Revision 5

#8929Store at -20C

5 µg

Cell Signaling Technology

Orders: 877-616-CELL (2355) [email protected]

Support: 877-678-TECH (8324)

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3 Trask LaneDanversMassachusetts01923USA
For Research Use Only. Not for Use in Diagnostic Procedures.
MW (kDa):

16-26

UniProt ID:

#P09603

Entrez-Gene Id:

1435

Background

Colony stimulating factor 1 (CSF-1)/macrophage colony stimulating factor (M-CSF) is produced by fibroblasts, endothelial cells, stromal cells, macrophages, osteoblasts, and other cell types (1). CSF-1/M-CSF is required for growth and differentiation of monocytes and macrophages (1,2). CSF-1/M-CSF polarizes macrophages into the M2 phenotype where anti-inflammatory IL-10 is produced, rather than the M1 phenotype where inflammatory cytokines are produced. CSF-1/M-CSF also recruits monocytes and enhances angiogenesis by inducing VEGF production (1,2). CSF-1/M-CSF binds to its receptor CSF1R; downstream signaling involves PI3K/Akt, Erk, and Stats 1, 3, and 5 (1,3). An increase in CSF-1/M-CSF expression may contribute to cancer progression, and high plasma CSF-1/M-CSF levels are associated with rheumatoid arthritis (1,4,5).

  1. Hamilton, J.A. (2008) Nat Rev Immunol 8, 533-44.
  2. Curry, J.M. et al. (2008) PLoS One 3, e3405.
  3. Hamilton, J.A. (1997) J Leukoc Biol 62, 145-55.
  4. Rioja, I. et al. (2008) Arthritis Rheum 58, 2257-67.
  5. Skrzypski, M. et al. (2008) Clin Cancer Res 14, 4794-9.

Endotoxin

Less than 0.01 ng endotoxin/1 μg hCSF-1/M-CSF.

Purity

>98% as determined by SDS-PAGE of 6 μg reduced (+) and non-reduced (-) recombinant hCSF-1/M-CSF. All lots are greater than 98% pure.

Source / Purification

Recombinant human CSF-1/M-CSF Glu33-Ser190 (Accession #P09603-3) was expressed in human 293 cells at Cell Signaling Technology.

Bioactivity

The bioactivity of recombinant hCSF-1M/CSF was determined in a M-NFS-60 cell proliferation assay. The ED50 of each lot is between 0.5-15.0 ng/ml.

Background

Colony stimulating factor 1 (CSF-1)/macrophage colony stimulating factor (M-CSF) is produced by fibroblasts, endothelial cells, stromal cells, macrophages, osteoblasts, and other cell types (1). CSF-1/M-CSF is required for growth and differentiation of monocytes and macrophages (1,2). CSF-1/M-CSF polarizes macrophages into the M2 phenotype where anti-inflammatory IL-10 is produced, rather than the M1 phenotype where inflammatory cytokines are produced. CSF-1/M-CSF also recruits monocytes and enhances angiogenesis by inducing VEGF production (1,2). CSF-1/M-CSF binds to its receptor CSF1R; downstream signaling involves PI3K/Akt, Erk, and Stats 1, 3, and 5 (1,3). An increase in CSF-1/M-CSF expression may contribute to cancer progression, and high plasma CSF-1/M-CSF levels are associated with rheumatoid arthritis (1,4,5).

Background References

    Cross-Reactivity Key

    H: human M: mouse R: rat Hm: hamster Mk: monkey Vir: virus Mi: mink C: chicken Dm: D. melanogaster X: Xenopus Z: zebrafish B: bovine Dg: dog Pg: pig Sc: S. cerevisiae Ce: C. elegans Hr: horse GP: Guinea Pig Rab: rabbit All: all species expected

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    Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.
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    Revision 5
    #8929

    Human CSF-1/M-CSF Recombinant Protein

    Human CSF-1/M-CSF Recombinant Protein: Image 1 Expand Image
    The proliferation of M-NFS-60 cells treated with increasing concentrations of hCSF-1/M-CSF was assessed. After 48 hour treatment with hCSF-1/M-CSF, cells were incubated with a tetrazolium salt and the OD450 - OD650 was determined.
    Human CSF-1/M-CSF Recombinant Protein: Image 2 Expand Image
    The purity of recombinant hCSF-1/M-CSF was determined by SDS-PAGE of 6 µg reduced (+) and non-reduced (-) recombinant hCSF-1/M-CSF and staining overnight with Coomassie Blue.
    Human CSF-1/M-CSF Recombinant Protein: Image 3 Expand Image
    Western blot analysis of extracts from M-NFS-60 cells, untreated or treated with hCSF-1/M-CSF for 10 minutes, using Phospho-p44/42 MAPK (Erk1/2) (Thr202/Tyr204) (D13.14.4E) XP® Rabbit mAb #4370 (upper) and p44/42 MAPK (Erk1/2) (137F5) Rabbit mAb #4695 (lower).