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Volume 7 Issue 7, July 2005

Severe telomere fusion phenotype upon loss of TRF2. The metaphase spread shown is derived from TRF2-/- p53-/- MEFs generated by Cre-mediated deletion of a floxed TRF2 allele.

Volume 7 Issue 7

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  • Many viruses and toxins enter the cytoplasm of cells by crossing endosomal membranes. New evidence now suggests that if entry occurs through multivesicular bodies, then they are first delivered into intraluminal vesicles before their final transfer into the cytoplasm via the 'back-fusion' of these vesicles.

    • Pradeep Uchil
    • Walther Mothes
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  • Cytoplasmic processing bodies, also known as P-bodies, concentrate enzymes that are involved in mRNA turnover and sequester mRNAs away from the translational machinery. Strong evidence now connects the RNA interference machinery with P-body formation.

    • John J. Rossi
    News & Views

  • New work reveals a key signal transduction pathway through which nitric oxide (NO) regulates apoptosis induced by disparate cellular stresses. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is S-nitrosylated by NO, which initiates an interaction with the E3 ligase Siah1, leading to nuclear translocation and ubiquitin-mediated degradation of nuclear target proteins.

    • Moran Benhar
    • Jonathan S. Stamler
    News & Views

  • The Nbs1 protein participates in the cell-cycle checkpoint response to DNA double-strand breaks (DSBs), but its precise mode of action — especially in relation to the checkpoint kinase Atm — has been debated. New mouse models suggest that Nbs1 is required for activation of Atm in response to DNA DSBs and that it also functions in an amplification loop with Atm that allows even a small number of DNA DSBs to mount a potent checkpoint response.

    • Elena S. Stavridi
    • Thanos D. Halazonetis
    News & Views
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