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Volume 10 Issue 9, September 2008

Images showing the extent of 'wound healing' after knockdown of 1081 genes in breast epithelial cells. This analysis identified 66 highly validated genes whose knockdown caused either acceleration or impairment of cell migration and involves diverse alterations in cellular processes.article p1027

Editorial

  • Thirty neuroscience journals share referee reports.

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  • The Nature journals upload manuscripts to PubMed Central on request.

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News & Views

  • Talin can activate integrins to bind the extracellular matrix and also connect matrix-engaged integrins to the actin cytoskeleton. New work shows that cell spreading can be dissected into three distinct phases according to their differential requirements for talin function.

    • Margaret Frame
    • Jim Norman
    News & Views
  • The self-perpetuating amyloid isoform, or prion, of the yeast translation termination factor eRF3 modulates programmed translational frameshifting that controls a regulatory circuit determining the polyamine levels in a yeast cell. But it is still unclear whether this effect is adaptive or pathological.

    • Yury O. Chernoff
    News & Views
  • The epithelial–mesenchymal transition (EMT) is a cellular transdifferentiation program that enables epithelial cancer cells to acquire traits of high-grade malignancy, notably invasive and metastatic powers. A new study indicates that it may also function early in tumour progression by preventing oncogene-induced senescence.

    • Robert A. Weinberg
    News & Views
  • Even though less than 2% of the mammalian genome encodes proteins, a significant fraction can be transcribed into non-coding RNAs. An elegant study identifies a function for non-coding RNA transcription in activating neighbouring genes.

    • Piero Carninci
    News & Views
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