Mouse CD25/IL-2R alpha Biotinylated Antibody
Mouse CD25/IL-2R alpha Biotinylated Antibody Summary
Accession # Q544I2
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Mouse CD25/IL-2 R alpha Sandwich Immunoassay
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Background: CD25/IL-2R alpha
IL-2 receptor alpha (IL-2 R alpha ), also known as CD25, is a 55 kDa type I membrane glycoprotein that belongs to the family of cytokine receptors that utilize the common gamma chain subunit ( gamma c). IL-2 R alpha is primarily expressed on activated T cells and on regulatory T cells (Treg) (1-3). The mouse IL-2 R alpha cDNA encodes a 268 amino acid (aa) precursor that includes a 21 aa signal peptide, a 215 aa extracellular domain (ECD) with two Sushi domains, a 21 aa transmembrane segment, and an 11 aa cytoplasmic domain (4, 5). Within the ECD, mouse IL-2 R alpha shares 81% and 58% aa sequence identity with rat and human IL-2 R alpha, respectively. It shares approximately 15% aa sequence identity with IL-4, -7, -9, -15, and -21 receptor subunits that also complex with gamma c. IL-2 R beta (CD122) and gamma c (IL-2 R gamma /CD132) dimerize to form a constitutively expressed intermediate affinity IL-2 receptor (6, 7). By itself, IL-2 R alpha binds IL-2 with low affinity. It associates with IL-2 R beta and gamma c to generate a ternary high affinity IL-2 receptor complex (8). A soluble form of IL-2 R alpha can be generated by proteolytic cleavage of the cell surface receptor, rendering the T cell unresponsive to IL-2 (9, 10). Increased serum levels of soluble IL-2 R alpha are found in some cancers and immune disorders (11). IL-2 R alpha is required for activation induced cell death (AICD) of naive T cells, a mechanism responsible for deleting autoreactive T cell clones (12, 13). IL-2 R alpha is also required for the development of CD4+CD25+ Treg which suppress autoreactive CD4+ T cells, thereby contributing to peripheral T cell homeostasis (12-14).
- Minami, Y. et al. (1993) Annu. Rev. Immunol. 11:245.
- Kovanen, P.E. and W.J. Leonard (2004) Immunol. Rev. 202:67.
- Bluestone, J.A. and Q. Tang (2005) Curr. Opin. Immunol. 17:638.
- Miller, J. et al. (1985) J. Immunol. 134:4212.
- Shimuzu, A. et al. (1985) Nucleic Acids Res. 13:1505.
- Hatakeyama, M. et al. (1989) Science 244:551.
- Takeshita, T. et al. (1992) Science 257:379.
- Wang, X. et al. (2005) Science 310:1159.
- Wagner, D.K. et al. (1986) J. Immunol. 137:592.
- Schulz, O. et al. (1998) J. Exp. Med. 187:271.
- Witkowska, A.M. (2005) Mediat. Inflamm. 2005:121.
- Willerford, D.M. et al. (1995) Immunity 3:521.
- Van Parijs, L. et al. (1997) J. Immunol. 158:3738.
- Almeida, A.R.M. et al. (2002) J. Immunol. 169:4850.
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