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Showing 1–6 of 6 results
Advanced filters: Author: Dena S. Leeman Clear advanced filters

  • CRISPR–Cas9 screens in cultures of young and old neural stem cells (NSCs) and in vivo in old mice identify gene knockouts that can boost old NSC activation and neurogenesis, with Slc2a4, which encodes the glucose transporter GLUT4, showing particular efficacy.

    • Tyson J. Ruetz
    • Angela N. Pogson
    • Anne Brunet
    ResearchOpen Access
    Nature
    Volume: 634, P: 1150-1159

  • Haematopoietic stem cells, from which blood cells originate, are shown to respond to oestrogen and divide more frequently in female mice than in males, probably preparing females for the increased demand for blood in pregnancy. See Letter p.555

    • Dena S. Leeman
    • Anne Brunet
    News & Views
    Nature
    Volume: 505, P: 488-489

  • The authors show that aged mammalian stem cells produce aberrant transcripts due to profound yet characteristic changes to chromatin during aging, a phenomenon only previously known to occur in simple invertebrate models, limiting their lifespan.

    • Brenna S. McCauley
    • Luyang Sun
    • Weiwei Dang
    Research
    Nature Aging
    Volume: 1, P: 684-697

  • Single-cell transcriptomic analysis of neurogenic niches in young and old mice reveals that T cells infiltrate the neurogenic niches of old mice and inhibit the proliferation of neural stem cells, in part through expression of interferon-γ.

    • Ben W. Dulken
    • Matthew T. Buckley
    • Anne Brunet
    Research
    Nature
    Volume: 571, P: 205-210

  • Using the GTEx data and others, a comprehensive analysis of adenosine-to-inosine RNA editing in mammals is presented; targets of the various ADAR enzymes are identified, as are several potential regulators of editing, such as AIMP2.

    • Meng How Tan
    • Qin Li
    • Jin Billy Li
    Research
    Nature
    Volume: 550, P: 249-254

  • It is shown here that the methylation of histone proteins regulates lifespan in Caenorhabditis elegans. Deficiencies in members of the ASH-2 complex, which trimethylates histone H3 at lysine 4 (H3K4), extend worm lifespan. Meanwhile, the H3K4 demethylase RBR-2 is required for normal lifespan. These findings are consistent with the idea that an excess of H3K4 trimethylation reduces longevity. The extension of lifespan caused by ASH-2 deficiency requires an intact adult germline and the continuous production of mature eggs.

    • Eric L. Greer
    • Travis J. Maures
    • Anne Brunet
    Research
    Nature
    Volume: 466, P: 383-387