SAB4500500
Anti-CSFR antibody produced in rabbit
affinity isolated antibody
Synonym(s):
CD115, CSF-1-R, CSF1R, CSFMR, c-fms
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About This Item
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biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen 107 kDa
species reactivity
human, rat, mouse
concentration
~1 mg/mL
technique(s)
ELISA: 1:5000
immunofluorescence: 1:100-1:500
immunohistochemistry: 1:50-1:100
NCBI accession no.
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... CSF1R(1436)
Related Categories
General description
Colony stimulating factor 1 receptor (CSF-1R) is encoded by the c-fms proto-oncogene mapped to human chromosome 5q33. The encoded protein acts as a receptor for CSF1 expressed in non-hematopoietic cells, such as macrophages, epithelial and fibroblasts cells and tumor cells.
Immunogen
The antiserum was produced against synthesized peptide derived from human CSFR.
Immunogen Range: 531-580
Immunogen Range: 531-580
Biochem/physiol Actions
Colony stimulating factor 1 receptor (CSF-1R)/ CSF-1 ligand system plays a vital role in the regulation of macrophage physiology in immune system.The encoded protein functions as a receptor and mediates the function of its ligand, colony stimulating factor 1, a cytokine involved in regulation of production, differentiation, and function of macrophages. Experimental analysis revealed that CSF-1/CSF-1R is overexpressed in patients with nasopharyngeal carcinoma when compared to patients with nasopharyngitis. Activated CSF-1R, is essential for monocyte differentiation to macrophages by oxidized low-density lipoprotein (Ox-LDL), which is a vital step in early atherogenesis. This protein is also associated with regulation of hematopoiesis. Deletion or mutation of this gene might be involved in the pathogenesis of myelodysplastic syndromes or of acute nonlymphocytic leukemia (ANLL).
Features and Benefits
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Physical form
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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flash_point_f
Not applicable
flash_point_c
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Find documentation for the products that you have recently purchased in the Document Library.
Evidence for the involvement of GM-CSF and FMS in the deletion (5q) in myeloid disorders.
Le Beau MM, et al.
Science, 231(4741), 984-987 (1986)
Ox-LDL induces monocyte-to-macrophage differentiation in vivo: Possible role for the macrophage colony stimulating factor receptor (M-CSF-R).
Fuhrman B, et al.
Atherosclerosis, 196(2), 598-607 (2008)
Overexpression of CSF-1R in nasopharyngeal carcinoma.
Huang L, et al.
Romanian Journal of Morphology and Embryology, 56(4), 1279-1283 (2015)
Myew-Ling Toh et al.
Arthritis & rheumatology (Hoboken, N.J.), 66(11), 2989-3000 (2014-03-14)
Colony-stimulating factor 1 receptor (CSF-1R) essentially modulates monocyte proliferation, migration, and activation, which are considered important for the pathogenesis of rheumatoid arthritis (RA). We undertook this study to determine CSF-1R expression in human RA as well as the efficacy of
Hirotake Tsukamoto et al.
Cancer immunology research, 1(1), 64-76 (2014-04-30)
Collaborative action between tumor cells and host-derived suppressor cells leads to peripheral tolerance of T cells to tumor antigens. Here, we showed that in tumor-bearing mice, generation of tumor antigen-specific effector T-helper cells (TH1) was significantly attenuated, and impaired TH1
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