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Merck

G5296

Sigma-Aldrich

Anti-Granulocyte Colony Stimulating Factor antibody produced in goat

IgG fraction of antiserum, lyophilized powder

Sinónimos:

Anti-G-CSF

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About This Item

MDL number:
UNSPSC Code:
51111800
NACRES:
NA.41

biological source

goat

Quality Level

conjugate

unconjugated

antibody form

IgG fraction of antiserum

antibody product type

primary antibodies

clone

polyclonal

form

lyophilized powder

species reactivity

mouse

technique(s)

neutralization: suitable
western blot: 1-2 μg/mL

UniProt accession no.

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

mouse ... Csf3(12985)

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General description

Mature myeloid cells are derived from bone-marrow derived precursor cells by the activity of three colony stimulating factors, granulocyte/macrophage colony-stimulating factor (GM-CSF), macrophage colony-stimulating factor (M-CSF) and granulocyte colony-stimulating factor (G-CSF). The expression of G-CSF is the result of activation of pathways in response to tumor necrosis factor-α, LPS and toll-like receptor ligands. The pathways that induce the effects of G-CSF are PI3K, ERK1/2 and p38. The generation of neutrophils and induction of the circulation of hematopoietic stem cells from the bone marrow are the main functions of G-CSF. There are additional activities attributed to G-CSF such as neuroprotection, immunomodulation and generation of cardiac cells and dendritic cells. Large quantities of G-CSF are secreted in a variety of myeloid and non-myeloid cancers and rheumatoid arthritis
Monoclonal anti-granulocyte colony stimulating factor recognizes mouse G-CSF. The antibody shows less than 20% cross-reactivity with recombinant human G-CSF.

Immunogen

purified, recombinant mouse granulocyte colony stimulating factor, expressed in E. coli.

Application

Anti-granulocyte colony stimulating factor antibody may be used for immunoblotting at a working concentration of 1-2 μg/ml. The antibody is suitable for neutralization reactions.

Physical form

Lyophilized from a 0.2 μm filtered solution in phosphate buffered saline containing carbohydrates.

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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Storage Class

13 - Non Combustible Solids

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)


Certificados de análisis (COA)

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R R Ji et al.
Nature neuroscience, 2(12), 1114-1119 (1999-11-26)
We investigated the involvement of extracellular signal-regulated protein kinases (ERK) within spinal neurons in producing pain hypersensitivity. Within a minute of an intense noxious peripheral or C-fiber electrical stimulus, many phosphoERK-positive neurons were observed, most predominantly in lamina I and
Sophie Pezet et al.
The European journal of neuroscience, 21(7), 1785-1797 (2005-05-05)
The serine/threonine kinase Akt/PKB has been implicated in cell survival signalling in many cell types, including the dorsal root ganglion (DRG). However, little is known about its role in physiological and pathophysiological conditions in the adult sensory and nociceptive system.
Sebastian Stösser et al.
Journal of molecular medicine (Berlin, Germany), 89(4), 321-329 (2010-11-17)
A variety of cancers are accompanied by debilitating pain, which constitutes the primary reason for poor quality of life in cancer patients. There is an urgent demand for the development of specific mechanism-based therapies against cancer pain. Recently, important advances
Rong L He et al.
Blood, 113(2), 429-437 (2008-10-28)
The acute-phase protein serum amyloid A (SAA) is commonly considered a marker for inflammatory diseases; however, its precise role in inflammation and infection, which often result in neutrophilia, remains ambiguous. In this study, we demonstrate that SAA is a potent
F Liu et al.
Immunity, 5(5), 491-501 (1996-11-01)
We have generated mice carrying a homozygous null mutation in the granulocyte colony-stimulating factor receptor (G-CSFR) gene. G-CSFR-deficient mice have decreased numbers of phenotypically normal circulating neutrophils. Hematopoietic progenitors are decreased in the bone marrow, and the expansion and terminal

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