The structural shift of a DNA template between a hairpin and a dimer tunes the emission color of DNA-templated AgNCs.

The scaffolding DNA sequence and the size of silver nanoclusters (AgNCs), confined in a DNA template are the key parameters in determining the fluorescent properties of DNA-stabilized silver nanoclusters (DNA/AgNCs). In addition, we suggest here that the structural shift of a DNA hairpin-dimer is as important as the DNA sequence in determining the emission wavelength of DNA/AgNCs. Furthermore, we show that the structural shift post AgNC formation can be triggered by incubation time and pre-AgNC formation under salt conditions.

Improvement of treatment outcome over 2 decades in children with acute myeloid leukemia.

Background: The prognosis of pediatric acute myeloid leukemia (AML) has recently improved. This study aimed to describe the epidemiology, changes in treatment strategies, and improvement of outcomes in Gwangju-Chonnam children with AML over 2 decades.

Methods: Medical records of 116 children with newly diagnosed AML were retrospectively reviewed for demographic characteristics, prognostic groups including cytogenetic risks, treatment protocols, and survival rates over the periods between 1996 and 2005 (Period I, N=53), and 2006 and 2015 (Period II, N=38).

Direct interaction of menin leads to ubiquitin-proteasomal degradation of β-catenin.

Menin, encoded by the multiple endocrine neoplasia type 1 (MEN1) gene, is a tumor suppressor and transcription regulator. Menin interacts with various proteins as a scaffold protein and is proposed to play important roles in multiple physiological and pathological processes by controlling gene expression, proliferation, and apoptosis. The mechanisms underlying menin's suppression of tumorigenesis are largely elusive.

A Pediatric Case of Severe Fever with Thrombocytopenia Syndrome in Korea.

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease and elderly people living in rural areas have the greatest risk of infection. We report the first pediatric case of SFTS in Korea and the clinical characteristics and disease progression in children. A 10-year-old child from Chonnam province visited the hospital with myalgia and a history of fever over the previous 8 days.

Differential regulation of the histone chaperone HIRA during muscle cell differentiation by a phosphorylation switch.

Replication-independent incorporation of variant histone H3.3 has a profound impact on chromatin function and numerous cellular processes, including the differentiation of muscle cells. The histone chaperone HIRA and H3.

Identification of small molecules that inhibit the histone chaperone Asf1 and its chromatin function.

The eukaryotic genome is packed into chromatin, which is important for the genomic integrity and gene regulation. Chromatin structures are maintained through assembly and disassembly of nucleosomes catalyzed by histone chaperones. Asf1 (anti-silencing function 1) is a highly conserved histone chaperone that mediates histone transfer on/off DNA and promotes histone H3 lysine 56 acetylation at globular core domain of histone H3.

The role of tumor suppressor menin in IL-6 regulation in mouse islet tumor cells.

Menin is a gene product of multiple endocrine neoplasia type1 (Men1), an inherited familial cancer syndrome characterized by tumors of endocrine tissues. To gain insight about how menin performs an endocrine cell-specific tumor suppressor function, we investigated the possibility that menin was integrated in a cancer-associated inflammatory pathway in a cell type-specific manner. Here, we showed that the expression of IL-6, a proinflammatory cytokine, was specifically elevated in mouse islet tumor cells upon depletion of menin and Men(-/-) MEF cells, but not in hepatocellular carcinoma cells.

The role of histone chaperones in osteoblastic differentiation of C2C12 myoblasts.

Cellular differentiation is a process in which the cells gain a more specialized shape, metabolism, and function. These cellular changes are accompanied by dynamic changes in gene expression programs. In most cases, DNA methylation, histone modification, and variant histones drive the epigenetic transition that reprograms the gene expression.