Recombinant Anti-GM-CSF/CSF2 Antibody, Rabbit Monoclonal sinobiological 51048-R017

$1,900.00
In stock
SKU
51048-R017
Catalog No.SizePrice (USD)
51048-R017-11 mL$1,969.87
51048-R017-2020 µL$118.49
51048-R017-5050 µL$177.58
51048-R017-100100 µL$340.51

General Information

Product nameRecombinant Anti-GM-CSF/CSF2 Antibody, Rabbit Monoclonal
Validated applicationsELISA (FAQ Protocol), ELISA(Cap) (FAQ Protocol)
Species reactivityReacts with: Mouse
SpecificityMouse GM-CSF/CSF2
ImmunogenRecombinant Mouse GM-CSF/CSF2 Protein (Catalog#51048-M07H)
PreparationThis antibody was obtained from a rabbit immunized with purified, recombinant Mouse GM-CSF/CSF2 (rM GM-CSF/CSF2; Catalog#51048-M07H; P01587; Ala18-Lys141).
SourceMonoclonal Rabbit IgG Clone #017
PurificationProtein A
Formulation0.2 μm filtered solution in PBS
ConjugateUnconjugated
FormLiquid
ShippingThis antibody is shipped as liquid solution at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
StorageThis antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free. Avoid repeated freeze-thaw cycles.

Synonyms: Anti-CSF Antibody; Anti-Csf2 Antibody; Anti-Csfgm Antibody; Anti-Gm-CSf Antibody; Anti-GMCSF Antibody; Anti-MGI-IGM Antibody

Background Information

Full Namecolony stimulating factor 2 (granulocyte-macrophage)
DescriptionGranulocyte-macrophage colony-stimulating factor (GM-CSF) is one of an array of cytokines with pivotal roles in embryo implantation and subsequent development. Several cell lineages in the reproductive tract and gestational tissues synthesise GM-CSF under direction by ovarian steroid hormones and signalling agents originating in male seminal fluid and the conceptus. The pre-implantation embryo, invading placental trophoblast cells and the abundant populations of leukocytes controlling maternal immune tolerance are all subject to GM-CSF regulation. GM-CSF stimulates the differentiation of hematopoietic progenitors to monocytes and neutrophils, and reduces the risk for febrile neutropenia in cancer patients. GM-CSF also has been shown to induce the differentiation of myeloid dendritic cells (DCs) that promote the development of T-helper type 1 (cellular) immune responses in cognate T cells. The active form of the protein is found extracellularly as a homodimer, and the encoding gene is localized to a related gene cluster at chromosome region 5q31 which is known to be associated with 5q-syndrome and acute myelogenous leukemia. 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 been utilized in the clinical management of multiple disease processes. Most recently, GM-CSF has been incorporated into the treatment of malignancies as a sole therapy, as well as a vaccine adjuvant. While the benefits of GM-CSF in this arena have been promising, recent reports have suggested the potential for GM-CSF to induce immune suppression and, thus, negatively impact outcomes in the management of cancer patients. GM-CSF deficiency in pregnancy adversely impacts fetal and placental development, as well as progeny viability and growth after birth, highlighting this cytokine as a central maternal determinant of pregnancy outcome with clinical relevance in human fertility.
Research Areas
  • Cancer Drug Targets
Related Pathways
  • IL17 signaling pathway
Tags
  • Cancer Immunotherapy
  • Immune Checkpoint
  • Immunotherapy
  • Targeted Therapy
References
  1. Robertson SA. (2007) GM-CSF regulation of embryo development and pregnancy. Cytokine Growth Factor Rev. 18(3-4): 287-98.
  2. Waller EK. (2007) The role of sargramostim (rhGM-CSF) as immunotherapy. Oncologist. 12 Suppl 2: 22-6.
  3. Clive KS, et al. (2010) Use of GM-CSF as an adjuvant with cancer vaccines: beneficial or detrimental? Expert Rev Vaccines. 9(5): 519-25.

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