IRF-4 (E8H3S) XP® Rabbit mAb (InTraSeq™ 3' Conjugate 3107) #54847
- SCA
Product Specifications
| REACTIVITY | H M |
| SENSITIVITY | Endogenous |
| MW (kDa) | |
| Source/Isotype | Rabbit IgG |
Application Key:
- SCA-Single Cell Analysis
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
Product Information
Storage
Protocol
Specificity / Sensitivity
Species Reactivity:
Source / Purification
Background
IRF-4 was independently cloned by three groups and demonstrated to have roles in different contexts of lymphoid regulation (3-5). First, IRF-4 (Pip) was found to associate with PU.1, a hematopoietic specific member of the ETS family, and to regulate the expression of B-cell specific genes (3). Second, it was characterized as a lymphoid-specific member of the IRF family (LSIRF) able to bind to ISRE (4). Third, it was identified in activated T cells as a factor that binds to the promoter of the interleukin-5 gene (ICSAT), and it was shown to repress gene activation induced by IFN (5). IRF-4 is expressed in all stages of B cell development and in mature T cells, and is inducible in primary lymphocytes by antigen mimetic stimuli such as concavalin A, CD3 crosslinking, anti-IgM and PMA treatment (4,5). Mice deficient in IRF-4 show normal distribution of B and T lymphocytes at 4 to 5 weeks, but later develop progressive generalized lymphadenopathy, suggesting a role for IRF-4 in the function and homeostasis of mature B- and T-lymphocytes (6).
- Taniguchi, T. et al. (2001) Annu Rev Immunol 19, 623-55.
- Honda, K. and Taniguchi, T. (2006) Nat Rev Immunol 6, 644-58.
- Eisenbeis, C.F. et al. (1995) Genes Dev 9, 1377-87.
- Matsuyama, T. et al. (1995) Nucleic Acids Res 23, 2127-36.
- Yamagata, T. et al. (1996) Mol Cell Biol 16, 1283-94.
- Mittrücker, H.W. et al. (1997) Science 275, 540-3.
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