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Sökning: L773:0028 0836 OR L773:1476 4687 > (2010-2019) > (2011)

  • Resultat 41-49 av 49
  • Föregående 1234[5]
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  • O'Neill, John S., et al. (författare)
  • Circadian rhythms persist without transcription in a eukaryote
  • 2011
  • Ingår i: Nature. - Nature Publishing Group. - 0028-0836. ; 469:7331, s. 554-558
  • Tidskriftsartikel (refereegranskat)abstract
    • Circadian rhythms are ubiquitous in eukaryotes, and coordinate numerous aspects of behaviour, physiology and metabolism, from sleep/wake cycles in mammals to growth and photosynthesis in plants. This daily timekeeping is thought to be driven by transcriptionaltranslational feedback loops, whereby rhythmic expression of clock- gene products regulates the expression of associated genes in approximately 24-hour cycles. The specific transcriptional components differ between phylogenetic kingdoms. The unicellular pico-eukaryotic alga Ostreococcus tauri possesses a naturally minimized clock, which includes many features that are shared with plants, such as a central negative feedback loop that involves the morning-expressed CCA1 and evening-expressed TOC1 genes. Given that recent observations in animals and plants have revealed prominent post-translational contributions to timekeeping, a reappraisal of the transcriptional contribution to oscillator function is overdue. Here we show that non-transcriptional mechanisms are sufficient to sustain circadian timekeeping in the eukaryotic lineage, although they normally function in conjunction with transcriptional components. We identify oxidation of peroxiredoxin proteins as a transcription-independent rhythmic biomarker, which is also rhythmic in mammals. Moreover we show that pharmacological modulators of the mammalian clock mechanism have the same effects on rhythms in Ostreococcus. Post-translational mechanisms, and at least one rhythmic marker, seem to be better conserved than transcriptional clock regulators. It is plausible that the oldest oscillator components are non-transcriptional in nature, as in cyanobacteria, and are conserved across kingdoms.
  • Parker, Thomas (författare)
  • Cutting Science's electricity bill
  • 2011
  • Ingår i: Nature. - Nature Publishing Group. - 0028-0836. ; 480, s. 315-316
  • Tidskriftsartikel (populärvet., debatt m.m.)
  • Regot, Sergi, et al. (författare)
  • Distributed biological computation with multicellular engineered networks.
  • 2011
  • Ingår i: Nature. - 1476-4687. ; 469:7329, s. 207-11
  • Tidskriftsartikel (refereegranskat)abstract
    • Ongoing efforts within synthetic and systems biology have been directed towards the building of artificial computational devices using engineered biological units as basic building blocks. Such efforts, inspired in the standard design of electronic circuits, are limited by the difficulties arising from wiring the basic computational units (logic gates) through the appropriate connections, each one to be implemented by a different molecule. Here, we show that there is a logically different form of implementing complex Boolean logic computations that reduces wiring constraints thanks to a redundant distribution of the desired output among engineered cells. A practical implementation is presented using a library of engineered yeast cells, which can be combined in multiple ways. Each construct defines a logic function and combining cells and their connections allow building more complex synthetic devices. As a proof of principle, we have implemented many logic functions by using just a few engineered cells. Of note, small modifications and combination of those cells allowed for implementing more complex circuits such as a multiplexer or a 1-bit adder with carry, showing the great potential for re-utilization of small parts of the circuit. Our results support the approach of using cellular consortia as an efficient way of engineering complex tasks not easily solvable using single-cell implementations.
  • Schmitz, Birger (författare)
  • Earth science: Mind your head
  • 2011
  • Ingår i: Nature. - Nature Publishing Group. - 0028-0836. ; 471:7340, s. 573-574
  • Recension (övrigt vetenskapligt)
  • Ikeda, Fumiyo, et al. (författare)
  • SHARPIN forms a linear ubiquitin ligase complex regulating NF-κB activity and apoptosis.
  • 2011
  • Ingår i: Nature. - 1476-4687 EISSN. ; 471:7340, s. 637-641
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>SHARPIN is a ubiquitin-binding and ubiquitin-like-domain-containing protein which, when mutated in mice, results in immune system disorders and multi-organ inflammation. Here we report that SHARPIN functions as a novel component of the linear ubiquitin chain assembly complex (LUBAC) and that the absence of SHARPIN causes dysregulation of NF-κB and apoptotic signalling pathways, explaining the severe phenotypes displayed by chronic proliferative dermatitis (cpdm) in SHARPIN-deficient mice. Upon binding to the LUBAC subunit HOIP (also known as RNF31), SHARPIN stimulates the formation of linear ubiquitin chains in vitro and in vivo. Coexpression of SHARPIN and HOIP promotes linear ubiquitination of NEMO (also known as IKBKG), an adaptor of the IκB kinases (IKKs) and subsequent activation of NF-κB signalling, whereas SHARPIN deficiency in mice causes an impaired activation of the IKK complex and NF-κB in B cells, macrophages and mouse embryonic fibroblasts (MEFs). This effect is further enhanced upon concurrent downregulation of HOIL-1L (also known as RBCK1), another HOIP-binding component of LUBAC. In addition, SHARPIN deficiency leads to rapid cell death upon tumour-necrosis factor α (TNF-α) stimulation via FADD- and caspase-8-dependent pathways. SHARPIN thus activates NF-κB and inhibits apoptosis via distinct pathways in vivo.</p>
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  • Föregående 1234[5]
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