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Dendritic cells are specialized antigen-presenting cells. As such, they exhibit limited degradation of phagocytosed antigens, which favours efficient antigen presentation to T lymphocytes. Work now shows that the restricted proteolysis is due to alkalinization of the phagosome through Rab27a-dependent fusion with a subset of lysosomal vesicles bearing NADPH–oxidase complexes.
Nine inherited neurodegenerative disorders are caused by polyglutamine (polyQ) expansions in diverse proteins. A study now suggests that polyQ-mediated depletion of nonhistone chromatin proteins enhances genotoxic stress induced by the disease protein.
The detrimental effects of nuclear factor-kappa B (NF-κB) signalling in cancer cells lacking the oestrogen receptor have now become clear, with the demonstration that increased NF-κB levels induce expression of Bcl-2 to both suppress apoptosis and induce epithelial–mesenchymal transitions (EMTs).
In mammalian cells, DNA double-strand breaks (DSBs) are repaired by the non-homologous end-joining (NHEJ) pathway. A key component of this repair mechanism is the DNA binding protein, Ku. A recent study shows that Par-3, a protein involved in cell polarity and the assembly of tight junctions, interacts with Ku and is involved in NHEJ, suggesting an intriguing new role for Par-3 and links between cell morphology and DNA damage response pathways.
