases, Phosphorylation, Protein Kinase C, Protein-Tyrosine Kinases, Proteins, Proto-Oncogene Proteins, Signal Transduction, Trans-Activators, Macrophage Colony-Stimulating Factor, Receptor, Macrophage Colony-Stimulating Factor, Proto-Oncogene Proteins p21(ras), Protein Tyrosine Phosphatases, Protein Serine-Threonine Kinases, Phosphotransferases (Alcohol Group Acceptor), Calcium-Calmodulin-Dependent Protein Kinases, Sodium-Hydrogen Exchangers, Cell Cycle Proteins, Phosphotyrosine, GTP-Binding Proteins, Dimerization, Phosphatidylinositol 3-Kinases, Ribosomal Protein S6 Kinases, Adaptor Proteins, Vesicular Transport, Ubiquitin-Protein Ligases, Intracellular Signaling Peptides and Proteins, Adaptor Proteins, Signal Transducing, Proto-Oncogene Proteins c-cbl, STAT1 Transcription Factor, Mice, GRB2 Adaptor Protein, Proto-Oncogene Proteins c-vav, Janus Kinase 1, Protein Tyrosine Phosphatase, Non-Receptor Type 6, Shc Signaling Adaptor Proteins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
