The DOI matches its Crossref record; 17 of the 17 references it cites were found in a registry or an index.
Axon degeneration: Molecular mechanisms of a self-destruction pathway
Open accessAbstract
Axon degeneration is a characteristic event in many neurodegenerative conditions including stroke, glaucoma, and motor neuropathies. However, the molecular pathways that regulate this process remain unclear. Axon loss in chronic neurodegenerative diseases share many morphological features with those in acute injuries, and expression of the Wallerian degeneration slow (WldS) transgene delays nerve degeneration in both events, indicating a common mechanism of axonal self-destruction in traumatic injuries and degenerative diseases. A proposed model of axon degeneration is that nerve insults lead to impaired delivery or expression of a local axonal survival factor, which results in increased intra-axonal calcium levels and calcium-dependent cytoskeletal breakdown.
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1 retracted
RETRACTED ARTICLE: APP binds DR6 to trigger axon pruning and neuron death via distinct caspases
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Close Contacts with the Endoplasmic Reticulum as Determinants of Mitochondrial Ca 2+ Responses
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Absence of Wallerian Degeneration does not Hinder Regeneration in Peripheral Nerve
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The Drosophila Cell Corpse Engulfment Receptor Draper Mediates Glial Clearance of Severed Axons
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Metadata
- Authors
- Wang, J. T., Medress, Z. A., & Barres, B. A.
- Venue
- Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2012-01-09
- Volume
- 196
- Issue
- 1
- Pages
- 7-18
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- OpenAlex
- W2131673631
- Cited by
- 442
- References
- 17
- FWCI
- 14.53
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Wang, J. T., Medress, Z. A., & Barres, B. A. (2012). Axon degeneration: Molecular mechanisms of a self-destruction pathway. Journal of Cell Biology. https://doi.org/10.1083/jcb.201108111
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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