Academic literature on the topic 'Axonal ER'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Axonal ER.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Axonal ER"

1

Lee, Soyeon, Wei Wang, Jinyeon Hwang, Uk Namgung, and Kyung-Tai Min. "Increased ER–mitochondria tethering promotes axon regeneration." Proceedings of the National Academy of Sciences 116, no. 32 (2019): 16074–79. http://dx.doi.org/10.1073/pnas.1818830116.

Full text
Abstract:
Translocation of the endoplasmic reticulum (ER) and mitochondria to the site of axon injury has been shown to facilitate axonal regeneration; however, the existence and physiological importance of ER–mitochondria tethering in the injured axons are unknown. Here, we show that a protein linking ER to mitochondria, the glucose regulated protein 75 (Grp75), is locally translated at axon injury site following axotomy, and that overexpression of Grp75 in primary neurons increases ER–mitochondria tethering to promote regrowth of injured axons. We find that increased ER–mitochondria tethering elevates
APA, Harvard, Vancouver, ISO, and other styles
2

Sun, Jingbo, Raihanah Harion, Tomoki Naito, and Yasunori Saheki. "INPP5K and Atlastin-1 maintain the nonuniform distribution of ER–plasma membrane contacts in neurons." Life Science Alliance 4, no. 11 (2021): e202101092. http://dx.doi.org/10.26508/lsa.202101092.

Full text
Abstract:
In neurons, the ER extends throughout all cellular processes, forming multiple contacts with the plasma membrane (PM) to fine-tune neuronal physiology. However, the mechanisms that regulate the distribution of neuronal ER-PM contacts are not known. Here, we used the Caenorhabditis elegans DA9 motor neuron as our model system and found that neuronal ER-PM contacts are enriched in soma and dendrite and mostly absent in axons. Using forward genetic screen, we identified that the inositol 5-phosphatase, CIL-1 (human INPP5K), and the dynamin-like GTPase, ATLN-1 (human Atlastin-1), help to maintain
APA, Harvard, Vancouver, ISO, and other styles
3

Robinson, Richard. "Axonal Signaling Proteins Take the ER Highway." PLoS Biology 8, no. 10 (2010): e1000504. http://dx.doi.org/10.1371/journal.pbio.1000504.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Lu, Meng, Francesca W. van Tartwijk, Julie Qiaojin Lin, et al. "The structure and global distribution of the endoplasmic reticulum network are actively regulated by lysosomes." Science Advances 6, no. 51 (2020): eabc7209. http://dx.doi.org/10.1126/sciadv.abc7209.

Full text
Abstract:
The endoplasmic reticulum (ER) comprises morphologically and functionally distinct domains: sheets and interconnected tubules. These domains undergo dynamic reshaping in response to changes in the cellular environment. However, the mechanisms behind this rapid remodeling are largely unknown. Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status: The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection. We validate this causal link via the chemo- and optogeneticall
APA, Harvard, Vancouver, ISO, and other styles
5

Glynn, Paul. "Axonal Degeneration and Neuropathy Target Esterase." Archives of Industrial Hygiene and Toxicology 58, no. 3 (2007): 355–58. http://dx.doi.org/10.2478/v10004-007-0029-z.

Full text
Abstract:
Axonal Degeneration and Neuropathy Target EsteraseThis brief review summarises recent observations which suggest a possible mechanism for organophosphate-induced delayed neuropathy (OPIDN). Neuropathy target esterase (NTE) has been shown to deacylate endoplasmic reticulum (ER) membrane phosphatidylcholine (PtdCho). Raised levels of PtdCho are present in the brains of swiss cheese/NTE mutant Drosophila together with abnormal membrane structures, axonal and dendritic degeneration and neural cell loss. Similar vacuolated pathology is found in the brains of mice with brain-specific deletion of the
APA, Harvard, Vancouver, ISO, and other styles
6

Fuentes, Federico, and Carlos O. Arregui. "Microtubule and Cell Contact Dependency of ER-bound PTP1B Localization in Growth Cones." Molecular Biology of the Cell 20, no. 6 (2009): 1878–89. http://dx.doi.org/10.1091/mbc.e08-07-0675.

Full text
Abstract:
PTP1B is an ER-bound protein tyrosine phosphatase implied in the regulation of cell adhesion. Here we investigated mechanisms involved in the positioning and dynamics of PTP1B in axonal growth cones and evaluated the role of this enzyme in axons. In growth cones, PTP1B consistently localizes in the central domain, and occasionally at the peripheral region and filopodia. Live imaging of GFP-PTP1B reveals dynamic excursions of fingerlike processes within the peripheral region and filopodia. PTP1B and GFP-PTP1B colocalize with ER markers and coalign with microtubules at the peripheral region and
APA, Harvard, Vancouver, ISO, and other styles
7

Gan, Kathlyn J., та Michael A. Silverman. "Dendritic and axonal mechanisms of Ca2+ elevation impair BDNF transport in Aβ oligomer–treated hippocampal neurons". Molecular Biology of the Cell 26, № 6 (2015): 1058–71. http://dx.doi.org/10.1091/mbc.e14-12-1612.

Full text
Abstract:
Disruption of fast axonal transport (FAT) and intracellular Ca2+ dysregulation are early pathological events in Alzheimer's disease (AD). Amyloid-β oligomers (AβOs), a causative agent of AD, impair transport of BDNF independent of tau by nonexcitotoxic activation of calcineurin (CaN). Ca2+-dependent mechanisms that regulate the onset, severity, and spatiotemporal progression of BDNF transport defects from dendritic and axonal AβO binding sites are unknown. Here we show that BDNF transport defects in dendrites and axons are induced simultaneously but exhibit different rates of decline. The spat
APA, Harvard, Vancouver, ISO, and other styles
8

Allison, Rachel, James R. Edgar, Guy Pearson, et al. "Defects in ER–endosome contacts impact lysosome function in hereditary spastic paraplegia." Journal of Cell Biology 216, no. 5 (2017): 1337–55. http://dx.doi.org/10.1083/jcb.201609033.

Full text
Abstract:
Contacts between endosomes and the endoplasmic reticulum (ER) promote endosomal tubule fission, but the mechanisms involved and consequences of tubule fission failure are incompletely understood. We found that interaction between the microtubule-severing enzyme spastin and the ESCRT protein IST1 at ER–endosome contacts drives endosomal tubule fission. Failure of fission caused defective sorting of mannose 6-phosphate receptor, with consequently disrupted lysosomal enzyme trafficking and abnormal lysosomal morphology, including in mouse primary neurons and human stem cell–derived neurons. Consi
APA, Harvard, Vancouver, ISO, and other styles
9

Tabb, J. S., B. J. Molyneaux, D. L. Cohen, S. A. Kuznetsov, and G. M. Langford. "Transport of ER vesicles on actin filaments in neurons by myosin V." Journal of Cell Science 111, no. 21 (1998): 3221–34. http://dx.doi.org/10.1242/jcs.111.21.3221.

Full text
Abstract:
Axoplasmic organelles in the giant axon of the squid have been shown to move on both actin filaments and microtubules and to switch between actin filaments and microtubules during fast axonal transport. The objectives of this investigation were to identify the specific classes of axoplasmic organelles that move on actin filaments and the myosin motors involved. We developed a procedure to isolate endoplasmic reticulum (ER) from extruded axoplasm and to reconstitute its movement in vitro. The isolated ER vesicles moved on exogenous actin filaments adsorbed to coverslips in an ATP-dependent mann
APA, Harvard, Vancouver, ISO, and other styles
10

Wang, Bingjie, You Yu, Lai Wei, and Yan Zhang. "Inhibition of ER stress improves progressive motor deficits in a REEP1-null mouse model of hereditary spastic paraplegia." Biology Open 9, no. 9 (2020): bio054296. http://dx.doi.org/10.1242/bio.054296.

Full text
Abstract:
ABSTRACTHereditary spastic paraplegias (HSPs) are genetic neurodegenerative diseases. HSPs are characterized by lower-extremity weakness and spasticity. However, there is no specific clinical treatment strategy to prevent or reverse nerve degeneration in HSPs. Mutations in receptor expression-enhancing protein 1 (REEP1) are well-recognized and relatively common causes of autosomal dominant HSPs. REEP1 modifies the endoplasmic reticulum (ER) shape, and is implicated in the ER stress response. Defects in the ER stress response seem to be crucial mechanisms underlying HSP neurodegeneration. Here,
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Axonal ER"

1

Sohail, Anood. "Visualizing roles of spastic paraplegia proteins in organizing axonal ER in live Drosophila." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/290113.

Full text
Abstract:
Axons possess a continuous network of smooth tubular endoplasmic reticulum (ER), extending from the nuclear envelope throughout the neuron to synapses. Mutations affecting proteins with intramembrane hairpin domains that model tubular ER membrane can lead to the axon degenerative disease, hereditary spastic paraplegia (HSP). However, the extent and mechanisms by which HSP proteins contribute to axonal ER organization and dynamics are unclear. To understand these mechanisms, there is a need to visualize axonal ER in wild-type and mutant live axons. I have therefore aimed to develop these tools
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Axonal ER"

1

González-Maciel, Angélica, Rafael Reynoso-Robles, Ricardo Torres-Jardón, Partha S. Mukherjee, and Lilian Calderón-Garcidueñas. "Combustion-Derived Nanoparticles in Key Brain Target Cells and Organelles in Young Urbanites: Culprit Hidden in Plain Sight in Alzheimer’s Disease Development." In Advances in Alzheimer’s Disease. IOS Press, 2021. http://dx.doi.org/10.3233/aiad210005.

Full text
Abstract:
Millions of children and young adults are exposed to fine particulate matter (PM2.5) and ozone, associated with Alzheimer’s disease (AD) risk. Mexico City (MC) children exhibit systemic and brain inflammation, low cerebrospinal fluid (CSF) Aβ1-42, breakdown of nasal, olfactory, alveolar-capillary, duodenal, and blood-brain barriers, volumetric and metabolic brain changes, attention and short-term memory deficits, and hallmarks of AD and Parkinson’s disease. Airborne iron-rich strongly magnetic combustion-derived nanoparticles (CDNPs) are present in young urbanites’ brains. Using transmission electron microscopy, we documented CDNPs in neurons, glia, choroid plexus, and neurovascular units of young MC residents versus matched clean air controls. CDNPs are associated with pathology in mitochondria, endoplasmic reticulum (ER), mitochondria-ER contacts (MERCs), axons,and dendrites. There is a significant difference in size and numbers between spherical CDNPs (>85%) and the angular, euhedral endogenous NPs (<15%). Spherical CDNPs (dogs 21.2 ± 7.1 nm in diameter versus humans 29.1 ± 11.2 nm, p = 0.002) are present in neurons, glia, choroid plexus, endothelium, nasal and olfactory epithelium, and in CSF at significantly higher in numbers in MC residents (p < 0.0001). Degenerated MERCs, abnormal mitochondria, and dilated ER are widespread, and CDNPs in close contact with neurofilaments, glial fibers, and chromatin are a potential source for altered microtubule dynamics, mitochondrial dysfunction, accumulation and aggregation of unfolded proteins, abnormal endosomal systems, altered insulin signaling, calcium homeostasis, apoptotic signaling, autophagy, and epigenetic changes. Highly oxidative, ubiquitous CDNPs constitute a novel path into AD pathogenesis. Exposed children and young adults need early neuroprotection and multidisciplinary prevention efforts to modify the course of AD at early stages.
APA, Harvard, Vancouver, ISO, and other styles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!