The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Early and Sustained Activation of Autophagy in Degenerating Axons after Spinal Cord Injury
Abstract
Axonal degeneration is one of the initial steps in many neurological disorders and has been associated with increased autophagic activity. Although there are increasing data on the regulation of autophagy proteins in the neuronal soma after spinal cord injury (SCI), their characterization in the axon is scarce. Here, we examined the regulation of autophagy during axonal degeneration in a rat model of SCI following a lesion at Th 8. We analyzed the morphological and ultrastructural changes in injured axons by immunohistochemical evaluation of autophagy‐related proteins and electron microscopy at different time points following SCI. The expression of ULK 1, A tg7 and A tg5 in damaged axons was rapidly upregulated within hours after SCI. The number of axonal LC 3‐positive autophagosomes was also rapidly increased after SCI and remained at an increased level for up to 6 weeks. Ultrastructural analysis showed early signs of axonal degeneration and increased autophagy. In conclusion, we show that autophagy is increased early and for a sustained period in degenerating axons after SCI and that it might be an important executive step involved in axonal degeneration. Therefore, autophagy may represent a promising target for future therapeutic interventions in the treatment of axonal degeneration in traumatic central nervous system disorders.
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“Complex II replaces ATG14/Atg14 with UVRAG, or Vps38 for mammals and yeast, respectively [789-793].”
From Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1 (2021) · cites this paper as [792]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
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“Complex I is composed of PIK3C3/VPS34, PIK3R4/VPS15/p150, BECN1, ATG14 and NRBF2 for mammals, or Vps34, Vps15, Vps30/Atg6, Atg14 and Atg38 for yeast.”
From Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1 (2021) · cites this paper as [792]
Experimental — accuracy not yet measuredIn the citing paper
“and a human homolog, named ATG14/ATG14L/BARKOR, has been identified [789, 792, 793, 818].”
From Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1 (2021) · cites this paper as [792]
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Guidelines for the use and interpretation of assays for monitoring autophagy
Klionsky, D. J., Abdalla, F. C., Abeliovich, H., Abraham, R. T., Acevedo-Arozena, A., Adeli, K., Agholme, L., Agnello, M., Agostinis, P., Aguirre-Ghiso, J. A., et al. (2012) · Autophagy · doi:10.4161/auto.19496 · Cited by 3,996 · cited 1×
“The LC3 protein regulates autophagosome formation and expansion, and its active form (LC3-II) becomes inserted into the membrane of the autophagosome and is used extensively as an autophagosome marker (14, 18).”
Self-citationNutrient-dependent mTORC1 Association with the ULK1–Atg13–FIP200 Complex Required for Autophagy
Hosokawa, N., Hara, T., Kaizuka, T., Kishi, C., Takamura, A., Miura, Y., Iemura, S.-I., Natsume, T., Takehana, K., Yamada, N., et al. (2009) · Molecular Biology of the Cell · doi:10.1091/mbc.e08-12-1248 · Cited by 2,076
Mizushima, N., Kuma, A., Kobayashi, Y., Yamamoto, A., Matsubae, M., Takao, T., Natsume, T., Ohsumi, Y., & Yoshimori, T. (2003) · Journal of Cell Science · doi:10.1242/jcs.00381 · Cited by 791
Autophagosomes initiate distally and mature during transport toward the cell soma in primary neurons
Maday, S., Wallace, K. E., & Holzbaur, E. L. F. (2012) · Journal of Cell Biology · doi:10.1083/jcb.201106120 · Cited by 681
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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1
Klionsky, D. J., Abdel-Aziz, A. K., Abdelfatah, S., Abdellatif, M., Abdoli, A., Abel, S., Abeliovich, H., Abildgaard, M. H., Abudu, Y. P., Acevedo-Arozena, A., et al. (2021) · Autophagy · doi:10.1080/15548627.2020.1797280 · Cited by 2,897
Self-citation
Metadata
- Authors
- Ribas, V. T., Schnepf, B., Challagundla, M., Koch, J. C., Bähr, M., & Lingor, P.
- Affiliations
- Department of Neurology University Medicine Göttingen Göttingen Germany
- Venue
- Brain Pathology
- Publisher
- Wiley
- Published
- 2014-09-12
- Volume
- 25
- Issue
- 2
- Pages
- 157-170
- ISSN
- 1015-6305
- 1750-3639
- Cited by
- 40
- References
- 7
- Language
- en
- Funders
- International Foundation for Research in Paraplegia (IRP - P 112)
- Deutsche Forschungsgemeinschaft (LI 1308/3-1)
- Center for Nanoscale Microscopy and Molecular Physiology of the Brain
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