Suppression of terminal axonal sprouting at the neuromuscular junction by monoclonal antibodies against a muscle-derived antigen of 56,000 daltons.
Open accessAbstract
After the partial denervation or paralysis of a muscle, the remaining motor axon terminals may sprout fine, neuritic processes (terminal sprouts) which escape the endplate region of the neuromuscular junction. We previously identified a muscle-derived, protein antigen of 56,000 daltons (56 kD) which plays a necessary role in terminal sprouting. A panel of monoclonal antibodies have been produced against the 56-kD antigen, some of which also partially suppress motor axon terminal sprouting. These monoclonal antibodies define at least two different epitopes upon the surface of the antigen, one of which is necessary for it to effect its biological role in vivo.
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NLK may support survival of sensory and spinal neurons and stimulate axonal growth.
“may support survival of sensory and spinal neurons and stimulate axonal growth [10–13]”
From Cerebrospinal fluid levels of the neurotrophic factor neuroleukin are increased in early Alzheimer’s disease, but not in cerebral amyloid angiopathy (2021) · cites this paper as [10]
The discussion (page not identified in our copy) associates the 56-kD antigen with spinal-neuron survival activity in culture, and reports that antibodies against it suppress motor-axon terminal sprouting. It does not identify the antigen as NLK or report that it supports sensory-neuron survival, so those parts of the claim are not established by this paper. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIn the extracellular space, NLK supports neuronal survival and stimulates axonal growth.
“In the extracellular space NLK supports neuronal survival and stimulates axonal growth [10–13]”
From Cerebrospinal fluid levels of the neurotrophic factor neuroleukin are increased in early Alzheimer’s disease, but not in cerebral amyloid angiopathy (2021) · cites this paper as [10]
The Discussion (p. 2271) associates the soluble, muscle-derived 56-kD antigen with spinal-neuron survival activity in preliminary culture results and finds it necessary for motor-axon terminal sprouting. It does not identify the antigen as NLK or establish that it independently stimulates axonal growth; the authors explicitly leave open whether it is a sprouting factor or a necessary co-factor. (LLM, conf=0.85)
Experimental — accuracy not yet measured
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- Authors
- Gurney, M. E., Apatoff, B. R., & Heinrich, S. P.
- Affiliations
- University of Chicago (US)
- ORCID
- Gurney, M E
- Venue
- The Journal of cell biology
- Publisher
- Rockefeller University Press
- Published
- 1986-06-01
- Volume
- 102
- Issue
- 6
- Pages
- 2264-2272
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC2114250
- OpenAlex
- W1969910567
- Cited by
- 35
- References
- 42
- Citations by year
- 2021: 1 · 2013: 1
- FWCI
- 1.96
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Cell Biology (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (P01NS021442, 5P01 NS-21442)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Axon Guidance and Neuronal Signaling
- Keywords
- neuromuscular junction, axonal sprouting, monoclonal antibodies, antigenic determinants, denervation, paralysis, endplate
- MeSH terms
- Animals, Antibodies, Monoclonal, Antibody Specificity, Antigens, Axons, Cell Fusion, Chromatography, Ion Exchange, Female, Hybridomas, Immune Sera, Immune Tolerance, Male, Mice, Inbred ICR, Molecular Weight, Motor Endplate, Motor Neurons, Muscles, Nerve Regeneration, Neuromuscular Junction, Rats, Inbred Lew, Rats, Inbred Strains, Mice, Rats
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