14 results found
    1. Medicine

    Direct reprogramming of human smooth muscle and vascular endothelial cells reveals defects associated with aging and Hutchinson-Gilford progeria syndrome

    Simone Bersini et al.
    Direct reprogramming of smooth muscle cells from HGPS patients revealed that BMP4 is a key contributor of vascular degeneration and might represent a new therapeutic target.
    1. Cell Biology

    A small-molecule ICMT inhibitor delays senescence of Hutchinson-Gilford progeria syndrome cells

    Xue Chen et al.
    Knockout of the methyltransferase ICMT prevents progerin methylation and improves survival in mice with Hutchinson-Gilford progeria syndrome (HGPS) and an ICMT inhibitor delays senescence and stimulates proliferation of HGPS cells.
    1. Chromosomes and Gene Expression

    Progerin reduces LAP2α-telomere association in Hutchinson-Gilford progeria

    Alexandre Chojnowski et al.
    Expression of the lamina-associated polypeptide α (LAP2α) prevents premature cellular ageing caused by expression of progerin in Hutchinson-Gilford progeria syndrome.
    1. Immunology and Inflammation

    Ribosome biogenesis restricts innate immune responses to virus infection and DNA

    Christopher Bianco, Ian Mohr
    Ribosome production is unexpectedly integrated into innate cell-intrinsic responses that regulate double strand DNA-sensing and inflammatory cytokine induction in infected and uninfected cells.
    1. Cell Biology

    Role of SAGA in the asymmetric segregation of DNA circles during yeast ageing

    Annina Denoth-Lippuner et al.
    The SAGA complex binds non-chromosomal DNA circles and prevents their spreading by attaching them to nuclear pores, thereby leading to the concomitant accumulation of DNA circles and pores in ageing yeast mother cells.
    1. Cell Biology

    LAP2alpha maintains a mobile and low assembly state of A-type lamins in the nuclear interior

    Nana Naetar et al.
    The lamin A/C binding protein LAP2α inhibits formation of higher order lamin structures in the nuclear interior in a lamin A/C-phosphorylation-independent manner, thereby regulating chromatin mobility.
    1. Genetics and Genomics

    DNA damage—how and why we age?

    Matt Yousefzadeh et al.
    There is now sufficient and diverse evidence to support a cogent argument that DNA damage plays a causal role in aging.
    1. Chromosomes and Gene Expression

    Ssd1 and Gcn2 suppress global translation efficiency in replicatively aged yeast while their activation extends lifespan

    Zheng Hu et al.
    Activation of the stress response pathway in young cells extends replicative lifespan, not by reducing global protein synthesis per se, but by Gcn4-mediated autophagy induction.
    1. Computational and Systems Biology
    2. Neuroscience

    Suppression of transcriptional drift extends C. elegans lifespan by postponing the onset of mortality

    Sunitha Rangaraju et al.
    A transcriptome-based metric for aging reveals a longevity mechanism that specifically prolongs the duration of young adulthood rather than slowing overall aging.
    1. Biochemistry and Chemical Biology
    2. Structural Biology and Molecular Biophysics

    A molecular mechanism for LINC complex branching by structurally diverse SUN-KASH 6:6 assemblies

    Manickam Gurusaran, Owen Richard Davies
    The LINC complex has a core 6:6 structure in which KASH-binding induces head-to-head interactions between SUN trimers, suggesting force transduction between cytoskeletal and nuclear components through branched LINC complex networks.

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