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Showing 1–17 of 17 results
Advanced filters: Author: John H. Brumell Clear advanced filters

  • Zhu et al show that LRRK2 kinase promotes invagination of the plasma membrane to create ‘reservoirs’, which dynamically store or release excess membrane. Salmonella can exploit these membrane reservoirs during invasion of host cells by controlling the activity of LRRK2.

    • Hongxian Zhu
    • Andrew M. Sydor
    • John H. Brumell
    ResearchOpen Access
    Nature Communications
    Volume: 16, P: 1-18

  • The plasma membrane of eukaryotic cells can fold inwards to create reservoirs that store or release excess membrane. Zhu et al. show that Salmonella-secreted effectors modulate these reservoirs to facilitate host cell invasion.

    • Hongxian Zhu
    • Andrew M. Sydor
    • John H. Brumell
    ResearchOpen Access
    Nature Communications
    Volume: 15, P: 1-16

  • Interferon (IFN) is an important component of antiviral immunity, but can also be exploited by bacteria for immune evasion. Here the authors show that Listeria monocytogenes (Lm) induces type I IFN to suppress the degradation of Lm virulence proteins, ActA and LLO, and promote Lm infection in an IFITM3-dependent manner, thereby hinting at a potential target for antimicrobial therapy.

    • Joel M. J. Tan
    • Monica E. Garner
    • John H. Brumell
    ResearchOpen Access
    Nature Communications
    Volume: 12, P: 1-15

  • Salmonella secretes the effector protein SopD into the host cell cytoplasm, leading to scission of the plasma membrane through unclear mechanisms. Here, Boddy et al. show that SopD binds to and inhibits the small GTPase Rab10, thus promoting removal of Rab10 and recruitment of dynamin-2 to drive plasma membrane scission.

    • Kirsten C. Boddy
    • Hongxian Zhu
    • John H. Brumell
    ResearchOpen Access
    Nature Communications
    Volume: 12, P: 1-15

  • Autophagy not only degrades components of host cells but can also target intracellular bacteria and thus contribute to host defences. Here, Huang and Brumell discuss the canonical and selective pathways of antibacterial autophagy, as well as the ways in which bacteria can escape from them and sometimes even use them to promote infection.

    • Ju Huang
    • John H. Brumell
    Reviews
    Nature Reviews Microbiology
    Volume: 12, P: 101-114

  • Pathogens have many ways of subverting their hosts' molecular machinery. A striking example of such a ploy comes to light from investigations of the species of bacterium that causes listeriosis.

    • Grace Y. Lam
    • John H. Brumell
    News & Views
    Nature
    Volume: 455, P: 1186-1187

  • Cells can destroy invading bacteria through a digestive process called autophagy. A study finds that sugar molecules, exposed by bacterial damage to the cell's membrane, can trigger this process. See Letter p.414

    • Ju Huang
    • John H. Brumell
    News & Views
    Nature
    Volume: 482, P: 316-317

  • The intracellular bacterial pathogen Listeria monocytogenes is shown to exploit efferocytosis—the process by which dead or dying cells are removed by phagocytosis—to promote cell-to-cell spread during infection.

    • Mark A. Czuczman
    • Ramzi Fattouh
    • John H. Brumell
    Research
    Nature
    Volume: 509, P: 230-234

  • Getting synthetic biology circuit-based sensors into field applications is still a challenge. Here the authors combine a circuit sensor with a glucose meter for small analyte and nucleic acid detection.

    • Evan Amalfitano
    • Margot Karlikow
    • Keith Pardee
    ResearchOpen Access
    Nature Communications
    Volume: 12, P: 1-10

  • ARPC1B is a component of the actin-related protein 2/3 complex (Arp2/3), which is required for actin filament branching. Kahret al. show that ARPC1B deficiency in humans is associated with severe multisystem disease that includes platelet abnormalities, eosinophilia, eczema and other indicators of immune disease.

    • Walter H. A. Kahr
    • Fred G. Pluthero
    • Aleixo M Muise
    ResearchOpen Access
    Nature Communications
    Volume: 8, P: 1-14

  • HACE1 is an E3 ubiquitin ligase known to regulate various cell biological processes. Here, Zhang et al.identify HACE1 as a protective factor in the heart, demonstrating that HACE1 inhibits the development of heart failure in response to haemodynamic stress by regulating protein degradation pathways.

    • Liyong Zhang
    • Xin Chen
    • Peter P. Liu
    ResearchOpen Access
    Nature Communications
    Volume: 5, P: 1-14

  • Listeria monocytogenes multiplies rapidly in the cytosol of infected cells, but has also been found in intracellular vacuoles during persistent infection. Now, these vacuoles are described as sites of comparably slow bacterial replication, which may promote bacterial survival in face of the host immune response.

    • Cheryl L. Birmingham
    • Veronica Canadien
    • John H. Brumell
    Research
    Nature
    Volume: 451, P: 350-354