Temporal coordination of the transcription factor response to HO stress.

Oxidative stress from excess HO activates transcription factors that restore redox balance and repair oxidative damage. Although many transcription factors are activated by HO, it is unclear whether they are activated at the same HO concentration, or time. Dose-dependent activation is likely as oxidative stress is not a singular state and exhibits dose-dependent outcomes including cell-cycle arrest and cell death.

Blocked Presentation Leads Participants to Overutilize Domain Familiarity as a Cue for Judgments of Learning (JOLs).

The accuracy of judgments of learning (JOLs) is vital for efficient self-regulated learning. We examined a situation in which participants overutilize their prior knowledge of a topic ("domain familiarity") as a basis for JOLs, resulting in substantial overconfidence in topics they know the most about. College students rank ordered their knowledge across ten different domains and studied, judged, and then completed a test on facts from those domains.

Temporal Coordination of the Transcription Factor Response to HO stress.

Oxidative stress from excess HO activates transcription factors (TFs) that restore redox balance and repair oxidative damage. Though many TFs are activated by HO, it is unknown whether they are activated at the same HO concentration or time after HO stress. We found TF activation is tightly coordinated over time and dose dependent.

Temporal Coordination of the Transcription Factor Response to HO stress.

The p53 and FOXO transcription factors (TFs) share many similarities despite their distinct evolutionary origins. Both TFs are activated by a variety of cellular stresses and upregulate genes in similar pathways including cell-cycle arrest and apoptosis. Oxidative stress from excess HO activates both FOXO1 and p53, yet whether they are activated at the same time is unclear.

FOXO nuclear shuttling dynamics are stimulus-dependent and correspond with cell fate.

FOXO transcription factors are regulators of cellular homeostasis linked to increased lifespan and tumor suppression. FOXOs are activated by diverse cell stresses including serum starvation and oxidative stress. FOXO activity is regulated through posttranslational modifications that control shuttling of FOXO proteins to the nucleus.