Increased Nuclear NAD Biosynthesis and SIRT1 Activation Prevent Axonal Degeneration
By T. Araki, Y. Sasaki, J. Milbrandt. Science, 2004
1,106 citations recorded by the source corpus.
Subfields: Epidemiology, Geriatrics and Gerontology, Physiology
View Paper: https://www.semanticscholar.org/paper/1996780d4f02373cdca2639251af4d9974ec5860
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In Epidemiology
In Geriatrics and Gerontology
- Johan Auwerx
- D. Sinclair
- L. Guarente
- C. Cantó
- M. Haigis
- R. Houtkooper
- Joseph A. Baur
- Keir J. Menzies
In Physiology
Citations in the corpus
- Poly(ADP-ribosyl)ation by PARP-1: 'PAR-laying' NAD+ into a nuclear signal. (2005, background): “More conclusive evidence for the regulation of NADdependent nuclear enzymes by NAD biosynthetic pathways comes from studies on the activity of yeast Sir2/ mammalian SIRT1, an NAD-dependent nuclear protein deacetylase whose activity is modulated by PNC1, NMNATs, and NAMPT (Anderson et al. 2002, 2003;”
- Neural mechanisms of ageing and cognitive decline (2010, background): “Evidence for the benefits of SIRT1 in brain ageing includes the finding that increased SIRT1 activity protects against axon degeneration after injury in a mouse mutant known as Wallerian degeneration slo”
- NAD+ metabolism and the control of energy homeostasis - a balancing act between mitochondria and the nucleus (2015, background): “Efforts from diverse labs have since confirmed that it is the NMNAT enzymatic activity that is required to delay axon degeneration (Araki et al., 2004; Conforti et al., 2009; Gilley and Coleman, 2010; Llopis et al., 2000; Sasaki et al., 2009; Yahata et al., 2009; Yan et al., 2010), probably by…”
- Poly(ADP-ribose): novel functions for an old molecule (2006, background): “This type of cell death, which can be attributed to a robust PARP-1 activation and a depletion of the cellular NAD + pool, relies also in part on the subsequent reduction of SIRT1 deacetylase activity, which is due to substrate deprivation and a high level of the reaction-product nicotinamid”
- NAD+ metabolism: pathophysiologic mechanisms and therapeutic potential (2020, background): “Furthermore, Sir2, as a mammalian homolog of SIRT1, is the downstream effector of increased Nmnat activity, which can lead to axon protection in Wallerian degeneration slow mice.(491) Additionally, SARM1 protein is required for NMN to promote axon degeneration and Ca influx.”
- Calorie restriction, SIRT1 and metabolism: understanding longevity (2005, background): “This mutation increases the levels of an enzyme that is involved in NAD synthesi”
- Nutrient-sensitive mitochondrial NAD+ levels dictate cell survival. (2007, background): “Cell 130 the cytoplasmic form of Nmnat (Nmnat-1) has no effect on NAD levels (Araki et al., 2004; Revollo et al., 2004).”
- DNA damage-induced alterations in chromatin contribute to genomic integrity and age-related changes in gene expression (2008, neutral): “Cells were infected with either a luciferase-specific or a SIRT1-specific shRNA lentiviral vector (Araki et al., 2004).”
- SIRTUIN 1 AND SIRTUIN 3: PHYSIOLOGICAL MODULATORS OF METABOLISM (2012, background): “Recent studies have suggested that SIRT1 is responsible for protection from neuronal, and specifically axonal, degeneration (16, 90, 169, 336), suggesting that the activation of SIRT1 might be important in the treatment of Alzheimer’s disease or other neurodegenerative diseases such as Huntington’s ”
- Neuronal Cell Death. (2018, neutral): “To examine whether microglial activation occurs in AD, a microglial PET marker that detects the microglial protein 18-kDa translocator protein TSPO (18)F-DPA-714, as an indicator of microglial activation, was delivered to a small cohort of individuals with prodromal AD or AD dementia or controls who”
- Axon degeneration mechanisms: commonality amid diversity (2005, neutral): “fcgi?db=gene&cmd=Retrieve&dopt=full_report&list_uids=93759">SIRT1”
- Resveratrol improves mitochondrial function and protects against metabolic disease by activating SIRT1 and PGC-1alpha. (2006, background): “A potential connection with SIRT1 becomes apparent in the remarkable protection against axonal degeneration afforded by SIRT1 activation in the Wallerian degeneration slow mice, an effect that can be reproduced in vitro on dorsal root ganglion cultures by RSV (Araki et al., 2004).”