Wallerian degeneration of injured axons and synapses is delayed by a Ube4b/Nmnat chimeric gene

By T. Mack, M. Reiner, B. Beirowski, Weiqian Mi, M. Emanuelli, Diana Wagner, D. Thomson, T. Gillingwater, F. Court, L. Conforti and 8 more. Nature Neuroscience, 2001

643 citations recorded by the source corpus.

Subfields: Developmental Neuroscience, Epidemiology, Geriatrics and Gerontology

View Paper: https://www.semanticscholar.org/paper/e19b3714770c0566213d22130b79ec73c223ab19

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Developmental Neuroscience

1. D. O'Leary
2. Liqun Luo
3. J. Scholz
4. Clifford J. Woolf

In Epidemiology

1. Guy C. Brown
2. W. Kraus
3. Michael Coleman
4. Johan Auwerx
5. M. Coleman
6. V. Borutaite
7. M. Fricker
8. A. Tolkovsky

In Geriatrics and Gerontology

1. Johan Auwerx
2. C. Cantó
3. Keir J. Menzies
4. R. Houtkooper
5. W. Kraus
6. R. Wanders
7. S. Imai
8. E. Verdin

Citations in the corpus

• Clinical Progression in Parkinson's Disease and the Neurobiology of Axons (2010, background): “The mutation was identified as an 85kb tandem triplication, which results in a novel chimeric mRNA that encodes for the N-terminal 70 amino acids of ubiquitination factor E4B, followed by the complete coding sequence for the nicotinamide adenine dinucleotide-synthesizing enzyme nicotinamide mononucl”
• Neuronal Cell Death. (2018, positive): “The identification of Wallerian degeneration slow (Wld), a mutant fusion protein, revealed a key role for NAD-related metabolism (438).”
• The neuropathic pain triad: neurons, immune cells and glia (2007, background): “Mutant C57BL/6OlaHsd-Wld mice express a chimeric nuclear protein that interferes with ubiquitination and proteolysis and protects from wallerian degeneratio”
• NAD+ metabolism and the control of energy homeostasis - a balancing act between mitochondria and the nucleus (2015, background): “The WldS mutant protein is a chimeric protein composed of the complete sequence of NMNAT1 fused to the ubiquitination factor E4B at the N terminus (Conforti et al., 2000; Mack et al., 2001).”
• Poly(ADP-ribosyl)ation by PARP-1: 'PAR-laying' NAD+ into a nuclear signal. (2005, background): “In fact, overexpression of NMNAT-1 in mammalian cells does not increase total cellular NAD levels, but is still able to regulate NAD-dependent nuclear processes (Mack et al. 2001; Araki et al. 2004).”
• The secret life of NAD+: an old metabolite controlling new metabolic signaling pathways. (2010, background): “The protective gene in this mouse was found to consist of the N-terminal 70 amino acids of a ubiquitination assembly factor (Ube4B), the full coding sequence of NMNAT1, and a small linking region (213, 214).”
• Axon degeneration mechanisms: commonality amid diversity (2005, methodology): “The slow Wallerian degeneration mutant ( Wld S ) mouse, in which WALLERIAN DEGENERATION is delayed for 2–3 weeks, has been used to show that both physical injury and a blockade of axonal transport trigger a proactive axon death programme, the molecular details of which are just beginning to emerg”
• Axon retraction and degeneration in development and disease. (2005, background): “Transgenic expression of Wlds protects distal axon degeneration after severing in a dose-dependent fashion (Mack et al. 2001).”