Selective retrieval of task-relevant information often facilitates memory retention of that information. However, it is still unclear if selective retrieval of task-relevant information can alter memory for task-irrelevant information, and the role of emotional arousal in it. In two experiments, we used emotional and neutral faces as stimuli, and participants were asked to memorise the name (who is this person?) and location (where does he/she come from?) associated with each face in initial study. Then, half of the studied faces were (...) presented as cues, and participants were asked to retrieve the corresponding names (Experiment 1) or locations (Experiment 2). Finally, all the faces were presented and participants were asked to retrieve both the corresponding names and locations. The results of the final test showed that retrieval practice not only enhanced memory of task-relevant information but also enhanced memory of task-irrelevant information. More importantly, negative emotion amplified the retrieval practice effect overall, with a larger retrieval-induced benefit for the negative than neutral condition. These findings demonstrated an emotional arousal amplification effect on retrieval-induced enhancement effects, suggesting that the advantage of the retrieved memory representations can be amplified by emotional arousal even without explicit goals in a task setting. (shrink)

Neddylation, a ubiquitylation‐like post‐translational modification, is catalyzed by a cascade composed of three enzymes: E1 activating enzyme, E2 conjugating enzyme, and E3 ligase with cullins as physiological substrates. Specifically, neddylation E2 UBE2M couples with E3 RBX1 to neddylate cullins 1–4, whereas neddylation E2 UBE2F couples with E3 RBX2/SAG to neddylate cullin 5, leading to activation of CRL1‐4 (Cullin‐RING ligases 1–4) and CRL5, respectively. While over‐activation of the neddylation‐CRLs axis occurs frequently in many human cancers, how neddylation‐CRLs regulate the function of (...) immune cells, particularly Treg cells was previously unknown. To this end, we recently performed Treg selective knockout of two neddylation E2s and two E3s, individually, driven by Foxp3‐Cre, and found that while the Ube2f‐Sag E2/E3 pair plays a minimal role, if any, the Ube2m‐Rbx1 pair is essential for the maintenance of Treg functionality, since their deletion triggers robust inflammatory response with autoimmune phenotypes. Milder phenotype severity upon Treg KO of upstream Ube2m than that of downstream Rbx1 strongly suggested that Rbx1 regulates Treg function in a manner dependent and independent of neddylation. (shrink)