Increased nuclear NAD biosynthesis and SIRT1 activation prevent axonal degeneration

Science

Volumn 305, Issue 5686, 2004, Pages 1010-1013

  Araki, Toshiyuki ^a   Sasaki, Yo ^a   Milbrandt, Jeffrey ^a  

^a WASHINGTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

DISEASE CONTROL; ENZYMES; PROTEINS;

AXONAL DEGENERATION; MUTATION;

BIOSYNTHESIS;

NICOTINAMIDE ADENINE DINUCLEOTIDE; PROTEIN; PROTEIN NMNAT1; PROTEIN UFD2A; SILENT INFORMATION REGULATOR PROTEIN 2; SIRT1 PROTEIN; SIRTUIN; UNCLASSIFIED DRUG;

MEDICINE;

ARTICLE; AXONAL INJURY; BIOSYNTHESIS; GENE OVEREXPRESSION; NERVE DEGENERATION; NERVE FIBER DEGENERATION; NEUROPATHY; NONHUMAN; PRIORITY JOURNAL; PROTEIN FUNCTION;

3T3 CELLS; ANIMALS; AXONS; AXOTOMY; BENZAMIDES; CELL LINE; CELL NUCLEUS; CELL SURVIVAL; CELLS, CULTURED; GANGLIA, SPINAL; HUMANS; LENTIVIRUS; MICE; MUTATION; NAD; NAPHTHOLS; NERVE TISSUE PROTEINS; NEUROPROTECTIVE AGENTS; NICOTINAMIDE-NUCLEOTIDE ADENYLYLTRANSFERASE; POLY(ADP-RIBOSE) POLYMERASES; RNA, SMALL INTERFERING; SIRTUINS; STILBENES; UBIQUITIN-PROTEIN LIGASES; VINCRISTINE; WALLERIAN DEGENERATION;

MAMMALIA; WALLERIA;

EID: 4043165678     PISSN: 00368075     EISSN: None     Source Type: Journal    
DOI: 10.1126/science.1098014     Document Type: Article

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29. We thank D. Baltimore for the lentiviral expression system, Kazusa DNA Research Institute for the murine Ufd2a cDNA, and J. Manchester and J. Gordon for assistance with NAD measurements. We thank members of the laboratory and our colleagues E. Johnson, J. Gordon, S. Imai, R. Van Gelder, and R. Heuckeroth for helpful discussion and comments on the manuscript. The work was supported by grants from the National Institute of Neurological Disorders and Stroke NS40745 and National Institute on Aging AG13730, and a pilot grant from the Alzheimer's Disease Research Center at Washington University (National Institute on Aging AG05681).