Enhancer of SUMO conjugation. Via its interaction with UBE2I/UBC9, increases SUMO conjugation to proteins by promoting the binding of E1 and E2 enzymes, thioester linkage between SUMO and UBE2I/UBC9 and transfer of SUMO to specific target proteins which include HIF1A, PIAS, NFKBIA, NR3C1 and TOP1. Isoform 1 and isoform 2 positively regulate the NF-kappa-B signaling pathway by enhancing the sumoylation of NF-kappa-B inhibitor alpha (NFKBIA), promoting its stabilization which consequently leads to an increased inhibition of NF-kappa-B transcriptional activity. Isoform 1 and isoform 2 negatively regulate the hypoxia-inducible factor-1 alpha (HIF1A) signaling pathway by increasing the sumoylation of HIF1A, promoting its stabilization, transcriptional activity and the expression of its target gene VEGFA during hypoxia. Isoform 2 promotes the sumoylation and transcriptional activity of the glucocorticoid receptor NR3C1 and enhances the interaction of SUMO1 and NR3C1 with UBE2I/UBC9. Has no effect on ubiquitination. Isoform 1 and isoform 2 interact with UBE2I/UBC9 (PubMed:17956732, PubMed:23469069, PubMed:25918163). Isoform 1 shows a greater interaction with NFKBIA and HIF1A as compared to isoform 2 (PubMed:17956732, PubMed:23469069). Isoform 2 interacts with NCOA2 and NR3C1 (PubMed:23508108). Colocalizes with UBC9/UBE2I in nuclear spots. Isoform 1 and isoform 2 are expressed in glioma tumors (at protein level). Expressed in a wide number of tissues with highest expression in cerebellum, pituitary, heart, kidney, liver, stomach, pancreas, prostate and spleen. Low levels in thalamus, spinal cord, esophagus, thymus, lung and peripheral blood leukocytes. A higher level expression seen in pituitary tumors as compared to the pituitary gland. Induced by hypoxia and heat shock. The RWD domain is required for the sumoylation enhancement activity.