ERG (A7L1G) Rabbit mAb (PE Conjugate) #16606
- F
Supporting Data
| REACTIVITY | H M |
| SENSITIVITY | Endogenous |
| MW (kDa) | |
| Source/Isotype | Rabbit IgG |
Application Key:
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
Product Information
Product Description
Product Usage Information
| Application | Dilution |
|---|---|
| Flow Cytometry (Fixed/Permeabilized) | 1:50 |
Storage
Protocol
Specificity / Sensitivity
ERG (A7L1G) Rabbit mAb (PE Conjugate) recognizes endogenous levels of total ERG protein. Based on sequence identity, this antibody should detect isoforms ERG1, ERG2, and ERG3. This antibody does not cross-react with Fli1.
Species Reactivity:
Human, Mouse
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:
Rat, Hamster, Pig, Horse, Guinea Pig
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human ERG protein.
Background
ETS-related gene (ERG) is a member of the E-26 transformation-specific (ETS) family of sequence-specific DNA-binding transcription factors (1). ERG plays important and highly conserved roles in vertebrate development. Early in embryonic development, ERG is highly expressed in the embryonic mesoderm and endothelium, where it plays a critical role in the formation of the vascular system, urogenital tract and bone development (2,3). Later in embryonic development, ERG functions to regulate the pluripotency of hematopoietic stem cells, endothelial cell homeostasis and angiogenesis (2,4-7). ERG expression is not restricted to development. In adult mouse, ERG is normally expressed in endothelial tissues, including adrenal, cartilage, heart, spleen, lymphatic endothelial and eosinophil cells (8). However, deregulation of ERG activity, often resulting from chromosomal rearrangements, has been implicated and linked to poor prognosis in a number of different cancers. Chromosomal translocations generating EWS/ERG chimeric proteins comprised of the amino-terminal transactivation domain of Ewing’s sarcoma breakpoint region 1 (EWS) and the carboxy-terminal ETS domain of ERG have been identified in 5-10% of Ewing’s sarcoma, an aggressive bone and soft tissue tumor (9). Chromosomal translocations between ERG and TLS/FUS or ERG and ELF4 have been implicated in acute myeloid leukemia (10, 11). Over-expression of ERG, resulting from gene fusion with the androgen-driven promoter of the TMPRSS2 gene, has been identified as a key driver of metastasis and marker for poor prognosis in prostate cancer (12).
- Adamo, P. and Ladomery, M.R. (2016) Oncogene 35, 403-14.
- Birdsey, G.M. et al. (2008) Blood 111, 3498-506.
- Vijayaraj, P. et al. (2012) Development 139, 3973-85.
- Ng, A.P. et al. (2011) Blood 118, 2454-61.
- Birdsey, G.M. et al. (2015) Dev Cell 32, 82-96.
- Lathen, C. et al. (2014) Circulation 130, 1179-91.
- McLaughlin, F. et al. (2001) Blood 98, 3332-9.
- Mohamed, A.A. et al. (2010) J Cancer 1, 197-208.
- Chen, S. et al. (2016) Genes Chromosomes Cancer 55, 340-9.
- Ichikawa, H. et al. (1994) Cancer Res 54, 2865-8.
- Moore, S.D. et al. (2006) Leuk Res 30, 1037-42.
- Tomlins, S.A. et al. (2005) Science 310, 644-8.
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