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Showing 1–10 of 10 results
Advanced filters: Author: Dean Clift Clear advanced filters

  • Hutchinson-Gilford Progeria Syndrome is characterized by premature aging with cardiovascular disease being the main cause of death. Here the authors show that inhibition of the NAT10 enzyme enhances cardiac function and fitness, and reduces age-related phenotypes in a mouse model of premature aging.

    • Gabriel Balmus
    • Delphine Larrieu
    • Stephen P. Jackson
    ResearchOpen Access
    Nature Communications
    Volume: 9, P: 1-14

  • Mitotic spindles assemble from two centrosomes, but oocytes lack centrosomes so how their spindles assemble is unclear. Here Clift and Schuh show that multiple acentriolar microtubule-organizing centres fragment in a three-step process to facilitate bipolar spindle assembly in mouse oocytes.

    • Dean Clift
    • Melina Schuh
    ResearchOpen Access
    Nature Communications
    Volume: 6, P: 1-12

  • Overexpression of human antigen R (HuR) correlates with high grade tumours and poor patient prognosis. Here, the authors engineer a TRIM21 biological PROTAC to demonstrate the benefit of a targeted protein degradation approach to deplete HuR, resulting in tumour growth inhibition in pre-clinical cancer models by altering the HuR-regulated proteome.

    • Alice Fletcher
    • Dean Clift
    • James Hunt
    ResearchOpen Access
    Nature Communications
    Volume: 14, P: 1-14

  • Fertilization triggers a complex cellular programme that leads to a totipotent mitotic embryo. The molecular mechanisms underlying the meiosis to mitosis transition include changes in sister chromatid linkages, the reintroduction of a centrosome, a shift to symmetric cell division and changes in genomic imprinting and protein expression control.

    • Dean Clift
    • Melina Schuh
    Reviews
    Nature Reviews Molecular Cell Biology
    Volume: 14, P: 549-562

  • Non-neutralizing antibodies against the nucleoprotein (NP) of Crimean-Congo hemorrhagic fever virus are protective against lethal challenge in mice. Here, the authors show that these anti-NP antibodies protect through the intracellular antibody receptor TRIM21 and that protection is independent of T cells.

    • Shanna S. Leventhal
    • Thomas Bisom
    • David W. Hawman
    ResearchOpen Access
    Nature Communications
    Volume: 15, P: 1-14

  • The mechanism by which RING E3-anchored ubiquitin chains are formed is not well understood. Here, the authors solve a crystal structure of the RING E3 enzyme TRIM21 trapped in the process of self-anchored chain elongation and provide biochemical and cellular insights into the mechanism of ubiquitin conjugation.

    • Leo Kiss
    • Dean Clift
    • Leo C. James
    ResearchOpen Access
    Nature Communications
    Volume: 12, P: 1-12

  • TRIM21 mediates intracellular antibody immunity and is exploited for targeted protein degradation using Trim-Away technology. Here, the authors dissect the ubiquitination requirements for Trim-Away, providing an explanation for how TRIM21 can target diverse substrates for degradation.

    • Leo Kiss
    • Tyler Rhinesmith
    • Leo C. James
    ResearchOpen Access
    Nature Communications
    Volume: 14, P: 1-17

  • The mechanism behind Trim-Away, a protein-depletion approach using E3 ligase, TRIM21 and an antibody against the target, is now clarified, allowing expansion of the toolbox.

    • Jingwei Zeng
    • Ana Filipa Santos
    • Leo C. James
    Research
    Nature Structural & Molecular Biology
    Volume: 28, P: 278-289

  • This protocol describes Trim-Away, an approach for rapid protein depletion in different cell types. TRIM21–mediated proteasomal degradation is induced by microinjection or electroporation of an antibody into the protein of interest.

    • Dean Clift
    • Chun So
    • Melina Schuh
    Protocols
    Nature Protocols
    Volume: 13, P: 2149-2175