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CSF1R  -  colony stimulating factor 1 receptor

Homo sapiens

 
 
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Disease relevance of CSF1R

 

Psychiatry related information on CSF1R

  • However, participation in physical activity (PA) benefits people with FMS [5].
  • There was a significant difference between FMS patients and healthy controls on the measures of depression, difficulty in identifying feelings subscale of TAS (TAS-dif), and total alexithymia scores [6].
  • RESULTS: FMS participants reported lower levels of positive affect (p < .01) and extraversion (p < .01) than OA participants [7].
  • CONCLUSIONS: These findings suggest that self-efficacy may play a critical role in both the present and long-term PA of women with FMS [5].
  • Chronic episodic disorders, such as depressive disorders, IBS, migraine, and FMS, have important commonalities, including cormorbidities, an absence of classic anatomic pathology in the tissues, a lack of objective findings on physical examination, and a lack of abnormal findings by routine laboratory and radiologic tests [8].
 

High impact information on CSF1R

  • This was corroborated by multipoint analysis, indicating a close proximity to CSF1R as the most likely location of SM1 [9].
  • DTD maps to distal chromosome 5q and, based on linkage disequilibrium studies in the Finnish population, we had previously predicted that the DTD gene should lie about 64 kb away from the CSF1R locus [10].
  • The as yet unidentified c-fms promoter/enhancer sequences may be confined to the nucleotides separating the two genes or could potentially lie within the PDGF receptor gene itself [11].
  • A 5' untranslated exon of the human CSF-1 receptor gene (c-fms) is separated by a 26 kb intron from the 32 kb receptor coding sequences [11].
  • A point mutation in the extracellular domain of the human CSF-1 receptor (c-fms proto-oncogene product) activates its transforming potential [12].
 

Chemical compound and disease context of CSF1R

 

Biological context of CSF1R

  • We have found, using restriction fragment length polymorphism analysis and gene dosage experiments, that all 10 patients showed deletion of CSF1R; 6 of 10 were hemizygous and 4 of 10 homozygous for CSF1R loss [1].
  • We tested five tetranucleotide microsatellite markers (UT5085, L17686, D9S753, ACTBP2, and CSF1R) in the tumor specimens and paired surgical margins of the patients whose margins were negative on pathological examination [18].
  • Thus, although both chimeric genes have similar effects in transactivation of the CSF1R promoter, they affect cell growth as tumor promoters differently in vivo [19].
  • A 1-Mb YAC contig encompassing the CSF1R gene has been used to screen a fetal brain cDNA library, and this has resulted in the identification of two genes comprising one known gene previously localized to the region (ADRB2) and one known gene previously unlocalized [20].
  • Sixty-two pedigrees from Finland gave a lod score of 1.36 at the CSF1R locus approximately 14 cM distal to IL9/D5S393, where positive results from three pedigree collections converged at the 1997 workshop [21].
 

Anatomical context of CSF1R

  • The expression of two upregulated genes, HOXA4 and CSF1R, was significantly higher in patients with a white blood cell count higher than 30 x 10(9)/L cells [22].
  • These results demonstrate that leukemic myeloblasts from a subset of patients with AML express transcripts for both the CSF-1 and CSF-1 receptor genes, often in the same leukemic cells in vitro [3].
  • Expression vectors containing either normal or oncogenic point-mutated human c-fms genes were transfected into interleukin 3 (IL-3)-dependent 32D cells in order to determine the effects of CSF-1 signaling in this murine clonal myeloid progenitor cell line [23].
  • Tumor necrosis factor-alpha (TNF-alpha) stimulated the terminal differentiation of the DC by downregulating the expression of the M-CSF receptor, cfms mRNA, and aborting the potential to convert to macrophages [24].
  • NIH 3T3 cells cotransfected with the human c-fms proto-oncogene together with a 1.6-kilobase cDNA clone encoding a 256-amino-acid precursor of the human mononuclear phagocyte colony-stimulating factor CSF-1 (M-CSF) undergo transformation by an autocrine mechanism [25].
 

Associations of CSF1R with chemical compounds

  • The human CSF1 receptor (CSF1R) is a 150-kDa transmembrane glycoprotein whose cytoplasmic tyrosine kinase domain is split by a kinase insert (KI) region of approximately 70 amino acids [26].
  • The common region of loss in these three 5q- syndrome patients includes the macrophage colony-stimulating factor-1 receptor (CSF1R), secreted protein, acidic, cysteine-rich (SPARC), and glutamate receptor (GR1A1) genes [27].
  • TGF-beta 1 did not affect kinase activity, cellular phosphotyrosine response, or internalization of FMS [28].
  • Accelerated turnover of the human CSF-1 receptor was observed in response to CSF-1 and phorbol esters, but not after stimulation with IL-3 or bacterial lipopolysaccharide [29].
  • FMS receptor for M-CSF (CSF-1) is sensitive to the kinase inhibitor imatinib and mutation of Asp-802 to Val confers resistance [30].
 

Physical interactions of CSF1R

 

Enzymatic interactions of CSF1R

  • FMS overexpression also progressively increased the relative amount of dephosphorylated RB protein induced, while reducing the total amount of RB protein [33].
  • Although c-fms and several other proteins were shown to be phosphorylated in response to M-CSF, the functional consequences of this phosphorylation remain unclear [34].
  • CSF-1-treated cells expressing the CSF1R/IRDelta960 are unable to phosphorylate IRS-1 and Shc (Chaika, O. V., Chaika, N., Volle, D. J., Wilden, P. A. , Pirrucello, S. J., and Lewis, R. E. (1997) J. Biol. Chem. 272, 11968-11974) [35].
 

Regulatory relationships of CSF1R

 

Other interactions of CSF1R

  • The effects of CSF-1 are mediated through binding to specific, high-affinity surface receptors encoded by the c-fms gene [3].
  • Epigenetic consequences of AML1-ETO action at the human c-FMS locus [40].
  • The AML1-ETO complex does not disrupt binding of other transcription factors, indicating that c-FMS is not irreversibly epigenetically silenced [40].
  • In contrast, whatever the concentration, G-CSF had no effect on c-fms mRNA or protein levels [41].
  • We provide evidence that this multiprotein complex can interact with the tyrosine phosphorylated CSF-1 receptor through the unoccupied SH2 domain of Grb2 [42].
 

Analytical, diagnostic and therapeutic context of CSF1R

References

  1. Loss of both CSF1R (FMS) alleles in patients with myelodysplasia and a chromosome 5 deletion. Boultwood, J., Rack, K., Kelly, S., Madden, J., Sakaguchi, A.Y., Wang, L.M., Oscier, D.G., Buckle, V.J., Wainscoat, J.S. Proc. Natl. Acad. Sci. U.S.A. (1991) [Pubmed]
  2. Structural alteration of viral homologue of receptor proto-oncogene fms at carboxyl terminus. Coussens, L., Van Beveren, C., Smith, D., Chen, E., Mitchell, R.L., Isacke, C.M., Verma, I.M., Ullrich, A. Nature (1986) [Pubmed]
  3. Expression of the macrophage colony-stimulating factor and c-fms genes in human acute myeloblastic leukemia cells. Rambaldi, A., Wakamiya, N., Vellenga, E., Horiguchi, J., Warren, M.K., Kufe, D., Griffin, J.D. J. Clin. Invest. (1988) [Pubmed]
  4. Expression of the colony stimulating factor-1 receptor (c-fms product) by cells at the human uteroplacental interface. Jokhi, P.P., Chumbley, G., King, A., Gardner, L., Loke, Y.W. Lab. Invest. (1993) [Pubmed]
  5. Correlates of physical activity among women with fibromyalgia syndrome. Oliver, K., Cronan, T.A. Annals of behavioral medicine : a publication of the Society of Behavioral Medicine. (2005) [Pubmed]
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  9. Genetic localization of a locus controlling the intensity of infection by Schistosoma mansoni on chromosome 5q31-q33. Marquet, S., Abel, L., Hillaire, D., Dessein, H., Kalil, J., Feingold, J., Weissenbach, J., Dessein, A.J. Nat. Genet. (1996) [Pubmed]
  10. The diastrophic dysplasia gene encodes a novel sulfate transporter: positional cloning by fine-structure linkage disequilibrium mapping. Hästbacka, J., de la Chapelle, A., Mahtani, M.M., Clines, G., Reeve-Daly, M.P., Daly, M., Hamilton, B.A., Kusumi, K., Trivedi, B., Weaver, A. Cell (1994) [Pubmed]
  11. Tandem linkage of human CSF-1 receptor (c-fms) and PDGF receptor genes. Roberts, W.M., Look, A.T., Roussel, M.F., Sherr, C.J. Cell (1988) [Pubmed]
  12. A point mutation in the extracellular domain of the human CSF-1 receptor (c-fms proto-oncogene product) activates its transforming potential. Roussel, M.F., Downing, J.R., Rettenmier, C.W., Sherr, C.J. Cell (1988) [Pubmed]
  13. Co-expression of M-CSF transcripts and protein, FMS (M-CSF receptor) transcripts and protein, and steroid receptor content in adenocarcinomas of the ovary. Kommoss, F., Wölfle, J., Bauknecht, T., Pfisterer, J., Kiechle-Schwarz, M., Pfleiderer, A., Sauerbrei, W., Kiehl, R., Kacinski, B.M. J. Pathol. (1994) [Pubmed]
  14. Macrophage colony-stimulating factor receptor c-fms is a novel target of imatinib. Dewar, A.L., Cambareri, A.C., Zannettino, A.C., Miller, B.L., Doherty, K.V., Hughes, T.P., Lyons, A.B. Blood (2005) [Pubmed]
  15. Increasing c-FMS (CSF-1 receptor) expression decreases retinoic acid concentration needed to cause cell differentiation and retinoblastoma protein hypophosphorylation. Yen, A., Sturgill, R., Varvayanis, S. Cancer Res. (1997) [Pubmed]
  16. Post-transcriptional regulation of c-fms proto-oncogene expression by dexamethasone and of CSF-1 in human breast carcinomas in vitro. Chambers, S.K., Wang, Y., Gilmore-Hebert, M., Kacinski, B.M. Steroids (1994) [Pubmed]
  17. Identification and characterization of heparin binding regions of the Fim2 subunit of Bordetella pertussis. Geuijen, C.A., Willems, R.J., Hoogerhout, P., Puijk, W.C., Meloen, R.H., Mooi, F.R. Infect. Immun. (1998) [Pubmed]
  18. Tetranucleotide microsatellite instability in surgical margins for prediction of local recurrence of head and neck squamous cell carcinoma. Temam, S., Casiraghi, O., Lahaye, J.B., Bosq, J., Zhou, X., Julieron, M., Mamelle, G., Lee, J.J., Mao, L., Luboinski, B., Benard, J., Janot, F. Clin. Cancer Res. (2004) [Pubmed]
  19. Rearrangements of the AML1/CBFA2 gene in myeloid leukemia with the 3;21 translocation: in vitro and in vivo studies. Zent, C., Rowley, J.D., Nucifora, G. Leukemia (1997) [Pubmed]
  20. Novel genes mapping to the critical region of the 5q- syndrome. Boultwood, J., Fidler, C., Soularue, P., Strickson, A.J., Kostrzewa, M., Jaju, R.J., Cotter, F.E., Fairweather, N., Monaco, A.P., Müller, U., Lovett, M., Jabs, E.W., Auffray, C., Wainscoat, J.S. Genomics (1997) [Pubmed]
  21. Report of the Chromosome 5 Workshop of the Sixth World Congress on Psychiatric Genetics. Crowe, R.R., Vieland, V. Am. J. Med. Genet. (1999) [Pubmed]
  22. Overexpression of translocation-associated fusion genes of FGFRI, MYC, NPMI, and DEK, but absence of the translocations in acute myeloid leukemia. A microarray analysis. Larramendy, M.L., Niini, T., Elonen, E., Nagy, B., Ollila, J., Vihinen, M., Knuutila, S. Haematologica (2002) [Pubmed]
  23. Macrophage-colony-stimulating factor (CSF-1) induces proliferation, chemotaxis, and reversible monocytic differentiation in myeloid progenitor cells transfected with the human c-fms/CSF-1 receptor cDNA. Pierce, J.H., Di Marco, E., Cox, G.W., Lombardi, D., Ruggiero, M., Varesio, L., Wang, L.M., Choudhury, G.G., Sakaguchi, A.Y., Di Fiore, P.P. Proc. Natl. Acad. Sci. U.S.A. (1990) [Pubmed]
  24. Generation of CD1+RelB+ dendritic cells and tartrate-resistant acid phosphatase-positive osteoclast-like multinucleated giant cells from human monocytes. Akagawa, K.S., Takasuka, N., Nozaki, Y., Komuro, I., Azuma, M., Ueda, M., Naito, M., Takahashi, K. Blood (1996) [Pubmed]
  25. Synthesis of membrane-bound colony-stimulating factor 1 (CSF-1) and downmodulation of CSF-1 receptors in NIH 3T3 cells transformed by cotransfection of the human CSF-1 and c-fms (CSF-1 receptor) genes. Rettenmier, C.W., Roussel, M.F., Ashmun, R.A., Ralph, P., Price, K., Sherr, C.J. Mol. Cell. Biol. (1987) [Pubmed]
  26. A mutational analysis of phosphatidylinositol-3-kinase activation by human colony-stimulating factor-1 receptor. Choudhury, G.G., Wang, L.M., Pierce, J., Harvey, S.A., Sakaguchi, A.Y. J. Biol. Chem. (1991) [Pubmed]
  27. Molecular cytogenetic delineation of the critical deleted region in the 5q- syndrome. Jaju, R.J., Boultwood, J., Oliver, F.J., Kostrzewa, M., Fidler, C., Parker, N., McPherson, J.D., Morris, S.W., Müller, U., Wainscoat, J.S., Kearney, L. Genes Chromosomes Cancer (1998) [Pubmed]
  28. Mechanism of differential inhibition of factor-dependent cell proliferation by transforming growth factor-beta 1: selective uncoupling of FMS from MYC. Chen, A.R., Rohrschneider, L.R. Blood (1993) [Pubmed]
  29. Human colony-stimulating factor 1 (CSF-1) receptor confers CSF-1 responsiveness to interleukin-3-dependent 32DC13 mouse myeloid cells and abrogates differentiation in response to granulocyte CSF. Kato, J., Sherr, C.J. Blood (1990) [Pubmed]
  30. FMS receptor for M-CSF (CSF-1) is sensitive to the kinase inhibitor imatinib and mutation of Asp-802 to Val confers resistance. Taylor, J.R., Brownlow, N., Domin, J., Dibb, N.J. Oncogene (2006) [Pubmed]
  31. Transcription factor PU.1 mediates induction of c-fms in vascular smooth muscle cells: a mechanism for phenotypic change to phagocytic cells. Inaba, T., Gotoda, T., Ishibashi, S., Harada, K., Ohsuga, J.I., Ohashi, K., Yazaki, Y., Yamada, N. Mol. Cell. Biol. (1996) [Pubmed]
  32. Induction of macrophage colony-stimulating factor receptor (c-fms) expression in vascular medial smooth muscle cells treated with heparin binding epidermal growth factor-like growth factor. Inaba, T., Ishibashi, S., Harada, K., Ohsuga, J., Ohashi, K., Yagyu, H., Yazaki, Y., Higashiyama, S., Kawata, S., Matsuzawa, Y., Yamada, N. J. Biol. Chem. (1996) [Pubmed]
  33. FMS (CSF-1 receptor) prolongs cell cycle and promotes retinoic acid-induced hypophosphorylation of retinoblastoma protein, G1 arrest, and cell differentiation. Yen, A., Sturgill, R., Varvayanis, S., Chern, R. Exp. Cell Res. (1996) [Pubmed]
  34. C-fms protein expression by B-cells, with particular reference to the hairy cells of hairy-cell leukaemia. Till, K.J., Lopez, A., Slupsky, J., Cawley, J.C. Br. J. Haematol. (1993) [Pubmed]
  35. Anti-apoptotic signaling by a colony-stimulating factor-1 receptor/insulin receptor chimera with a juxtamembrane deletion. Boehm, J.E., Chaika, O.V., Lewis, R.E. J. Biol. Chem. (1998) [Pubmed]
  36. Human monocyte-derived dendritic cells produce macrophage colony-stimulating factor: enhancement of c-fms expression by interleukin-10. Rieser, C., Ramoner, R., Böck, G., Deo, Y.M., Höltl, L., Bartsch, G., Thurnher, M. Eur. J. Immunol. (1998) [Pubmed]
  37. Lack of KIT or FMS internal tandem duplications but co-expression with ligands in AML. Zheng, R., Klang, K., Gorin, N.C., Small, D. Leuk. Res. (2004) [Pubmed]
  38. IL-2 enhances c-fms expression in human monocytes. Espinoza-Delgado, I., Longo, D.L., Gusella, G.L., Varesio, L. J. Immunol. (1990) [Pubmed]
  39. Expression of the c-mpl proto-oncogene in human hematologic malignancies. Vigon, I., Dreyfus, F., Melle, J., Viguié, F., Ribrag, V., Cocault, L., Souyri, M., Gisselbrecht, S. Blood (1993) [Pubmed]
  40. Epigenetic consequences of AML1-ETO action at the human c-FMS locus. Follows, G.A., Tagoh, H., Lefevre, P., Hodge, D., Morgan, G.J., Bonifer, C. EMBO J. (2003) [Pubmed]
  41. IL-3, GM-CSF and CSF-1 modulate c-fms mRNA more rapidly in human early monocytic progenitors than in mature or transformed monocytic cells. Panterne, B., Hatzfeld, A., Sansilvestri, P., Cardoso, A., Monier, M.N., Batard, P., Hatzfeld, J. J. Cell. Sci. (1996) [Pubmed]
  42. CSF-1 stimulation induces the formation of a multiprotein complex including CSF-1 receptor, c-Cbl, PI 3-kinase, Crk-II and Grb2. Husson, H., Mograbi, B., Schmid-Antomarchi, H., Fischer, S., Rossi, B. Oncogene (1997) [Pubmed]
  43. Colony-stimulating factor-1 stimulates the formation of multimeric cytosolic complexes of signaling proteins and cytoskeletal components in macrophages. Yeung, Y.G., Wang, Y., Einstein, D.B., Lee, P.S., Stanley, E.R. J. Biol. Chem. (1998) [Pubmed]
  44. Characterization of the 5q- breakpoint in an acute nonlymphocytic leukemia patient using pulsed-field gel electrophoresis. Thornton, D.E., Theil, K., Payson, R., Balcerzak, S.P., Chiu, I.M. Am. J. Med. Genet. (1991) [Pubmed]
  45. Direct comparison of the effects of CSF-1 (M-CSF) and GM-CSF on human monocyte DNA synthesis and CSF receptor expression. Finnin, M., Hamilton, J.A., Moss, S.T. J. Interferon Cytokine Res. (1999) [Pubmed]
 
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