Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Insensitive Nuclei Enhanced by Polarization Transfer (INEPT)01:15

Insensitive Nuclei Enhanced by Polarization Transfer (INEPT)

Insensitive Nuclei Enhanced by Polarization Transfer (INEPT) is an advanced Nuclear Magnetic Resonance (NMR) technique specifically designed to detect and enhance the signals of low-abundance nuclei, such as carbon-13 and nitrogen-15, in small molecules. The fundamental principle behind INEPT is the transfer of polarization from a more abundant and highly polarizable nucleus, typically hydrogen-1, to the low-abundance nucleus of interest. This process effectively boosts the NMR signal of the...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Age-dependent association of the METTL23 c.84+60delAT variant with normal-tension glaucoma.

Journal of human genetics·2026
Same author

Initial Site of Macular Involvement in Central Retinal Dystrophies Revealed by Fundus Autofluorescence and Optical Coherence Tomography.

Investigative ophthalmology & visual science·2026
Same author

Noise-Matched Blending Level Selection for 1024-Matrix CT Images Using Hybrid-Iterative Reconstruction: Comparison With 512-Matrix Images.

Journal of computer assisted tomography·2026
Same author

Genotype-Phenotype Correlations in RPGRIP1-Associated Retinal Dystrophy in a Nationwide Japanese Cohort.

American journal of ophthalmology·2026
Same author

Longitudinal evaluation of peripheral photoreceptor atrophy in fundus albipunctatus.

Japanese journal of ophthalmology·2026
Same author

DELETION INVOLVING EXON 18 OF RPGRIP1 IS a MAJOR CAUSE OF ACHROMATOPSIA.

Retina (Philadelphia, Pa.)·2026

Related Experiment Video

Updated: Jun 6, 2026

Optic Nerve Transection: A Model of Adult Neuron Apoptosis in the Central Nervous System
12:06

Optic Nerve Transection: A Model of Adult Neuron Apoptosis in the Central Nervous System

Published on: May 12, 2011

Processing of optineurin in neuronal cells.

Xiang Shen1, Hongyu Ying, Ye Qiu

  • 1Department of Ophthalmology and Visual Sciences, College of Medicine, University of Illinois, Chicago, Illinois 60612, USA.

The Journal of Biological Chemistry
|November 10, 2010
PubMed
Summary

Optineurin protein turnover primarily uses the ubiquitin-proteasome pathway (UPP). When mutated or overexpressed, autophagy compensates for impaired UPP, impacting glaucoma disease progression.

More Related Videos

An Enhanced Green Fluorescence Protein-based Assay for Studying Neurite Outgrowth in Primary Neurons
08:02

An Enhanced Green Fluorescence Protein-based Assay for Studying Neurite Outgrowth in Primary Neurons

Published on: October 19, 2019

An Optic Nerve Crush Injury Murine Model to Study Retinal Ganglion Cell Survival
09:07

An Optic Nerve Crush Injury Murine Model to Study Retinal Ganglion Cell Survival

Published on: April 25, 2011

Related Experiment Videos

Last Updated: Jun 6, 2026

Optic Nerve Transection: A Model of Adult Neuron Apoptosis in the Central Nervous System
12:06

Optic Nerve Transection: A Model of Adult Neuron Apoptosis in the Central Nervous System

Published on: May 12, 2011

An Enhanced Green Fluorescence Protein-based Assay for Studying Neurite Outgrowth in Primary Neurons
08:02

An Enhanced Green Fluorescence Protein-based Assay for Studying Neurite Outgrowth in Primary Neurons

Published on: October 19, 2019

An Optic Nerve Crush Injury Murine Model to Study Retinal Ganglion Cell Survival
09:07

An Optic Nerve Crush Injury Murine Model to Study Retinal Ganglion Cell Survival

Published on: April 25, 2011

Area of Science:

  • Neuroscience
  • Cell Biology
  • Genetics

Background:

  • Optineurin (OPTN) gene mutations are linked to glaucoma, a leading cause of blindness.
  • Understanding OPTN processing is crucial for neurodegenerative disease research.

Purpose of the Study:

  • Investigate the roles of the ubiquitin-proteasome pathway (UPP) and autophagy in optineurin (OPTN) processing.
  • Examine how OPTN mutations affect protein clearance mechanisms.

Main Methods:

  • Utilized RGC5 and PC12 cell lines to study endogenous and overexpressed OPTN.
  • Employed proteasomal and autophagic inhibitors, western blotting, and electron microscopy.
  • Analyzed E50K transgenic mouse models for in vivo validation.

Main Results:

  • Endogenous OPTN levels increased with proteasome inhibition, suggesting UPP involvement.
  • Ubiquitination of OPTN was confirmed.
  • Overexpression of wild-type and mutant E50K OPTN reduced proteasome activity (PSMB5) and enhanced autophagy markers (LC3).
  • Autophagosome formation increased with autophagic inhibition and decreased with rapamycin treatment.
  • Rapamycin reduced OPTN-induced apoptosis.

Conclusions:

  • In homeostasis, UPP primarily clears endogenous OPTN.
  • UPP is compromised in conditions of OPTN upregulation or mutation, leading to autophagy activation.
  • Findings in E50K transgenic mice validate in vitro results, highlighting the relevance of these pathways in glaucoma.