Publications by authors named "Bryce A Wilson"

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.

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Article Synopsis
  • Both p53 and FOXO transcription factors (TFs) are activated by cellular stresses and regulate similar cellular processes like cell-cycle arrest and apoptosis, even though they evolved separately.
  • Cells respond to high levels of oxidative stress (HO) in two phases: initially, FOXO1 moves to the nucleus while p53 remains low, and later, FOXO1 exits the nucleus as p53 levels increase.
  • Different sets of TFs are activated during each phase, leading to significant variations in gene expression, and the timing of these phases is influenced by 2-Cys peroxiredoxins in response to oxidative stress.
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Amyotrophic lateral sclerosis (ALS) is a fatal, complex neurodegenerative disorder that causes selective degeneration of motor neurons. ALS patients exhibit symptoms consistent with altered cellular energetics such as hypermetabolism, weight loss, dyslipidemia, insulin resistance, and altered glucose tolerance. Although evidence supports metabolic changes in ALS patients, metabolic alterations at a cellular level remain poorly understood.

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Cohort-based whole exome and whole genome sequencing and copy number variant (CNV) studies have identified genetic etiologies for a sizable proportion of patients with cerebral palsy (CP). These findings indicate that genetic mutations collectively comprise an important cause of CP. We review findings in CP genomics and propose criteria for CP-associated genes at the level of gene discovery, research study, and clinical application.

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