- SynonymGM-CSF,CSF2,MGC131935
- SourceActiveMax® Human GM-CSF, Tag Free (GMF-H4214) is expressed from human 293 cells (HEK293). It contains AA Ala 18 - Glu 144 (Accession # NP_000749.2).Predicted N-terminus: Ala 18Request for sequence
- Molecular Characterization
This protein carries no "tag".
The protein has a calculated MW of 14.5 kDa. The protein migrates as 18-26 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.
- EndotoxinLess than 0.1 EU per μg by the LAL method.
- Purity
>95% as determined by SDS-PAGE.
- Formulation
Lyophilized from 0.22 μm filtered solution in PBS, pH7.4. Normally trehalose is added as protectant before lyophilization.
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- Reconstitution
Please see Certificate of Analysis for specific instructions.
For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.
- Storage
For long term storage, the product should be stored at lyophilized state at -20°C or lower.
Please avoid repeated freeze-thaw cycles.
This product is stable after storage at:
-20°C to -70°C for 12 months in lyophilized state;
-70°C for 3 months under sterile conditions after reconstitution.
ActiveMax® Human GM-CSF, Tag Free on SDS-PAGE under reducing (R) condition. The gel was stained overnight with Coomassie Blue. The purity of the protein is greater than 95%.
Loaded Human GM-CSF R alpha, Fc Tag (Cat. No. GRA-H5255) on Protein A Biosensor, can bind ActiveMax® Human GM-CSF, Tag Free (Cat. No. GMF-H4214) with an affinity constant of 9.21 nM as determined in BLI assay (ForteBio Octet Red96e) (Routinely tested).
The bio-activity was determined by dose-dependent stimulation of the proliferation of TF-1 cells. The ED50 < 0.1 ng/mL, corresponding to a specific activity of > 1x107 Unit/mg.
- Citations
Linoleic acid inhibits in vitro function of human and murine dendritic cells, CD4+T cells and retinal pigment epithelial cells.
Authors: Huang X, Yi S, Hu J, et al.
Journal: Graefes Arch Clin Exp Ophthalmol 2020
Application: Cell culture
Request for Full-text
Disabled-2 (DAB2) Overexpression Inhibits Monocyte-Derived Dendritic Cells' Function in Vogt-Koyanagi-Harada Disease
Authors: Yi, S., et al.
Journal: Immunology and Microbiology 43325
Application: Cell Culture
Request for Full-text
Decreased expression of A20 is associated with ocular Behcet's disease (BD) but not with Vogt-Koyanagi-Harada (VKH) disease
Authors: He Y, et al.
Journal: Br J Ophthalmol 2018
Application: Cell Culture
Request for Full-text
- BackgroundGranulocyte-macrophage colony-stimulating factor (GM-CSF) is also known as Colony stimulating factor 2 (granulocyte-macrophage), is a cytokine initially characterized by its ability to induce colonies of granulocytes and macrophages from myeloid progenitor cells, and is secreted by macrophages, T cells, mast cells, endothelial cells and fibroblasts. GM-CSF is a cytokine that functions as a white blood cell growth factor. GM-CSF stimulates stem cells to produce granulocytes (neutrophils, eosinophils, and basophils) and monocytes. Monocytes exitthe circulation and migrate into tissue, whereupon they mature into macrophages and dendritic cells. Thus, it is part of the immune/inflammatory cascade, by which activation of a small number of macrophages can rapidly lead to an increase in their numbers, a process crucial for fighting infection. The active form of the protein is found extracellularly as a homodimer. Human GM-CSF glycosylated in its mature form. As a part of the immune/inflammatory cascade, GM-CSF promotes Th1 biased immune response, angiogenesis, allergic inflammation, and the development of autoimmunity, and thus worthy of consideration for therapeutic target. GM-CSF has also recently been evaluated in clinical trials for its potential as a vaccine adjuvant in HIV-infected patients. The preliminary results have been promising. GM-CSF is also used as a medication to stimulate the production of white blood cells following chemotherapy.
- References
(1)Volmar, C.H. et al., 2008, Cytokine. 42(3): 336-344.
(2)Breitbach CJ, et al., 2010, Nature 477 (7362): 99–102.
(3)Korzenik J, et al., 2005, N Engl J Med 352 (21): 2193–201.
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