Human CellExp CSF1R / CD115 / CD6, human recombinant protein
CD6, CD-6, Cluster of Differentiation 6, FLJ44171, TP120
|Calculated MW||This protein rhCSF1R is fused with a C-terminal 6×his tag and has a calculated MW of 55.1 kDa. The predicted N-terminus is Ile 20. DTT-reduced protein migrates as 80-95 kDa polypeptide in SDS-PAGE.|
|Other Names||CD6, CD-6, Cluster of Differentiation 6, FLJ44171, TP120|
|Results||The ED50 for this effect is typically 1.5-8.7 pg/ml in the presence of 1 ng/ml of rhMCSF.|
|Target/Specificity||CSF1R / CD115 / CD6|
|Application Notes||Centrifuge the vial prior to opening. Reconstitute in PBS, pH 7.4. Do not vortex.|
|Storage||-20°C; Lyophilized from 0.22 µm filtered solution in PBS, pH 7.4. Normally Mannitol or Trehalose are added as protectants before lyophilization.|
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Provided below are standard protocols that you may find useful for product applications.
Colony stimulating factor 1 receptor (CSF1R), also known as macrophage colony-stimulating factor receptor (M-CSFR), CD115 Cluster of Differentiation 115 (CD115), C-FMS, CSFR, FIM2, FMS, and is a member of the type III subfamily of receptor tyrosine kinases (RTKs). CSF1R is a receptor for a cytokine called colony stimulating factor 1, The protein encoded by the CSFR1 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 CSFR1 through a process of oligomerization and transphosphorylation. Mutations in CSF1R are associated with chronic myelomonocytic leukemia and type M4 acute myeloblastic leukemia. Increased levels of CSF1R1 are found in microglia in Alzheimer's disease and after brain injuries. The increased receptor expression causes microglia to become more active. Both CSF1R, and its ligand colony stimulating factor 1 play an important role in the development of the mammary gland and may be involved in the process of mammary gland carcinogenesis.
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Jin P.,et al.Arthritis Res. Ther. 10:R73-R73(2008).
Schmutz J.,et al.Nature 431:268-274(2004).
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