Recombinant Human SNRP70/U1-70K protein

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

SNRP70 also known as U1-70K is a protein component of the spliceosomal U1 small nuclear ribonucleoprotein (snRNP) complex. It has a molecular mass of approximately 70 kDa. This protein is mainly expressed in the nucleus of eukaryotic cells. SNRP70 binds to the U1 snRNA facilitating the early stages of pre-mRNA splicing. It stabilizes the binding of the U1 snRNP to the 5' splice site therefore playing a role in recognizing and defining correct splice sites necessary for mRNA maturation.

Biological function summary

This protein is integral to the spliceosome a large multi-component complex responsible for removing introns from pre-mRNA. SNRP70 interacts with other core components of the U1 snRNP such as U1A and U1C proteins to assemble the complex. It ensures the accuracy of splice site recognition and contributes to the dynamic rearrangement of the spliceosome during splicing. These interactions importantly influence the regulation of gene expression by facilitating alternative splicing which allows a single gene to code for multiple proteins.

Pathways

SNRP70 is actively involved in the mRNA processing pathway a critical process in gene expression regulation. Its function directly links to the RNA splicing pathway ensuring the generation of mature mRNA from precursor transcripts. SNRP70's role in the spliceosomal complex places it in association with other spliceosome-related proteins such as SF3B1. This interconnectedness with SF3B1 supports the protein's engagement in ensuring accurate splicing and modulating gene expression through alternative splicing events.

Disruptions in SNRP70 function associate with certain autoimmune conditions and neurodegenerative diseases. For instance autoantibodies against SNRP70 are characteristic in patients with systemic lupus erythematosus (SLE) an autoimmune disorder. Also aberrant splicing events involving SNRP70 contribute to the pathology of certain neurodegenerative diseases such as spinal muscular atrophy. In these conditions the misregulation of splicing factors can exacerbate disease progression linking SNRP70 with other autoantigen proteins like Sm proteins in SLE.