Anti-SENP1 Rabbit mAb

Uncategorized

Ambient temperature

73

SENP1 is a member of the sentrin/SUMO-specific protease (SENP) family. SENP1 localizes to the nucleoplasm and catalyzes the release of SUMO1, SUMO2, and SUMO3 monomers from sumoylated substrates. SENP1 has been reported to be responsible for intracellular SUMO homeostasis in the control of normal cellular function. The removal of sumoylation by SENP1 from many important target proteins, such as HDAC1, HIF-1α, , Stat5, p300, Elk-1, and SirT1, leads to the regulation of the related biological pathways. SENP1-induced desumoylation ofHIF-1α stabilizes the target during hypoxia, activating downstream VEGF expression and angiogenesis. SENP1 desumoylates Stat5 andcontributes to Stat5 acetylation and subsequent signaling during normal lymphocyte development. Under stress conditions, SENP1 interactswith and inactivates SirT1 by desumoylation, protecting cells from apoptosis. SENP1 has been reported to target the progesterone andandrogen receptors, either directly or indirectly through HDAC1, thereby upregulating their transcriptional function and potentially affectingreceptor-related cancer progression

PBS, Glycerol, BSA

Peptide

SENP1 is a member of the sentrin/SUMO-specific protease (SENP) family. SENP1 localizes to the nucleoplasm and catalyzes the release of SUMO1, SUMO2, and SUMO3 monomers from sumoylated substrates. SENP1 has been reported to be responsible for intracellular SUMO homeostasis in the control of normal cellular function. The removal of sumoylation by SENP1 from many important target proteins, such as HDAC1, HIF-1α, , Stat5, p300, Elk-1, and SirT1, leads to the regulation of the related biological pathways. SENP1-induced desumoylation of
HIF-1α stabilizes the target during hypoxia, activating downstream VEGF expression and angiogenesis. SENP1 desumoylates Stat5 and
contributes to Stat5 acetylation and subsequent signaling during normal lymphocyte development. Under stress conditions, SENP1 interacts
with and inactivates SirT1 by desumoylation, protecting cells from apoptosis. SENP1 has been reported to target the progesterone and
androgen receptors, either directly or indirectly through HDAC1, thereby upregulating their transcriptional function and potentially affecting
receptor-related cancer progression