Wss1 is both a metalloprotease and SUMO ligase found in association with Cdc48 and Doa1 and accumulating in the vacuole upon DNA damage.

Analyses using His6-HA-SUMO1 and SUMO1 KO mice indicate that SUMO1 modification of synaptic proteins is either absent or cannot be detected in brain and cultured neurons.

The SUMO-Ub-Cdc48 pathway is a novel regulatory mechanism of Pol III and a potential therapeutic target for Pol III-related human diseases.

Simulations of molecular dynamics suggest how the binding of the β-grasp domain of SUMO1 induces conformational and dynamic effects to activate SENP1.

Hinokiflavone is identified as a splicing modulator that blocks progression from spliceosome complex A to complex B and inhibits SUMO protease SENP1, causing hyper-SUMOylation affecting 6 U2 snRNP proteins.

Ptch1/2 can lower the sensitivity of Smo to activation by Shh via the secretion of a sterol precursor.

Multi-fiber photometry recording and circuit-based manipulation in vivo identify a long-range SuM-DG circuit linking two highly correlated subcortical regions to regulate spatial memory retrieval through SuM glutamate transmission.

The immediate response of the brain to a sudden, harmful drop in oxygen supply is the addition of SUMO proteins to sodium ion channels in neurons, increasing their activity.

In vivo inhibition of SUMO activating E1-enzymes by pyrophosphate reveals a mode of integrating metabolism and stress tolerance that is conserved across kingdoms.

The FDA-approved compound and plant extract tannic acid is a non-toxic chemical tool for modulating sumoylation in multiple platforms.