SOCS3 Antibody #2923
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Inquiry Info. # 2923
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Supporting Data
| REACTIVITY | H M R |
| SENSITIVITY | Endogenous |
| MW (kDa) | 26 |
| SOURCE | Rabbit |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
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 and 50% glycerol. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
SOCS3 Antibody detects endogenous levels of total SOCS3 protein.
Species Reactivity:
Human, Mouse, Rat
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Lys195 of SOCS3. Antibodies were purified by protein A and peptide affinity chromatography.
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 levels 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 levels 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).
- Alexander, W.S. et al. (1999) J Leukoc Biol 66, 588-92.
- Chen, X.P. et al. (2000) Immunity 13, 287-90.
- Hilton, D.J. et al. (1998) Proc Natl Acad Sci USA 95, 114-9.
- Starr, R. et al. (1997) Nature 387, 917-21.
- Bjørbaek, C. et al. (1998) Mol Cell 1, 619-25.
- Adams, T.E. et al. (1998) J Biol Chem 273, 1285-7.
- Soriano, S.F. et al. (2002) J Exp Med 196, 311-21.
- Emanuelli, B. et al. (2000) J Biol Chem 275, 15985-91.
- Stoiber, D. et al. (1999) J Immunol 163, 2640-7.
- Stoiber, D. et al. (2001) J Immunol 166, 466-72.
- Roberts, A.W. et al. (2001) Proc Natl Acad Sci USA 98, 9324-9.
- Seki, Y. et al. (2003) Nat Med 9, 1047-54.
- Shouda, T. et al. (2001) J Clin Invest 108, 1781-8.
- 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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