FUS
FUS (FUS DNA/RNA binding protein, also known as TLS, FUS1, hnRNP-P2 and HNRNPP2) is a nuclear DNA/RNA-binding protein of the FET family. It contributes to transcription regulation, RNA splicing, RNA transport and DNA repair, and defects in the FUS gene cause amyotrophic lateral sclerosis type 6. Browse Assay Genie's current range of FUS research reagents below, or read on for the biology behind the target.
FUS is a multifunctional DNA/RNA-binding protein that plays a role in transcription regulation, RNA splicing, RNA transport, DNA repair and the damage response. It binds single-stranded RNA containing the consensus sequence 5'-AGGUAA-3'. By binding nascent pre-mRNAs, FUS acts as a molecular mediator between RNA polymerase II and U1 small nuclear ribonucleoprotein, thereby coupling transcription and splicing. It also binds its own pre-mRNA and autoregulates its expression, a mechanism mediated by non-sense-mediated decay.
In DNA repair, FUS promotes D-loop formation and homologous recombination during double-strand break repair. In neuronal cells it has crucial roles in dendritic spine formation and stability, RNA transport, mRNA stability and synaptic homeostasis. The protein localises to the nucleus. Anyone working with a FUS antibody, FUS ELISA kit or recombinant FUS protein will usually be studying these RNA-processing and genome-maintenance functions.
The FUS gene encodes a component of the heterogeneous nuclear ribonucleoprotein (hnRNP) complex, which is involved in pre-mRNA splicing and export of fully processed mRNA to the cytoplasm. FUS belongs to the FET family of RNA-binding proteins, implicated in regulation of gene expression, maintenance of genomic integrity and mRNA/microRNA processing, and to the RRM TET family. Its HGNC gene group memberships include RANBP2-type zinc fingers, RNA binding motif containing proteins and hnRNPs. Alternative splicing produces multiple transcript variants. The name fused in sarcoma reflects the original description of the gene in the t(12;16) translocation of malignant liposarcoma, and defects in the gene result in amyotrophic lateral sclerosis type 6 (ALS6). The mouse ortholog is Fus.
Defects in the FUS gene result in amyotrophic lateral sclerosis type 6, making FUS central to studies of motor neuron disease.
FUS binds nascent pre-mRNAs and links RNA polymerase II to U1 snRNP, coupling transcription with splicing.
FUS promotes D-loop formation and homologous recombination during double-strand break repair, supporting work on genomic integrity.
In neuronal cells FUS contributes to dendritic spine formation and stability, RNA transport, mRNA stability and synaptic homeostasis.
FUS is a DNA/RNA-binding protein involved in transcription regulation, RNA splicing, RNA transport and DNA repair. It couples transcription to splicing by bridging RNA polymerase II and U1 snRNP, and it promotes homologous recombination in double-strand break repair. In neurons it supports synaptic homeostasis.
FUS is also called TLS, FUS1, hnRNP-P2, HNRNPP2 and ALS6. Earlier names include fused in sarcoma and fusion, derived from t(12;16) malignant liposarcoma. UniProt lists the protein as RNA-binding protein FUS, and alternative splicing yields multiple transcript variants.
Defects in the FUS gene result in amyotrophic lateral sclerosis type 6. The mouse has an ortholog, Fus, so rodent models can be used to study the protein. Check the datasheet of any product for its validated reactivity.
RNA-binding proteins, hnRNP family members and neurodegeneration markers with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt P35637; product specifications from Assay Genie datasheets.