CISH (D4D9) Rabbit mAb #8731
- WB
- IP
- F
Supporting Data
| REACTIVITY | H M |
| SENSITIVITY | Endogenous |
| MW (kDa) | 32, 37 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:100 |
| Flow Cytometry (Fixed/Permeabilized) | 1:50 - 1:200 |
Storage
For a carrier free (BSA and azide free) version of this product see product #39434.
Protocol
Specificity / Sensitivity
Species Reactivity:
The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.
Species predicted to react based on 100% sequence homology:
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro176 of human CISH 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.
CISH/CIS1, the first described member of the SOCS family, is induced by a number of cytokines including IL-2, IL-3, GM-CSF, and EPO (4). The CISH protein appears as a doublet around 32 and 37 kDa, the nature of which is unknown (4). CISH binds to phosphorylated cytokine receptors and can inhibit Stat5 activity (4-6). Expression of CISH is regulated by Stat5, thereby providing feedback modulation (5). Transgenic mice overexpressing CISH display phenotypes similar to Stat5 knockouts, including defects in mammary gland development and in T and NK cell regulation (6). Research studies have shown that polymorphisms within the CISH gene are associated with susceptibility to infectious diseases (7).
- 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.
- Yoshimura, A. et al. (1995) EMBO J 14, 2816-26.
- Matsumoto, A. et al. (1997) Blood 89, 3148-54.
- Matsumoto, A. et al. (1999) Mol Cell Biol 19, 6396-407.
- Khor, C.C. et al. (2010) N Engl J Med 362, 2092-101.
Limited Uses
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