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Showing 1–6 of 6 results
Advanced filters: Author: Dimitra K. Georgiou Clear advanced filters

  • Mutations in the type I ryanodine receptor (RYR1), a calcium channel, leads to stimulus-induced pathological muscle contractions, including malignant hyperthermia. Currently there are no pharmacological agents to protect against this condition, but Susan Hamilton and her colleagues have now identified AICAR as one possible candidate compound. To date, AICAR has been thought to be an AMPK activator, but her group shows that in a mouse model of malignant hyperthermia it does not target this kinase, but rather RYR1, to prevent improper calcium leakage and pathology.

    • Johanna T Lanner
    • Dimitra K Georgiou
    • Susan L Hamilton
    Research
    Nature Medicine
    Volume: 18, P: 244-251

  • Oncogenic transformation can render cancer cells dependent on aberrant expression of glycolytic enzyme isoforms. Lin et al. describe a novel enolase inhibitor, POMHEX, that can selectively kill ENO1-deleted glioblastomas.

    • Yu-Hsi Lin
    • Nikunj Satani
    • Florian L. Muller
    Research
    Nature Metabolism
    Volume: 2, P: 1413-1426

  • Mutations in the RyR1 channel cause core myopathies. Here the authors show that ER stress and the unfolded protein response underlie the pathology caused by a common RyR1 channel mutation, and show that treatment with a chemical chaperone restores muscle function in mice.

    • Chang Seok Lee
    • Amy D. Hanna
    • Susan L. Hamilton
    ResearchOpen Access
    Nature Communications
    Volume: 8, P: 1-15

  • The metabolite methylthioadenosine (MTA) inhibits PRMT5. Therefore, MTA accumulation due to MTA phosphorylase (MTAP) deletion has been proposed as a vulnerability for PRMT5-targeted therapy in cancer. Here, the authors show that MTA does not accumulate in MTAP-deficient cancer cells but is secreted and metabolized by MTAP-intact cells in the tumour microenvironment.

    • Yasaman Barekatain
    • Jeffrey J. Ackroyd
    • Florian L. Muller
    ResearchOpen Access
    Nature Communications
    Volume: 12, P: 1-13