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Volume 18 Issue 7, July 2016

Prolonged expression of p21 in p53-null cells triggers replication stress.

[article p777]

Review Article

  • Sanchez and Dynlacht discuss recent insights into the mechanisms of primary cilia assembly and disassembly, and the relationships between ciliogenesis and cell cycle regulation as well as disease.

    • Irma Sánchez
    • Brian David Dynlacht
    Review Article

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News & Views

  • Tumour-associated macrophages facilitate cancer progression, but whether they can be reprogrammed to elicit an anti-tumour response remains unclear. Deletion of the microRNA-processing enzyme Dicer is now shown to rewire macrophages to an anti-tumour mode, leading to an enhanced response to immunotherapy and inhibition of tumour progression.

    • Yunqin Lee
    • Subhra K. Biswas
    News & Views
  • During development, tubular networks form through the joining of lumenized branches. Further insights into tracheal tube fusion in Drosophila melanogaster now reveal the molecular steps that promote the connection of two apical membrane compartments within a single cell through secretory lysosomes.

    • Vahap Aydogan
    • Heinz-Georg Belting
    • Markus Affolter
    News & Views
  • Although known to induce cellular senescence, an important tumour suppressor mechanism, mutation of CDKN1A — the gene encoding p21 (also known as WAF1 or CIP1) — is rare in human cancers. Now, a study reports a previously unappreciated oncogenic effect of p21 overexpression that shapes cancer genome evolution through induction of replication stress.

    • Vasily S. Romanov
    • K. Lenhard Rudolph

    Collection:

    News & Views
  • Clearing misfolded proteins from the cytoplasm is essential to maintain cellular homeostasis. Now, a parallel clearance system is described that uses the deubiquitylase USP19 to enable secretion of misfolded cytoplasmic proteins when conventional proteasomal degradation is compromised. Misfolding-associated protein secretion (MAPS) has important implications for protein quality control and prion-like transmission.

    • Norbert Volkmar
    • Emma Fenech
    • John C. Christianson
    News & Views
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Letter

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Corrigendum

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Erratum

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