RESUMO
We report on the experimental evidence for a nanosecond timescale spin memory based on nonradiative excitons with large in-plane wave vector. The effect manifests itself in magnetic-field-induced oscillations of the energy of the optically active (radiative) excitons. The oscillations detected by a spectrally resolved pump-probe technique applied to a GaAs/AlGaAs quantum well structure in a transverse magnetic field persist over a timescale, which is orders of magnitude longer than the characteristic decoherence time in the system. The effect is attributed to the spin-dependent electron-electron exchange interaction of the optically active and inactive excitons. The spin relaxation time of the electrons belonging to nonradiative excitons appears to be much longer than the hole spin relaxation time.
RESUMO
The tumor-suppressor p53 can induce various biological responses. Yet, it is not clear whether it is p53 in vivo promoter selectivity that triggers different transcription programs leading to different outcomes. Our analysis of genome-wide chromatin occupancy by p53 using chromatin immunoprecipitation (ChIP)-seq revealed 'p53 default program', that is, the pattern of major p53-bound sites that is similar upon p53 activation by nutlin3a, reactivation of p53 and induction of tumor cell apoptosis (RITA) or 5-fluorouracil in breast cancer cells, despite different biological outcomes. Parallel analysis of gene expression allowed identification of 280 novel p53 target genes, including p53-repressed AURKA. We identified Sp1 as one of the p53 modulators, which confer specificity to p53-mediated transcriptional response upon RITA. Further, we found that STAT3 antagonizes p53-mediated repression of a subset of genes, including AURKA.
Assuntos
Cromatina/metabolismo , Genoma Humano , Proteína Supressora de Tumor p53/metabolismo , Aurora Quinase A , Aurora Quinases , Imunoprecipitação da Cromatina , Mapeamento Cromossômico , Furanos/farmacologia , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Células HCT116 , Humanos , Imidazóis/farmacologia , Células MCF-7 , Piperazinas/farmacologia , Regiões Promotoras Genéticas , Proteínas Serina-Treonina Quinases/genética , Proteínas Serina-Treonina Quinases/metabolismo , Elementos de Resposta , Fator de Transcrição STAT3/metabolismo , Fator de Transcrição Sp1/metabolismo , Transcrição Gênica , Proteína Supressora de Tumor p53/genéticaRESUMO
The aim of the present work was to identify the role of functional asymmetry in the cerebral hemispheres in the pathogenesis of infectious and oncological pathology in (CBAxC57BL/6)F1 mice. Mice with lefthemisphere dominance of motor functions ("right-handers") were found to be more resistant to infection with ectromelia virus and to show slower growth of tumors after subcutaneous injection of B-16 melanoma than animals with right-hemisphere dominance of motor control ("left-handers"). Thus, this report provides the first evidence for the role of functional asymmetry of the nervous system in the pathogenesis of ectromelia and melanoma (B-16) in (CBAxC57BL/6)F1 mice.