SUMO1 Human His

Small Ubiquitin-Related Modifier 1 (SUMO1) is a member of the SUMO protein family, which plays a crucial role in various cellular processes through a post-translational modification system known as SUMOylation. SUMOylation involves the attachment of SUMO proteins to target proteins, thereby altering their function, localization, and stability .

SUMO1 is a small protein consisting of 101 amino acids and has a molecular mass of approximately 12.6 kDa . The human recombinant version of SUMO1, tagged with a His (histidine) tag, is produced in E. coli and purified using chromatographic techniques . The His tag facilitates the purification process by allowing the protein to bind to metal affinity columns.

SUMO1 is similar to ubiquitin but differs in its function. Unlike ubiquitin, which primarily tags proteins for degradation, SUMO1 is involved in various cellular processes such as nuclear-cytosolic transport, transcriptional regulation, apoptosis, and protein stability . SUMOylation is a reversible process, and deSUMOylating enzymes can remove SUMO1 from target proteins, allowing for dynamic regulation of protein function .

The SUMOylation process involves an enzymatic cascade similar to ubiquitination. It begins with the activation of SUMO1 by the E1 enzyme complex (SAE1-SAE2), followed by its transfer to the E2 enzyme (UBE2I). The E3 ligases, such as PIAS1-4, RANBP2, or CBX4, then facilitate the attachment of SUMO1 to the target protein .

SUMO1 modification has been shown to influence various cellular outcomes, including altered localization and binding partners of target proteins . For example, the SUMOylation of RanGAP1 leads to its trafficking from the cytosol to the nuclear pore complex, while the SUMOylation of ninein results in its movement from the centrosome to the nucleus . Additionally, SUMO1 modification of transcriptional regulators often correlates with the inhibition of transcription .

Mutations or dysregulation of SUMO1 have been associated with several diseases, including Orofacial Cleft 10 and Amelogenesis Imperfecta, Type Ie . Understanding the role of SUMO1 in these conditions can provide insights into potential therapeutic targets and strategies.