FUS/TLS Antibody #4885
- WB
Supporting Data
| REACTIVITY | H M R Mk |
| SENSITIVITY | Endogenous |
| MW (kDa) | 70 |
| SOURCE | Rabbit |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
- Mk-Monkey
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
Storage
Protocol
Specificity / Sensitivity
FUS/TLS Antibody recognizes endogenous levels of total FUS/TLS protein.
Species Reactivity:
Human, Mouse, Rat, Monkey
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:
Hamster, Bovine, Horse, Guinea Pig
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly272 of human TLS/FUS protein. Antibodies are purified by protein A and peptide affinity chromatography.
Background
FUS/TLS (fused in sarcoma/translocated in liposarcoma) was initially identified by investigators as a component of fusion proteins found in a variety of cancers, such as myxoid liposarcoma, acute myeloid leukemia, and Ewing’s tumor (1). FUS/TLS fusion with the DNA-binding domain of transcription activators, such as CHOP and ERG, leads to aberrant transcription of target genes that is thought by researchers to lead to tumor development (1-5). FUS/TLS is involved in a wide range of RNA processing events, such as pre-mRNA splicing, mRNA transcription, and miRNA processing (1,6). In addition to its role in RNA metabolism, FUS/TLS maintains genomic stability and co-regulates gene expression by interacting with various transcription factors such as nuclear receptors, YB-1, p65 subunit of NF-κB, TFIID, and RUNX2 (1,6,7). More recently, researchers have found several mutations of FUS/TLS in ALS (amyotrophic lateral sclerosis) and FTLD (frontotemporal lobar degeneration) patients that causes cytoplasmic mislocalization of FUS/TLS (6,8-12).
- Yang, S. et al. (2010) Int J Biochem Cell Biol 42, 1408-11.
- Crozat, A. et al. (1993) Nature 363, 640-4.
- Rabbitts, T.H. et al. (1993) Nat Genet 4, 175-80.
- Law, W.J. et al. (2006) Brief Funct Genomic Proteomic 5, 8-14.
- Prasad, D.D. et al. (1994) Oncogene 9, 3717-29.
- Lagier-Tourenne, C. et al. (2010) Hum Mol Genet 19, R46-64.
- Baechtold, H. et al. (1999) J Biol Chem 274, 34337-42.
- Hewitt, C. et al. (2010) Arch Neurol 67, 455-61.
- Vance, C. et al. (2009) Science 323, 1208-11.
- Van Langenhove, T. et al. (2010) Neurology 74, 366-71.
- Da Cruz, S. and Cleveland, D.W. (2011) Curr Opin Neurobiol 21, 904-19.
- Hock, E.M. et al. (2018) Cell Rep 24, 987-1000.e7.
Limited Uses
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