ReviewProtein & cell2010
Wld(S), Nmnats and axon degeneration--progress in the past two decades.
Review in Protein & cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- NMNAT3 is protective against the effects of neonatal cerebral hypoxia-ischemia.Annals of clinical and translational neurology · 2017Article
- Wallerian degeneration and recovery of motor nerves after multiple focused cold therapies.Muscle & nerve · 2015Article
- Reduction in muscular motility by selective focused cold therapy: a preclinical study.Journal of neural transmission (Vienna, Austria : 1996) · 2014Article
- NMNATs, evolutionarily conserved neuronal maintenance factors.Trends in neurosciences · 2013Review
- Axon degeneration in Parkinson's disease.Experimental neurology · 2013Review
- The role of ubiquitin-mediated pathways in regulating synaptic development, axonal degeneration and regeneration: insights from fly and worm.The Journal of physiology · 2013Review
- Article
- Protective role of Wallerian degeneration slow (Wld(s)) gene against retinal ganglion cell body damage in a Wallerian degeneration model.Experimental and therapeutic medicine · 2013Article
- Protection of mouse retinal ganglion cell axons and soma from glaucomatous and ischemic injury by cytoplasmic overexpression of Nmnat1.Investigative ophthalmology & visual science · 2013Article
- Chaperoning the synapse--NMNAT protects Bruchpilot from crashing.EMBO reports · 2013Article
- Mutations in NMNAT1 cause Leber congenital amaurosis and identify a new disease pathway for retinal degeneration.Nature genetics · 2012Article
- Mutations in NMNAT1 cause Leber congenital amaurosis with early-onset severe macular and optic atrophy.Nature genetics · 2012Article
- Retinal ganglion cell survival and axon regeneration in WldS transgenic rats after optic nerve crush and lens injury.BMC neuroscience · 2012Article
- Simultaneous single-sample determination of NMNAT isozyme activities in mouse tissues.PloS one · 2012Article
- Nicotinamide mononucleotide adenylyltransferase 2 (Nmnat2) regulates axon integrity in the mouse embryo.PloS one · 2012Article
- Mutations in a P-type ATPase gene cause axonal degeneration.PLoS genetics · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A chimeric protein called Wallerian degeneration slow (Wld(S)) was first discovered in a spontaneous mutant strain of mice that exhibited delayed Wallerian degeneration. This provides a useful tool in elucidating the mechanisms of axon degeneration. Over-expression of Wld(S) attenuates the axon degeneration that is associated with several neurodegenerative disease models, suggesting a new logic for developing a potential protective strategy. At molecular level, although Wld(S) is a fusion protein, the nicotinamide mononucleotide adenylyl transferase 1 (Nmnat1) is required and sufficient for the protective effects of Wld(S), indicating a critical role of NAD biosynthesis and perhaps energy metabolism in axon degeneration. These findings challenge the proposed model in which axon degeneration is operated by an active programmed process and thus may have important implication in understanding the mechanisms of neurodegeneration. In this review, we will summarize these recent findings and discuss their relevance to the mechanisms of axon degeneration.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.