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Showing 1–9 of 9 results
Advanced filters: Author: Razq Hakem Clear advanced filters

  • Here the authors show that the nucleus undergoes a transient ‘metamorphosis’ within a nuclear–cytoplasmic DNA damage response linked to health and disease. Through this process, the nuclear envelope projects tubules that capture damaged DNA, mediating its repair.

    • Mitra Shokrollahi
    • Mia Stanic
    • Karim Mekhail
    Research
    Nature Structural & Molecular Biology
    Volume: 31, P: 1319-1330

  • Thomas, Egan et al. report that hexokinase 2 localizes to the nucleus of leukaemic and normal haematopoietic cells to maintain stemness by interacting with nuclear proteins and modulating chromatin accessibility independently of its kinase activity.

    • Geethu Emily Thomas
    • Grace Egan
    • Aaron D. Schimmer
    ResearchOpen Access
    Nature Cell Biology
    Volume: 24, P: 872-884

  • RNA polymerase II has an unexpected function in the nucleolus, helping to drive the expression of ribosomal RNA and to protect nucleolar structure through a mechanism involving triplex R-loop structures.

    • Karan J. Abraham
    • Negin Khosraviani
    • Karim Mekhail
    Research
    Nature
    Volume: 585, P: 298-302

  • Croker and colleagues show that the phosphatase Ptpn6 functions to suppress neutrophil cell death pathways and IL-1 release, thereby limiting autoinflammatory responses.

    • Mary Speir
    • Cameron J. Nowell
    • Ben A. Croker
    Research
    Nature Immunology
    Volume: 21, P: 54-64

  • The effect of hyaluronan-mediated motility receptor (HMMR) expression in BRCA1-associated breast cancer risk remains unknown. Here, HMMR overexpression induces the activation of cGAS-STING and non-canonical NF-κB signalling, instigating an immune permissive environment for breast cancer development.

    • Francesca Mateo
    • Zhengcheng He
    • Miquel Angel Pujana
    ResearchOpen Access
    Nature Communications
    Volume: 13, P: 1-16

  • Targeting a post-translational modification of Fas by recombinant Glrx reverses established lung fibrosis in a mouse model of age-related idiopathic pulmonary fibrosis.

    • Vikas Anathy
    • Karolyn G. Lahue
    • Yvonne M. W. Janssen-Heininger
    Research
    Nature Medicine
    Volume: 24, P: 1128-1135

  • Caspase-8 mediates apoptosis induced by death receptors. At the same time, this protease is able to prevent RIP-dependent necrosis. Without caspase-8 mice die during their embryonic development. Two papers now show that lethality is not caused by the absence of apoptosis, but by RIP3-dependent necrosis that is unleashed without caspase-8. Mice that lack both caspase-8 and RIP3 develop into viable, immunocompetent, fertile adult mice, but suffer from a progressive lymphoaccumulative disease similar to mice that lack the death receptor CD95. This paper further shows that caspase-8 forms a proteolytically active complex with FLIPL, and that this complex is required for protection against RIP3-dependent necrosis.

    • Andrew Oberst
    • Christopher P. Dillon
    • Douglas R. Green
    Research
    Nature
    Volume: 471, P: 363-367