CD25 / IL2RA (Activated Lymphocyte Marker) Antibody - With BSA and Azide
Mouse Monoclonal Antibody [Clone 143-13 ]
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| IF, FC |
---|---|
Primary Accession | P01589 |
Other Accession | 3559, 231367 |
Reactivity | Human |
Host | Mouse |
Clonality | Monoclonal |
Isotype | Mouse / IgG1, kappa |
Clone Names | 143-13 |
Calculated MW | 55kDa |
Gene ID | 3559 |
---|---|
Other Names | Interleukin-2 receptor subunit alpha, IL-2 receptor subunit alpha, IL-2-RA, IL-2R subunit alpha, IL2-RA, TAC antigen, p55, CD25, IL2RA |
Storage | Store at 2 to 8°C.Antibody is stable for 24 months. |
Precautions | CD25 / IL2RA (Activated Lymphocyte Marker) Antibody - With BSA and Azide is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | IL2RA |
---|---|
Function | Receptor for interleukin-2. The receptor is involved in the regulation of immune tolerance by controlling regulatory T cells (TREGs) activity. TREGs suppress the activation and expansion of autoreactive T-cells. |
Cellular Location | Membrane; Single-pass type I membrane protein. |
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Background
Recognizes a protein of 55kDa, identified as CD25 (Workshop IV; Code A27). CD25 is expressed on activated T- and B-cells and activated monocytes/macrophages. With respect to lymphomas, CD25 is present on malignant cells of Hodgkinā€™s disease, HTLV-1+ adult T-cell leukemia, cutaneous T-cell lymphoma, and hair cell leukemia. Increased levels of soluble CD25 are observed in the leukemias/lymphomas and inflammatory/ autoimmune diseases. CD25 molecule alone appears to function as a low affinity receptor and associates with CD122 (IL-2R ļ� � chain, p75) and CD132 (common ļ� � chain) to form the high affinity IL-2 receptor complex. CD25 antibodies detect three epitope regions, A, B and C. This MAb recognizes the epitope B, which is located at residue 3-104 of CD25 and can effectively block IL-2 binding to CD25.
References
Knapp W. et al. Leucocyte typing IV, p. 408- 411 and p. 1080, Oxford University Press, Oxford 1989
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