1. H3K36 methylation promotes longevity by enhancing transcriptional fidelity.

    Genes & Development 29(13):1362 (2015) PMID 26159996 PMCID PMC4511212

    Epigenetic mechanisms, including histone post-translational modifications, control longevity in diverse organisms. Relatedly, loss of proper transcriptional regulation on a global scale is an emerging phenomenon of shortened life span, but the specific mechanisms linking these observations remai...
  2. MicroRNA transcriptome analysis identifies miR-365 as a novel negative regulator of cell proliferation in Zmpste24-deficient mouse embryonic fibroblasts.

    PMID 25983189

    Zmpste24 is a metalloproteinase responsible for the posttranslational processing and cleavage of prelamin A into mature laminA. Zmpste24(-/-) mice display a range of progeroid phenotypes overlapping with mice expressing progerin, an altered version of lamin A associated with Hutchinson-Gilford p...
  3. PMT1 deficiency enhances basal UPR activity and extends replicative lifespan of Saccharomyces cerevisiae.

    Age 37(3):9788 (2015) PMID 25936926 PMCID PMC4417673

    Pmt1p is an important member of the protein O-mannosyltransferase (PMT) family of enzymes, which participates in the endoplasmic reticulum (ER) unfolded protein response (UPR), an important pathway for alleviating ER stress. ER stress and the UPR have been implicated in aging and age-related dis...
  4. Correction: Why Is Aging Conserved and What Can We Do about it?

    PLoS Biology 13(5):e1002176 (2015) PMID 25978048 PMCID PMC4433349

    [This corrects the article DOI: 10.1371/journal.pbio.1002131.].
  5. Why is aging conserved and what can we do about it?

    PLoS Biology 13(4):e1002131 (2015) PMID 25923592 PMCID PMC4414409

    The field of aging research has progressed rapidly over the past few decades. Genetic modulators of aging rate that are conserved over a broad evolutionary distance have now been identified. Several physiological and environmental interventions have also been shown to influence the rate of aging...
  6. Fertile waters for aging research.

    Cell 160(5):814 (2015) PMID 25723160

    The quest to slow aging has come far, and what used to be the domain of science fiction writers and snake oil salesmen may soon become science fact. Innovative new approaches, such as the use of the very short-lived African killifish (Harel et al.), are bridging the translational gap and bring t...
  7. Fertile Waters for Aging Research

    Cell 160(5):814 (2015)

    The quest to slow aging has come far, and what used to be the domain of science fiction writers and snake oil salesmen may soon become science fact. Innovative new approaches, such as the use of the very short-lived African killifish (Harel et al.), are bridging the translational gap a...
  8. Fertile waters for aging research.

    Cell 160(5):814 (2015) PMID 25723160

    The quest to slow aging has come far, and what used to be the domain of science fiction writers and snake oil salesmen may soon become science fact. Innovative new approaches, such as the use of the very short-lived African killifish (Harel et al.), are bridging the translational gap and bring t...
  9. Syringaresinol protects against hypoxia/reoxygenation-induced cardiomyocytes injury and death by destabilization of HIF-1α in a FOXO3-dependent mechanism.

    Oncotarget 6(1):43 (2015) PMID 25415049

    Hypoxia-inducible factor 1 (HIF-1) is a master regulator of hypoxic response and has been a prime therapeutic target for ischemia/reperfusion (I/R)-derived myocardial dysfunction and tissue damage. There is also increasing evidence that HIF-1 plays a central role in regulating aging, both throug...
  10. Syringaresinol protects against hypoxia/reoxygenation-induced cardiomyocytes injury and death by destabilization of HIF-1α in a FOXO3-dependent mechanism.

    Oncotarget 6(1):43 (2015) PMID 25415049 PMCID PMC4381577

    Hypoxia-inducible factor 1 (HIF-1) is a master regulator of hypoxic response and has been a prime therapeutic target for ischemia/reperfusion (I/R)-derived myocardial dysfunction and tissue damage. There is also increasing evidence that HIF-1 plays a central role in regulating aging, both throug...
  11. Modulating mTOR in aging and health.

    PMID 25341517

    The physiological responses to nutrient availability play a central role in aging and disease. Genetic and pharmacological studies have identified highly conserved cellular signaling pathways that influence aging by regulating the interface between nutrient and hormone cues and cellular growth a...
  12. Modulating mTOR in aging and health.

    PMID 25341517

    The physiological responses to nutrient availability play a central role in aging and disease. Genetic and pharmacological studies have identified highly conserved cellular signaling pathways that influence aging by regulating the interface between nutrient and hormone cues and cellular growth a...
  13. Enhanced longevity by ibuprofen, conserved in multiple species, occurs in yeast through inhibition of tryptophan import.

    PLoS Genetics 10(12):e1004860 (2014) PMID 25521617 PMCID PMC4270464

    The common non-steroidal anti-inflammatory drug ibuprofen has been associated with a reduced risk of some age-related pathologies. However, a general pro-longevity role for ibuprofen and its mechanistic basis remains unclear. Here we show that ibuprofen increased the lifespan of Saccharomyces ce...
  14. Enhanced Longevity by Ibuprofen, Conserved in Multiple Species, Occurs in Yeast through Inhibition of Tryptophan Import.

    PLoS Genetics 10(12):e1004860 (2014) PMID 25521617

    The common non-steroidal anti-inflammatory drug ibuprofen has been associated with a reduced risk of some age-related pathologies. However, a general pro-longevity role for ibuprofen and its mechanistic basis remains unclear. Here we show that ibuprofen increased the lifespan of Saccharomyces ce...
  15. Enhanced longevity by ibuprofen, conserved in multiple species, occurs in yeast through inhibition of tryptophan import.

    PLoS Genetics 10(12):e1004860 (2014) PMID 25521617 PMCID PMC4270464

    The common non-steroidal anti-inflammatory drug ibuprofen has been associated with a reduced risk of some age-related pathologies. However, a general pro-longevity role for ibuprofen and its mechanistic basis remains unclear. Here we show that ibuprofen increased the lifespan of Saccharomyces ce...
  16. Enhanced Longevity by Ibuprofen, Conserved in Multiple Species, Occurs in Yeast through Inhibition of Tryptophan Import.

    PLoS Genetics 10(12):e1004860 (2014) PMID 25521617 PMCID PMC4270464

    The common non-steroidal anti-inflammatory drug ibuprofen has been associated with a reduced risk of some age-related pathologies. However, a general pro-longevity role for ibuprofen and its mechanistic basis remains unclear. Here we show that ibuprofen increased the lifespan of Saccharomyces ce...
  17. Enhanced Longevity by Ibuprofen, Conserved in Multiple Species, Occurs in Yeast through Inhibition of Tryptophan Import.

    PLoS Genetics 10(12):e1004860 (2014) PMID 25521617 PMCID PMC4270464

    The common non-steroidal anti-inflammatory drug ibuprofen has been associated with a reduced risk of some age-related pathologies. However, a general pro-longevity role for ibuprofen and its mechanistic basis remains unclear. Here we show that ibuprofen increased the lifespan of Saccharomyces ce...
  18. A Drosophila model of mitochondrial disease caused by a complex I mutation that uncouples proton pumping from electron transfer.

    Disease Models & Mechanisms 7(10):1165 (2014) PMID 25085991 PMCID PMC4174527

    Mutations affecting mitochondrial complex I, a multi-subunit assembly that couples electron transfer to proton pumping, are the most frequent cause of heritable mitochondrial diseases. However, the mechanisms by which complex I dysfunction results in disease remain unclear. Here, we describe a D...
  19. A Drosophila model of mitochondrial disease caused by a complex I mutation that uncouples proton pumping from electron transfer.

    Disease Models & Mechanisms 7(10):1165 (2014) PMID 25085991 PMCID PMC4174527

    Mutations affecting mitochondrial complex I, a multi-subunit assembly that couples electron transfer to proton pumping, are the most frequent cause of heritable mitochondrial diseases. However, the mechanisms by which complex I dysfunction results in disease remain unclear. Here, we describe a D...
  20. A Drosophila model of mitochondrial disease caused by a complex I mutation that uncouples proton pumping from electron transfer.

    Disease Models & Mechanisms 7(10):1165 (2014) PMID 25085991 PMCID PMC4174527

    Mutations affecting mitochondrial complex I, a multi-subunit assembly that couples electron transfer to proton pumping, are the most frequent cause of heritable mitochondrial diseases. However, the mechanisms by which complex I dysfunction results in disease remain unclear. Here, we describe a D...