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The reversible posttranslational modification of proteins by the addition of small ubiquitin-like SUMO proteins (see SUMO1\; MIM 601912) is required for numerous biologic processes. Additionally we are shipping ULP1 Antibodies (55) and ULP1 Proteins (4) and many more products for this protein.
The present study examined dynamic changes in SENP3 expression in the cerebral cortex and in its cellular localization.
The p53-independent tumor suppressive functions of p19(Arf) may be mediated by its ability to antagonize Senp3, thereby inducing cell cycle arrest by abnormally elevating the cellular levels of SUMOylated proteins.
High SENP3 expression is associated with stomach neoplasms.
SENP3, which is increased in gastric cancer cells, potentiates the transcriptional activity of FOXC2 (show FOXC2 ELISA Kits) through de-SUMOylation, in favor of the induction of specific mesenchymal gene expression in gastric cancer metastasis.
Evidence show that mTOR (show FRAP1 ELISA Kits)-mediated phosphorylation of SENP3 facilitates the interaction with NPM1 (show NPM1 ELISA Kits), thereby promoting nucleolar targeting.
SENP3 is associated with MLL1/MLL2 (show MLL2 ELISA Kits) complexes and catalyzes deSUMOylation of RbBP5 (show RBBP5 ELISA Kits).
ROS (show ROS1 ELISA Kits) induced SENP3 redistribution from the nucleoli to the nucleoplasm.
In a novel adaptive pathway to extreme cell stress, dynamic changes in SENP3 stability and regulation of Drp1 (show CRMP1 ELISA Kits) SUMOylation are crucial determinants of cell fate.
The shift of HIF-1 (show HIF1A ELISA Kits) transactivation by reactive oxidative species is correlated with and dependent on the biphasic redox sensing of SENP3 that leads to the differential SENP3/p300 (show EP300 ELISA Kits) interaction and the consequent fluctuation in the p300 (show EP300 ELISA Kits) SUMOylation status.
These results suggest that SMT3IP1 is a new regulator of the p53 (show TP53 ELISA Kits)-Mdm2 (show MDM2 ELISA Kits) pathway.
Hsp90 (show HSP90 ELISA Kits)/SENP3 association protects SENP3 from CHIP-mediated ubiquitination and subsequent degradation, but this effect of Hsp90 (show HSP90 ELISA Kits) requires the presence of CHIP.
SENP3-mediated de-conjugation of SUMO2 (show SUMO2 ELISA Kits)/3 from promyelocytic leukemia (show PML ELISA Kits) is correlated with accelerated cell proliferation under mild oxidative stress.
The reversible posttranslational modification of proteins by the addition of small ubiquitin-like SUMO proteins (see SUMO1\; MIM 601912) is required for numerous biologic processes. SUMO-specific proteases, such as SENP3, are responsible for the initial processing of SUMO precursors to generate a C-terminal diglycine motif required for the conjugation reaction. They also have isopeptidase activity for the removal of SUMO from high molecular mass SUMO conjugates (Di Bacco et al., 2006
SUMO-1-specific protease 3
, SUMO/sentrin specific protease 3
, sentrin-specific protease 3
, sentrin/SUMO-specific protease SENP3
, smt3-specific isopeptidase 1
, sentrin/SUMO-specific protease 3
, SUMO/sentrin specific peptidase 3