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Related Concept Videos

Open Angle Glaucoma: Treatment01:27

Open Angle Glaucoma: Treatment

In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
Drugs such as carbonic anhydrase inhibitors, α2- and...
Glaucoma: Overview01:25

Glaucoma: Overview

Glaucoma is an eye condition characterized by increased intraocular pressure that damages the retina and optic nerve, leading to irreversible blindness if left untreated. The human eye has various components, including the cornea, iris, pupil, lens, and optic nerve. Aqueous humor is secreted by the epithelium of the ciliary body in the posterior chamber and flows through the trabecular meshwork and canal of Schlemm, maintaining normal intraocular pressure. The trabecular meshwork and the canal...
Angle Closure Glaucoma: Treatment01:28

Angle Closure Glaucoma: Treatment

Angle-closure glaucoma, or closed-angle glaucoma, is an eye condition where the iris bulges out and blocks the iridocorneal angle, resulting in a buildup of aqueous humor and increased intraocular pressure. Immediate medical attention is necessary due to the sudden onset of symptoms. The treatment for angle-closure glaucoma includes short-term and long-term approaches. Short-term treatment involves using eye drops like pilocarpine to lower intraocular pressure by increasing aqueous humor...
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Related Experiment Video

Updated: May 26, 2026

Assessing Early Stage Open-Angle Glaucoma in Patients by Isolated-Check Visual Evoked Potential
07:11

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Published on: May 25, 2020

Variants in ASB10 are associated with open-angle glaucoma.

Francesca Pasutto1, Kate E Keller, Nicole Weisschuh

  • 1Institute of Human Genetics, University Hospital Erlangen-Nuremberg, Erlangen, Germany.

Human Molecular Genetics
|December 14, 2011
PubMed
Summary

Genetic variants in ASB10 are linked to primary open angle glaucoma (POAG). This gene is crucial for aqueous humor outflow and retinal ganglion cell health, offering new insights into glaucoma

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Laser Capture Microdissection of Highly Pure Trabecular Meshwork from Mouse Eyes for Gene Expression Analysis
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Laser Capture Microdissection of Highly Pure Trabecular Meshwork from Mouse Eyes for Gene Expression Analysis
13:47

Laser Capture Microdissection of Highly Pure Trabecular Meshwork from Mouse Eyes for Gene Expression Analysis

Published on: June 3, 2018

Area of Science:

  • Ophthalmology
  • Genetics
  • Molecular Biology

Background:

  • Glaucoma, a leading cause of blindness, involves impaired aqueous humor outflow and retinal ganglion cell loss.
  • The precise molecular mechanisms underlying these glaucoma pathologies are not fully understood.

Purpose of the Study:

  • To investigate the role of ankyrin repeats and suppressor of cytokine signaling box-containing protein 10 (ASB10) in primary open angle glaucoma (POAG).
  • To identify genetic variants in ASB10 associated with POAG and elucidate their functional impact.

Main Methods:

  • Identified a synonymous ASB10 variant (c.765C>T) affecting mRNA splicing in a POAG family.
  • Conducted systematic sequence analysis in POAG patient cohorts and controls to find ASB10 missense variants.
  • Utilized molecular modeling to assess the impact of variants on ASB10 structure.
  • Performed ASB10 gene silencing in anterior segment organ cultures to evaluate effects on outflow facility.

Main Results:

  • A significant association was found between ASB10 missense variants and POAG (6.0% in patients vs. 2.8% in controls, P = 0.008).
  • ASB10 variants were predicted to alter protein net charge or ankyrin repeat stability.
  • ASB10 is highly expressed in ocular tissues, including the trabecular meshwork and retinal ganglion cells.
  • Silencing ASB10 reduced aqueous humor outflow facility by approximately 50%.

Conclusions:

  • Genetic and molecular evidence implicates ASB10 as a causative gene in glaucoma.
  • ASB10 plays a critical role in regulating aqueous humor outflow and maintaining retinal ganglion cell function.