A5006025447- Genetics, Aging, and Longevity in Model Organisms
- Epigenetics and DNA Methylation
- Sirtuins and Resveratrol in Medicine
- DNA Repair Mechanisms
- Calcium signaling and nucleotide metabolism
- Genomics and Chromatin Dynamics
- Bacterial Genetics and Biotechnology
- Birth, Development, and Health
- NF-κB Signaling Pathways
- Nutrition, Genetics, and Disease
- Genetics and Neurodevelopmental Disorders
- Neurogenesis and neuroplasticity mechanisms
- Pluripotent Stem Cells Research
- Biochemical effects in animals
- Inflammatory Bowel Disease
- TGF-β signaling in diseases
- Nuclear Receptors and Signaling
- Retinal Development and Disorders
- Health, Environment, Cognitive Aging
- Genetic Neurodegenerative Diseases
- Health and Well-being Studies
- Fungal and yeast genetics research
- Autophagy in Disease and Therapy
- PARP inhibition in cancer therapy
- Histone Deacetylase Inhibitors Research
Boston VA Research Institute
2019-2024
Harvard University
2013-2024
Biogen (United States)
2003-2008
New York State Department of Health
2003
Brandeis University
1999-2003
NAD + can influence DNA repair by modulating protein interactions.
TNF-like weak inducer of apoptosis (TWEAK) is a TNF family member with pleiotropic effects on variety cell types, one which the induction proinflammatory cytokines by synovial fibroblasts derived from rheumatoid arthritis (RA) patients. In this study, we report that serum TWEAK level was dramatically elevated during mouse collagen-induced (CIA) and blocking neutralizing mAb significantly reduced clinical severity CIA. Histological analyses also revealed inhibition diminished joint...
SUMMARY Nicotinamide adenine dinucleotide (NAD) is essential for many enzymatic reactions, including those involved in energy metabolism, DNA repair and the activity of sirtuins, a family defensive deacylases. During aging, levels NAD + can decrease by up to 50% some tissues, repletion which provides range health benefits both mice humans. Whether or not precursor nicotinamide mononucleotide (NMN) extends lifespan mammals known. Here we investigate effect long-term administration NMN on...
SUMMARY All living things experience entropy, manifested as a loss of inherited genetic and epigenetic information over time. As budding yeast cells age, changes result in cell identity sterility, both hallmarks aging. In mammals, is also lost time, but what causes it to be whether cause or consequence aging not known. Here we show that the transient induction genomic instability, form low number non-mutagenic DNA breaks, accelerates many chromatin tissue seen during aging, including erosion...
Rearrangements between tandemly repeated DNA sequences are a common source of genetic instability. Such rearrangements underlie several human diseases. In many organisms, the mismatch-repair (MMR) system functions to stabilize repeats when repeat unit is short or sequence imperfections present repeats. We show here that action single-stranded (ssDNA) exonucleases plays an additional, important role in stabilizing tandem repeats, independent their MMR. For perfect ≈100 bp Escherichia coli not...
SUMMARY There are numerous hallmarks of aging in mammals, but no unifying cause has been identified. In budding yeast, is associated with a loss epigenetic information that occurs response to genome instability, particularly DNA double-strand breaks (DSBs). Mammals also undergo predictable changes age, including alterations methylation patterns serve as “age” clocks, what drives these not known. Using transgenic mouse system called “ICE” (for inducible c hanges the e pigenome), we show...
Ageing is a degenerative process leading to tissue dysfunction and death. A proposed cause of ageing the accumulation epigenetic noise, which disrupts youthful gene expression patterns that are required for cells function optimally recover from damage 1–3 . Changes DNA methylation over time form basis an ‘ageing clock’ 4, 5 , but whether old individuals retain information reset clock and, if so, this would improve not known. Of all tissues in body, central nervous system (CNS) one first lose...
ABSTRACT The recJ gene, identified in Escherichia coli , encodes a Mg +2 -dependent 5′-to-3′ exonuclease with high specificity for single-strand DNA. Genetic and biochemical experiments implicate RecJ homologous recombination, base excision, methyl-directed mismatch repair. Genes encoding proteins strong similarities to have been found every eubacterial genome sequenced date, the exception of Mycoplasma Mycobacterium tuberculosis . Multiple genes similar are some eubacteria, including...
All living things experience entropy, manifested as a loss of inherited genetic and epigenetic information over time. As budding yeast cells age, changes result in cell identity sterility, both hallmarks aging. In mammals, is also lost time, but what causes it to be whether cause or consequence aging not known. Here we show that the transient induction genomic instability, form low number non-mutagenic DNA breaks, accelerates many chromatin tissue seen during aging, including erosion...
ABSTRACT The RecJ protein of Escherichia coli plays an important role in a number DNA repair and recombination pathways. catalyzes processive degradation single-stranded 5′-to-3′ direction. Sequences highly related to those encoding can be found most the eubacterial genomes sequenced date. From alignment these sequences, seven conserved motifs are apparent. At least five shared among large family proteins eubacteria, eukaryotes, archaea, including PPX1 polyphosphatase yeast Drosophila Prune....
There are numerous hallmarks of aging in mammals, but no unifying cause has been identified. In budding yeast, is associated with a loss epigenetic information that occurs response to genome instability, particularly DNA double-strand breaks (DSBs). Mammals also undergo predictable changes age, including alterations methylation patterns serve as "age" clocks, what drives these not known. Using transgenic mouse system called "ICE" (for inducible the epigenome), we show tissue's non-mutagenic...
All living things experience entropy, manifested as a loss of inherited genetic and epigenetic information over time. In yeast, changes result in cell identity sterility, both hallmarks yeast aging. mammals, is also lost time, but what causes it to be whether cause or consequence aging not known. Using transgenic mouse system called "ICE" (for Inducible Changes the Epigenome), we show that process repairing non-mutagenic DNA breaks accelerates age-related physiological, cognitive, molecular...
Abstract Levels of nicotinamide adenine dinucleotide (NAD+) decline by up to 50% in aging. NAD+ is an essential co-factor for many metabolic processes, including the deacetylase activity sirtuins, and previous studies have demonstrated that supplementing levels has a range health benefits both mice humans. Here we investigate effect long-term (from 13 months age) administration precursor mononucleotide (NMN) on frailty lifespan male female mice. NMN treatment delayed onset sexes, improved...