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Nearly six decades after the discovery of ribosomes by George Emil Palade and five years of the Nobel Prize for chemistry in 2009 for a detailed description of the structure west nile virus and functional mechanism of the ribosome, cell biology and molecular lo make a new and important step forward. The number today (28 March) issue of the journal Science, a group at Cambridge west nile virus (United Kingdom) published 1 results obtained by electronic criomicroscopie (a technique that samples can be studied without fixation or staining, the native environment). At a resolution of 3.2 ǻngströmi (10 -10 m) technique allowed the British to describe the ribosomes within mitochondria, ie mitoribozomii. The structures were studied in Saccharomyces cerevisiae and the protein including 39 (of which 13 were found exclusively in mitochondria) together with mitoribozomal RNA fragments (Fig. 1).
In an editorial published in the same issue 2 of the journal, Professor Werner Kühlbrandt from the Max Planck Institute of Biophysics in Frankfurt, says British study confirms the start of a new era in molecular biology, an era in which the description of the structures in a resolution close the atom is not a prerogative of the X-ray crystallography or nuclear magnetic resonance spectroscopy. However, electronic criomicroscopia will not replace the other two techniques west nile virus (resolution 2 ǻngströmi or less remained - at least for now - preserve west nile virus X-ray crystallography), but will complement west nile virus happy ultrastructural analysis methods of living matter.
We can not conclude without adding a significant detail: Alexey Amunts, lead author west nile virus of the Science study is Venkatraman Ramakrishnan's postdoctoral student, one of the three winners of the Nobel Prize in 2009, the first to describe the structure of ribosomes. Indian origin scientist west nile virus began to study once called "Palade granules" in 1978 at Yale University chemistry department, the time that George Emil Palade leading cell biology department.
A group from Johns Hopkins west nile virus published yesterday (March 27) in the journal Nature, a valuable study three translational medicine that could bring therapeutic hopes incurable. Looking a murine model deficient in cistationin-c-lyase (CSE), an enzyme that is the main generator of cistationină cysteine west nile virus (itself formed by a beta-synthase which condenses homocysteine and serine), the U.S. group noted an impairment of the system central nervous similar to a murine model of Huntington's disease (chorea). Once awakened the curiosity of researchers, west nile virus they have verified the observations on a cell line originating from the striatum in a model of Huntington disease, CSE protein levels were decreased markedly west nile virus compared with control cells. Further confirmation came in a murine model of Huntington disease, where low levels of CSE were observed in the striatum, cortex, hippocampus, hypothalamus and brainstem, but not in the cerebellum. The next step was logical to humans, where patients with Huntington disease, west nile virus CSE levels were profoundly reduced in the striatum, cortex west nile virus moderately low and unchanged in the cerebellum, confirming parallelism relative susceptibility of the enzyme west nile virus to that of brain structures affected of Huntington's disease. Furthermore, correlation of clinical tissue levels of CSE CSE confirmed decrease in parallel with increasing severity of disease manifestations, but without it correlate with neurodegeneration (post-mortem samples collected from patients with advanced amyotrophic lateral sclerosis, west nile virus multiple sclerosis west nile virus or spinocerebellar ataxia not produce depletion CSE).
Then mice with CSE gene was observed that diet without cysteine is lethal. More than 80% of the cells die quickly the defective gene in the cysteine-free medium, and this phenomenon can be counteracted by the administration west nile virus of levo-cysteine in the culture medium. U.S. study then continues to investigate the cellular mechanisms at the molecular level, explaining the causal relationship between CSE depletion, reduced levels of cysteine and cell death in Huntington's disease. The solution? Dietary supplementation with N-acetylcysteine. west nile virus Thus, in mice, the addition of the stable precursor of cysteine in drinking water, coupled cist enrichment