Anti-SF3A1 antibody [EPR7666] - BSA and Azide free

Supplementary info

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

Activity summary

The SF3A1 protein also known as SAP114 is a component of the spliceosomal subunit SF3a critical for pre-mRNA splicing. It is approximately 79 kDa in mass. SF3A1 is expressed in various tissues contributing to its broad functional role. The protein is central in assembling the active spliceosome complex facilitating the precise removal of introns from pre-mRNA through exon recognition. This mechanical role is vital for synthesizing mature mRNA molecules necessary for proper gene expression.

Biological function summary

SF3A1 operates as an integral part of the SF3a complex which also consists of SF3A2 and SF3A3. This complex associates with the U2 small nuclear ribonucleoprotein (snRNP) within the spliceosome. The role of SF3A1 in the assembly and stability of this complex is significant ensuring efficient splicing of pre-mRNA. By doing this SF3A1 contributes to the regulation of gene expression by allowing for the generation of multiple mRNA variants from single genes a process known as alternative splicing.

Pathways

SF3A1 plays an important role in the splicing of pre-mRNA an important step in the RNA processing pathway. This pathway ensures that non-coding regions are accurately removed and exons are joined to produce functional mRNA transcripts. SF3A1 works in conjunction with proteins like SF3B1 and U2AF both of which are also spliceosome components. Together these facilitate the selection of splice sites impacting the production of proteins within the cell by influencing mRNA variants that are translated.

Associated diseases and disorders

SF3A1 alterations have been implicated in myelodysplastic syndromes (MDS) and certain cancers. Mutations or dysregulation of SF3A1 are associated with aberrant splicing patterns contributing to the pathology of these diseases. For instance in MDS SF3A1 mutations may cause ineffective hematopoiesis through improper mRNA processing. SF3A1 interacts with other spliceosomal proteins like U2AF1 where alterations can lead to similar splicing defects that exacerbate disease conditions. Understanding SF3A1's role in such pathologies opens prospects for therapeutic interventions targeting splicing mechanisms.