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Journal Cover Nature Cell Biology
  [SJR: 14.131]   [H-I: 294]   [431 followers]  Follow
    
   Full-text available via subscription Subscription journal
   ISSN (Print) 1465-7392 - ISSN (Online) 1476-4679
   Published by NPG Homepage  [135 journals]
  • RIPK1-mediated induction of mitophagy compromises the viability of
           extracellular-matrix-detached cells
    • RIPK1-mediated induction of mitophagy compromises the viability of extracellular-matrix-detached cells

      RIPK1-mediated induction of mitophagy compromises the viability of extracellular-matrix-detached cells, Published online: 19 February 2018; doi:10.1038/s41556-018-0034-2

      Hawk et al. show that RIPK1 activation during extracellular matrix detachment induces mitophagy through mitochondrial phosphatase PGAM5 to increase reactive oxygen species and non-apoptotic cell death, and that antagonizing RIPK1/PGAM5 enhances tumour formation.RIPK1-mediated induction of mitophagy compromises the viability of extracellular-matrix-detached cells, Published online: 2018-02-19; doi:10.1038/s41556-018-0034-22018-02-19
      DOI: 10.1038/s41556-018-0034-2
       
  • Identification of distinct nanoparticles and subsets of extracellular
           vesicles by asymmetric flow field-flow fractionation
    • Identification of distinct nanoparticles and subsets of extracellular vesicles by asymmetric flow field-flow fractionation

      Identification of distinct nanoparticles and subsets of extracellular vesicles by asymmetric flow field-flow fractionation, Published online: 19 February 2018; doi:10.1038/s41556-018-0040-4

      Lyden and colleagues use asymmetric flow field-flow fractionation to classify nanoparticles derived from cell lines and human samples, including previously uncharacterized large, Exo-L and small, Exo-S, exosome subsets.Identification of distinct nanoparticles and subsets of extracellular vesicles by asymmetric flow field-flow fractionation, Published online: 2018-02-19; doi:10.1038/s41556-018-0040-42018-02-19
      DOI: 10.1038/s41556-018-0040-4
       
  • Publisher Correction: Affinity purification of cell-specific mitochondria
           from whole animals resolves patterns of genetic mosaicism
    • Publisher Correction: Affinity purification of cell-specific mitochondria from whole animals resolves patterns of genetic mosaicism

      Publisher Correction: Affinity purification of cell-specific mitochondria from whole animals resolves patterns of genetic mosaicism, Published online: 15 February 2018; doi:10.1038/s41556-018-0055-x

      Publisher Correction: Affinity purification of cell-specific mitochondria from whole animals resolves patterns of genetic mosaicismPublisher Correction: Affinity purification of cell-specific mitochondria from whole animals resolves patterns of genetic mosaicism, Published online: 2018-02-15; doi:10.1038/s41556-018-0055-x2018-02-15
      DOI: 10.1038/s41556-018-0055-x
       
  • Reactive oxygen species regulate axonal regeneration through the release
           of exosomal NADPH oxidase 2 complexes into injured axons
    • Reactive oxygen species regulate axonal regeneration through the release of exosomal NADPH oxidase 2 complexes into injured axons

      Reactive oxygen species regulate axonal regeneration through the release of exosomal NADPH oxidase 2 complexes into injured axons, Published online: 12 February 2018; doi:10.1038/s41556-018-0039-x

      Hervera et al. show that extracellular vesicles containing NOX2 complexes are released from macrophages and incorporated into injured axons, leading to axonal regeneration through PI3K–p-Akt signalling.Reactive oxygen species regulate axonal regeneration through the release of exosomal NADPH oxidase 2 complexes into injured axons, Published online: 2018-02-12; doi:10.1038/s41556-018-0039-x2018-02-12
      DOI: 10.1038/s41556-018-0039-x
       
  • Author Correction: Sister chromatid resolution is an intrinsic part of
           chromosome organization in prophase
    • Author Correction: Sister chromatid resolution is an intrinsic part of chromosome organization in prophase

      Author Correction: Sister chromatid resolution is an intrinsic part of chromosome organization in prophase, Published online: 12 February 2018; doi:10.1038/s41556-018-0044-0

      Author Correction: Sister chromatid resolution is an intrinsic part of chromosome organization in prophaseAuthor Correction: Sister chromatid resolution is an intrinsic part of chromosome organization in prophase, Published online: 2018-02-12; doi:10.1038/s41556-018-0044-02018-02-12
      DOI: 10.1038/s41556-018-0044-0
       
  • The mTOR–S6K pathway links growth signalling to DNA damage response
           by targeting RNF168
    • The mTOR–S6K pathway links growth signalling to DNA damage response by targeting RNF168

      The mTOR–S6K pathway links growth signalling to DNA damage response by targeting RNF168, Published online: 05 February 2018; doi:10.1038/s41556-017-0033-8

      Xie and colleagues find that activated mTORC1 growth signalling impairs DNA repair through S6K-mediated phosphorylation and inhibition of the RNF168 ligase.The mTOR–S6K pathway links growth signalling to DNA damage response by targeting RNF168, Published online: 2018-02-05; doi:10.1038/s41556-017-0033-82018-02-05
      DOI: 10.1038/s41556-017-0033-8
       
  • Nanopillar force measurements reveal actin-cap-mediated YAP
           mechanotransduction
    • Nanopillar force measurements reveal actin-cap-mediated YAP mechanotransduction

      Nanopillar force measurements reveal actin-cap-mediated YAP mechanotransduction, Published online: 05 February 2018; doi:10.1038/s41556-017-0030-y

      Using nanopillars with increased spatial resolution, Shiu et al. identify high perinuclear forces that originate from contractile apical actin filaments that span across the nucleus and are dependent on lamin A and the LINC complex.Nanopillar force measurements reveal actin-cap-mediated YAP mechanotransduction, Published online: 2018-02-05; doi:10.1038/s41556-017-0030-y2018-02-05
      DOI: 10.1038/s41556-017-0030-y
       
  • Tumour spheres with inverted polarity drive the formation of peritoneal
           metastases in patients with hypermethylated colorectal carcinomas
    • Tumour spheres with inverted polarity drive the formation of peritoneal metastases in patients with hypermethylated colorectal carcinomas

      Tumour spheres with inverted polarity drive the formation of peritoneal metastases in patients with hypermethylated colorectal carcinomas, Published online: 05 February 2018; doi:10.1038/s41556-017-0027-6

      Zajac et al. show that in colorectal cancer, decreased TGF-β signalling promotes apical actomyosin contractility and collective apical budding of invading tumour spheres with inverted polarity that drive metastatic spread.Tumour spheres with inverted polarity drive the formation of peritoneal metastases in patients with hypermethylated colorectal carcinomas, Published online: 2018-02-05; doi:10.1038/s41556-017-0027-62018-02-05
      DOI: 10.1038/s41556-017-0027-6
       
 
 
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