Sequence-specific DNA binding activity of rat cdc37-related gene product

AbstractThe rat cdc37-related gene product (RCdc37), which is possibly involved in the regulation of cell cycle progression, contains a putative basic/leucine zipper (bZIP) domain in its N-terminal portion. In this study, we have identified a rat genomic sequence which can interact with RCdc37 using an in vitro binding assay. The specificity of this interaction was confirmed by gel retardation experiments. These results raise a possibility that RCdc37 might play an important role in the control of cell cycle progression via a sequence-specific DNA binding mechanism

p53: The Attractive Tumor Suppressor in the Cancer Research Field

p53 is one of the most studied tumor suppressors in the cancer research field. Of note, over 50% of human tumors carry loss of function mutations, and thus p53 has been considered to be a classical Knudson-type tumor suppressor. From the functional point of view, p53 is a nuclear transcription factor to transactivate a variety of its target genes implicated in the induction of cell cycle arrest, DNA repair, and apoptotic cell death. In response to cellular stresses such as DNA damage, p53 is activated and promotes cell cycle arrest followed by the replacement of DNA lesions and/or apoptotic cell death. Therefore, p53 is able to maintain the genomic integrity to prevent the accumulation of genetic alterations, and thus stands at a crossroad between cell survival and cell death. In this paper, we describe a variety of molecular mechanisms behind the regulation of p53

p73-Binding Partners and Their Functional Significance

p73 is one of the tumor-suppressor p53 family of nuclear transcription factor. As expected from the structural similarity between p53 and p73, p73 has a tumor-suppressive function. However, p73 was rarely mutated in human primary tumors. Under normal physiological conditions, p73 is kept at an extremely low level to allow cells normal growth. In response to a certain subset of DNA damages, p73 is induced dramatically and transactivates an overlapping set of p53-target genes implicated in the promotion of cell cycle arrest and/or apoptotic cell death. Cells undergo cell cycle arrest and/or apoptotic cell death depending on the type and strength of DNA damages. p73 is regulated largely through the posttranslational modifications such as phosphorylation and acetylation. These chemical modifications are tightly linked to direct protein-protein interactions. In the present paper, the authors describe the functional significance of the protein-protein interactions in the regulation of proapoptotic p73

Characterization of the effect of ion irradiation on industrially produced GdBa₂Cu₃O₇−δ superconducting tapes using a slow positron beam

To investigate the effect of irradiation-induced defects on the superconducting characteristics of industrially produced superconductor—GdBa₂Cu₃O₇−δ (GdBCO)—coated conductors (CCs), we irradiated the GdBCO CCs with Au ions at 2 or 10 MeV and probed them using a slow positron beam. Vacancy clusters were detected in both unirradiated and irradiated GdBCO CCs. However, the effect of ion irradiation on the GdBCO CCs was characterized as a slight reduction in the positron annihilation rate with low-momentum electrons. We also found a correlation between the annihilation rate of low-momentum electrons and the superconducting transition temperature

Fabrication of binary FeSe superconducting wires by novel diffusion process

We report successful fabrication of multi- and mono-core FeSe wires with high transport critical current density Jc using a simple in-situ Fe-diffusion process based on the powder-in-tube (Fe-diffusion PIT) method. The seven-core wire showed transport Jc of as high as 1027 A/cm2 at 4.2 K. The superconducting transition temperature Tczero was observed at 10.5 K in the wire-samples, which is about 2 K higher than that of bulk FeSe. The Fe-diffusion PIT method is suitable for fabricating multi-core wires of the binary FeSe superconductors with superior properties.Comment: 14 pages, 5 figure