Ezh2 (D2C9) XP® Rabbit mAb (Alexa Fluor® 647 Conjugate) #45638
- F
Supporting Data
| REACTIVITY | H M R Mk |
| SENSITIVITY | Endogenous |
| MW (kDa) | |
| Source/Isotype | Rabbit IgG |
Application Key:
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
- Mk-Monkey
Product Information
Product Description
Product Usage Information
| Application | Dilution |
|---|---|
| Flow Cytometry (Fixed/Permeabilized) | 1:50 |
Storage
Protocol
Specificity / Sensitivity
Ezh2 (D2C9) XP® Rabbit mAb (Alexa Fluor® 647 Conjugate) detects endogenous levels of total Ezh2 protein.
Species Reactivity:
Human, Mouse, Rat, Monkey
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Arg354 of human Ezh2 protein.
Background
The polycomb group (PcG) proteins are involved in maintaining the silenced state of several developmentally regulated genes and contribute to the maintenance of cell identity, cell cycle regulation, and oncogenesis (1,2). Enhancer of zeste homolog 2 (Ezh2), a member of this large protein family, contains four conserved regions including domain I, domain II, and a cysteine-rich amino acid stretch that precedes the carboxy-terminal SET domain (3). The SET domain has been linked with histone methyltransferase (HMTase) activity. Moreover, mammalian Ezh2 is a member of a histone deacetylase complex that functions in gene silencing, acting at the level of chromatin structure (4). Ezh2 complexes methylate histone H3 at Lys9 and 27 in vitro, which is thought to be involved in targeting transcriptional regulators to specific loci (5). Ezh2 is deregulated in various tumor types, and its role, both as a primary effector and as a mediator of tumorigenesis, has become a subject of increased interest (6).
- Sellers, W.R. and Loda, M. (2002) Cancer Cell 2, 349-50.
- Visser, H.P. et al. (2001) Br J Haematol 112, 950-8.
- Chen, H. et al. (1996) Genomics 38, 30-7.
- Tonini, T. et al. (2004) Oncogene 23, 4930-7.
- Müller, J. et al. (2002) Cell 111, 197-208.
- Kleer, C.G. et al. (2003) Proc Natl Acad Sci U S A 100, 11606-11.
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