FUS/TLS (E3O8I) Rabbit mAb #67840

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).