Advanced search

Filter By:

Journal Check one or more journals to show results from those journals only.

Choose more journals

Article type Check one or more article types to show results from those article types only.
Subject Check one or more subjects to show results from those subjects only.
Date Choose a date option to show results from those dates only.

Custom date range

Clear all filters
Sort by:
Showing 1–5 of 5 results
Advanced filters: Author: Tanner O. Monroe Clear advanced filters

  • The role of ciliary/centriolar components in the postnatal brain is unclear. Here, the authors show via ablation of Pcm1 in mice that degenerative ciliary/centriolar phenotypes induce neuroanatomical and behavioral changes. Sequencing of PCM1 in human cohorts and zebrafish in vivo complementation suggests PCM1 mutations can contribute to schizophrenia.

    • Tanner O. Monroe
    • Melanie E. Garrett
    • Nicholas Katsanis
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-14

  • Defective autophagy is associated with the pathogenesis of Duchenne muscular dystrophy (DMD). Pal et al. reveal that activation of Src kinase by oxidative stress is responsible for impairment of autophagy in the muscles of mdxmice, and show that reducing oxidative stress rescues autophagy in this DMD model.

    • Rituraj Pal
    • Michela Palmieri
    • George G. Rodney
    Research
    Nature Communications
    Volume: 5, P: 1-10

  • This protocol describes how to coat polymeric nanoparticles (e.g., bare poly (lactic-co-glycolic acid) (50:50, acid terminated) Resomer 504H nanoparticles) with ionic liquids to improve their circulation half-life and biodistribution after intravenous injection. This is achieved via red blood cell hitchhiking in whole blood.

    • Christine M. Hamadani
    • Gaya S. Dasanayake
    • Eden E. L. Tanner
    Protocols
    Nature Protocols
    Volume: 18, P: 2509-2557

  • 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