CSF1R Primary Antibody
|Aliases||FMS; CSFR; FIM2; HDLS; C-FMS; CD115; CSF-1R; M-CSF-R|
|Formulation||Purified antibody in PBS with 0.05% sodium azide|
|Immunogen||Purified recombinant fragment of human CSF1R (AA: 344-497) expressed in E. Coli.|
|Shipping Information||This product will ship in a box containing blue ice at a temperature of 4°C. Learn More|
|IHC_P(Immunohistochemistry)||1/200 - 1/1000|
|FCM (Flow Cytometry)||1/200 - 1/400|
|WB (Western Blot)||1/500 - 1/2000|
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Figure 1: Western blot analysis using CSF1R mAb against human CSF1R (AA: 344-497) recombinant protein. (Expected MW is 43.3 kDa)
Figure 2: Western blot analysis using CSF1R mAb against HEK293 (1) and CSF1R (AA: 344-497)-hIgGFc transfected HEK293 (2) cell lysate.
Figure 3: Flow cytometric analysis of HepG2 cells using CSF1R mouse mAb (green) and negative control (red).
Figure 4: Immunohistochemical analysis of paraffin-embedded prostate cancer tissues using CSF1R mouse mAb with DAB staining.
Figure 5: Immunohistochemical analysis of paraffin-embedded cervical cancer tissues using CSF1R mouse mAb with DAB staining.
Black line: Control Antigen (100 ng); Purple line: Antigen(10ng); Blue line: Antigen (50 ng); Red line: Antigen (100 ng);
|Description||The protein encoded by this gene is the receptor for colony stimulating factor 1, a cytokine which controls the production, differentiation, and function of macrophages. This receptor mediates most if not all of the biological effects of this cytokine. Ligand binding activates the receptor kinase through a process of oligomerization and transphosphorylation. The encoded protein is a tyrosine kinase transmembrane receptor and member of the CSF1/PDGF receptor family of tyrosine-protein kinases. Mutations in this gene have been associated with a predisposition to myeloid malignancy. The first intron of this gene contains a transcriptionally inactive ribosomal protein L7 processed pseudogene oriented in the opposite direction. |
|References (references)||1. PLoS One. 2011;6(11):e27450. |
2. J Biochem. 2012 Jan;151(1):47-55.