Academic literature on the topic 'Optic neuropathy-inducing protein'

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Journal articles on the topic "Optic neuropathy-inducing protein"

1

Umezurike, Benedict C., Moses O. Akhimien, Chidinma Chukwuka, et al. "The Genetics of Primary Open Angle Glaucoma Interventions: Therapeutic Directions and Future Predictions." Ophthalmology Research: An International Journal 19, no. 5 (2024): 1–19. http://dx.doi.org/10.9734/or/2024/v19i5435.

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The “multifactorial chronic optic neuropathy” known as primary open angle glaucoma (POAG) is typified by a “progressive loss of retinal ganglion cells (RGC), structural damage to the retinal nerve fiber layer (RNFL) and optic nerve head (ONH), as well as abnormalities in the visual field.” High intraocular pressure (IOP), age, genetics, family history, race, etc. are the main risk factors. One of the pathological implications of POAG is “pressure-induced” ONH damage, which results in modifications to the expression of retinal genes. The ensuing fluid backup raises IOP, which damages optic nerv
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2

Clementi, Maria Elisabetta, Michela Pizzoferrato, Giada Bianchetti, et al. "Cytoprotective Effect of Idebenone through Modulation of the Intrinsic Mitochondrial Pathway of Apoptosis in Human Retinal Pigment Epithelial Cells Exposed to Oxidative Stress Induced by Hydrogen Peroxide." Biomedicines 10, no. 2 (2022): 503. http://dx.doi.org/10.3390/biomedicines10020503.

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Idebenone is a ubiquinone short-chain synthetic analog with antioxidant properties, which is believed to restore mitochondrial ATP synthesis. As such, idebenone is investigated in numerous clinical trials for diseases of mitochondrial aetiology and it is authorized as a drug for the treatment of Leber’s hereditary optic neuropathy. Mitochondria of retinal pigment epithelium (RPE) are particularly vulnerable to oxidative damage associated with cellular senescence. Therefore, the aim of this study was to explore idebenone’s cytoprotective effect and its underlying mechanism. We used a human-RPE
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3

Cao, Biyin, Tingjun Hou, Suning Chen, et al. "Clioquinol Arrests Cell Cycle at G1 Phase and Triggers Intrinsic Apoptosis In Myeloma and Leukemia Cells by Inhibiting Histone Deacetylases." Blood 116, no. 21 (2010): 1836. http://dx.doi.org/10.1182/blood.v116.21.1836.1836.

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Abstract Abstract 1836 Clioquinol (5-chloro-7-iodo-8-hydroxyquinoline, CQ) is an old and effective antifungal and amoebicidal drug but is restricted or discontinued in some countries because of its suspect causality in inducing subacute myelo-optic neuropathy, however it has been recently revitalized as an anti-cancer drug candidate at both in vitro and in vivo models. Our previous study suggested that CQ induced cell death and displayed anti-leukemia and anti-myeloma activity (Mao × et al, Leukemia, 2009), but its mechanisms are not well known. In this study, we demonstrated that clioquinol-i
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4

Shirvan, Anat, Michal Kimron, Vered Holdengreber, et al. "Anti-semaphorin 3A Antibodies Rescue Retinal Ganglion Cells from Cell Death following Optic Nerve Axotomy." Journal of Biological Chemistry 277, no. 51 (2002): 49799–807. http://dx.doi.org/10.1074/jbc.m204793200.

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Damage to the optic nerve in mammals induces retrograde degeneration and apoptosis of the retinal ganglion cell (RGC) bodies. The mechanisms that mediate the response of the neuronal cells to the axonal injury are still unknown. We have previously shown that semaphorins, axon guidance molecules with repulsive cues, are capable of mediating apoptosis in cultured neuronal cells (Shirvan, A., Ziv, I., Fleminger, G., Shina, R., He, Z., Brudo, I., Melamed, E., and Brazilai, A. (1999)J. Neurochem.73, 961–971). In this study, we examined the involvement of semaphorins in anin vivoexperimental animal
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5

Alsemeh, Amira Ebrahim, Mohey A. E. Hulail, Hanan E. L. Mokhtar, et al. "Tempol improves optic nerve histopathology and ultrastructures in cisplatin-induced optic neuropathy in rats by targeting oxidative stress—Endoplasmic reticulum stress—Autophagy signaling pathways." Frontiers in Cellular Neuroscience 17 (October 5, 2023). http://dx.doi.org/10.3389/fncel.2023.1256299.

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IntroductionOptic neuropathy is an affection of the optic neurons, which ends with blindness and occurs either primarily due to direct affection of the optic nerve or secondarily as a complication of chronic diseases and/or adverse effects of their therapy. The search for novel therapeutic tools is crucial in addressing the limited therapeutic approaches for optic neuropathy. Therefore, the present study was developed to investigate the possible ameliorative effect of tempol against cisplatin-induced optic neuropathy and its underlying mechanism.MethodsForty-eight adult male albino Wistar rats
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6

Alshafie, Walaa, Maryam Fotouhi, Irina Shlaifer, Thomas M. Durcan, Peter S. McPherson, and Carl Laflamme. "Antibody Characterization Report for Optineurin." April 30, 2021. https://doi.org/10.5281/zenodo.4730992.

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Head to head comparison of available commercial antibodies against Optineurin by immunoblot (Western blot), immunoprecipitation and immunofluorescence. The following study was funded in part by Genome Québec's Genomics Integration Program, awarded to the laboratory of Peter S. McPherson. This work is part of the ALS-Reproducible Antibody Platform (ALS-RAP), established as a public-private partnership by three prominent ALS charities - the ALS Association (USA), the Motor Neurone Disease Association (UK), and the ALS Society of Canada.
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7

Ruíz, Moleón Vera, Maryam Fotouhi, Charles Alende, et al. "Antibody Characterization Report for Optineurin (2023)." November 9, 2023. https://doi.org/10.5281/zenodo.10091740.

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This report presents a guide to selecting high-quality commercial antibodies against Optineurin by immunoblot (Western blot), immunoprecipitation and immunofluorescence, using a knockout based validation approach. The research displayed in this study can be considered a subsequent study following the initial Optineurin report published to the YCharOS community in 2021 (DOI:10.5281/zenodo.4730992). Antibodies ab213556**, 60293-1-Ig*, 702766** and 711879**, previously characterized in the initial report, were retested in all three applications, employing our revised standardized protocols.
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