Publications by authors named "L E Rieder"
To ensure that the embryo can package exponentially increasing amounts of DNA, replication-dependent histones are some of the earliest transcribed genes from the zygotic genome. However, how the histone genes are identified is not known. The pioneer factor CLAMP regulates the embryonic histone genes and helps establish the histone locus body, a suite of factors that controls histone mRNA biosynthesis, but CLAMP is not unique to the histone genes.
View Article and Find Full Text PDFIntroduction: The COVID-19 pandemic, led to significant global health challenges. Medical services worldwide had to reconfigure to manage the surge in COVID-19 cases, including oncological abdominal surgery (OAS). This study investigates the impact of the pandemic on the OAS workforce and aims to enhance future healthcare preparedness to potential pandemics.
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- The study examined the brain regions affected during seizures in 34 patients with epilepsy linked to hypothalamic hamartoma through long-term video-EEG monitoring.
- It found that seizure activity predominantly involved frontal and temporal areas, with advanced disease showing more frontal region involvement and distinct patterns based on seizure type.
- The findings suggest variations in cortical involvement based on disease stage and cognitive function, which may aid in understanding epilepsy progression and inform surgical treatment options.
Article Synopsis
- The () gene is identified as a maternal-effect lethal gene that regulates core histones, but existing mutant strains may have background genetic mutations affecting results.
- Researchers developed two new tools: a CRISPR/Cas9 knockout for genetic analysis and an epitope-tagged allele for studying cellular effects, confirming that the gene causes maternal-effect lethality that can be mitigated by reducing histone gene copies.
- Despite previous beliefs, they found that the gene does not repress core histone transcript levels, leaving the molecular reasons for its lethal effects still unclear.
Article Synopsis
- ER stress leads to overall repression of protein synthesis in cells, complicating understanding of localized translation effects.
- Live-cell imaging revealed that translation at mitochondria is surprisingly protected during ER stress, linked to the ATAD3A protein's interaction with the PERK protein.
- The binding of ATAD3A to PERK reduces local PERK signaling, enabling some mitochondrial proteins to continue being expressed despite the stress response.