19.1
#P09920
12985
Background
G-CSF is a hematopoietic cytokine essential for neutrophil development, survival, and egress from bone marrow (1-4). Macrophages and monocytes are the predominant producers of G-CSF (3) and endothelial cells, fibroblasts, and neuronal cells can produce G-CSF in response to inflammatory stimuli (3). G-CSF inhibits apoptosis in neutrophils and neurons (4,5). G-CSF stimulates proliferation and differentiation of neuronal progenitor cells (5). G-CSF binding to G-CSFR induces receptor dimerization and activation of Jak1/2 tyrosine phosphorylation (3,6). Signaling is through Stat3, ERK, p38, and Akt (5,6). Absence of functional G-CSF or its receptor in humans and mice causes neutropenia (7,8).
- Furze, R.C. and Rankin, S.M. (2008) Immunology 125, 281-8.
- Demetri, G.D. and Griffin, J.D. (1991) Blood 78, 2791-808.
- Srinivasa, S.P. and Doshi, P.D. (2002) Leukemia 16, 244-53.
- van Raam, B.J. et al. (2008) Blood 112, 2046-54.
- Schneider, A. et al. (2005) J Clin Invest 115, 2083-98.
- Nicholson, S.E. et al. (1994) Proc Natl Acad Sci U S A 91, 2985-8.
- Lieschke, G.J. et al. (1994) Blood 84, 1737-46.
- Dong, F. et al. (1994) Proc Natl Acad Sci U S A 91, 4480-4.
Endotoxin
Endotoxin levels are less than or equal to 1 EU / 1 μg mG-CSF.
Purity
A greater than or equal to 95% purity was determined by SDS-PAGE.
Source / Purification
Recombinant mouse G-CSF was expressed in E. coli and is supplied in a lyophilized form.
Bioactivity
The bioactivity of recombinant mG-CSF was determined in an NFS-60 cell proliferation assay. The ED50 of each lot is less than or equal to 50 pg/mL.
Background
G-CSF is a hematopoietic cytokine essential for neutrophil development, survival, and egress from bone marrow (1-4). Macrophages and monocytes are the predominant producers of G-CSF (3) and endothelial cells, fibroblasts, and neuronal cells can produce G-CSF in response to inflammatory stimuli (3). G-CSF inhibits apoptosis in neutrophils and neurons (4,5). G-CSF stimulates proliferation and differentiation of neuronal progenitor cells (5). G-CSF binding to G-CSFR induces receptor dimerization and activation of Jak1/2 tyrosine phosphorylation (3,6). Signaling is through Stat3, ERK, p38, and Akt (5,6). Absence of functional G-CSF or its receptor in humans and mice causes neutropenia (7,8).
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
Trademarks and Patents
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