R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
SOCS3 (D6E1T) Rabbit mAb #52113
Filter:
- WB
Supporting Data
| REACTIVITY | H M |
| SENSITIVITY | Endogenous |
| MW (kDa) | 28 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
SOCS3 (D6E1T) Rabbit mAb recognizes endogenous levels of total SOCS3 protein.
Species Reactivity:
Human, Mouse
Source / Purification
Monoclonal antibody is produced by immunizing animals with recombinant protein specific to human SOCS3 protein.
Background
The suppressor of cytokine signaling (SOCS) family members are negative regulators of cytokine signal transduction that inhibit the Jak/Stat pathway (1-3). The SOCS family consists of at least 8 members including the originally identified cytokine-inducible SH2-containing protein (CIS1), as well as SOCS1-7. Each SOCS family member contains a central SH2 domain and a conserved carboxy-terminal motif designated as the SOCS box. These proteins are important regulators of cytokine signaling, proliferation, differentiation, and immune responses.
Low levels of SOCS3 are observed in lung, spleen, and thymus and, like other SOCS family members, its expression is rapidly induced by a number of factors including interleukins, EPO, IFN-γ, CSF, and TNF-α (4). SOCS3 uses its SH2 domain to bind activated Jaks and their cognate receptors to provide negative feedback inhibition. In addition to the initially described inducers of SOCS3 expression, subsequent studies have described SOCS3-mediated negative feedback inhibition for leptin (5), GH (6), chemokine receptors (7), insulin (8), and certain pathogens (9,10). SOCS3 deletion results in embryonic lethality with placental insufficiency (11). SOCS3 signaling has been linked pathologically to allergic responses (12), inflammatory disease (13), endotoxic shock (14), wound repair (15), and obesity (16,17).
Low levels of SOCS3 are observed in lung, spleen, and thymus and, like other SOCS family members, its expression is rapidly induced by a number of factors including interleukins, EPO, IFN-γ, CSF, and TNF-α (4). SOCS3 uses its SH2 domain to bind activated Jaks and their cognate receptors to provide negative feedback inhibition. In addition to the initially described inducers of SOCS3 expression, subsequent studies have described SOCS3-mediated negative feedback inhibition for leptin (5), GH (6), chemokine receptors (7), insulin (8), and certain pathogens (9,10). SOCS3 deletion results in embryonic lethality with placental insufficiency (11). SOCS3 signaling has been linked pathologically to allergic responses (12), inflammatory disease (13), endotoxic shock (14), wound repair (15), and obesity (16,17).
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- Fang, M. et al. (2005) Cell Mol Immunol 2, 373-7.
- Goren, I. et al. (2006) J Invest Dermatol 126, 477-85.
- Mori, H. et al. (2004) Nat Med 10, 739-43.
- Howard, J.K. et al. (2004) Nat Med 10, 734-8.
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For Research Use Only. Not For Use In Diagnostic Procedures.
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KARPAS cell line source: Dr. Abraham Karpas at the University of Cambridge.
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