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.

Aberrant neddylation of non-cullin substrates disrupts normal cell cycle progression.

In cortical pyramidal neurons, subtype-specific SUMOylation of Na+ channels regulates input-output relationships, synaptic boosting, and action potential propagation from the axonal trigger zone back into the dendrites.

The Anaphase Promoting Complex/Cyclosome is regulated by sumoylation to ensure timely mitotic exit in human cells.

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.

The natural compounds cordycepin and mycophenolic acid stimulate alternative polyadenylation through opposing effects on transcriptional rate.

Shigella infection induces a calpain-mediated loss of SUMO conjugates that promotes bacterial entry.

When a protein involved in DNA repair malfunctions, it can anneal RNA molecules to DNA molecules, creating hybrids that increase the frequency of mutations in the DNA.

Near atomic resolution of late 40S ribosomal subunit assembly by cryo-EM reveals immature rRNA active sites stabilized by biogenesis factors.