Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Mutated myocilin and heterozygous Sod2 deficiency act synergistically in a mouse model of open-angle glaucoma.

Human molecular genetics - 15 Jun 2015

Joe Myung Kuk, Nakaya Naoki, Abu-Asab Mones, Tomarev Stanislav I

Abstract excerpt

Glaucoma is a multifactorial optic neuropathy characterized by retinal ganglion cell (RGC) death and axonal degeneration leading to irreversible blindness. Mutations in the myocilin (MYOC) gene are the most common genetic factors of primary open-angle glaucoma. To develop a genetic mouse model induced by the synergistic interaction of mutated myocilin and another significant risk factor, oxidative stress, we...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to E-Selectin
Share to Endoplasmic Reticulum Stress

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Glaucoma, Open-Angle

Share to Haploinsufficiency

Share to Intraocular Pressure

Share to Optic Nerve Diseases

Share to Retinal Ganglion Cells

Share to Trabecular Meshwork

Source

Open in PubMed Open full text

Identifiers

PMID: 25740847
DOI: 10.1093/hmg/ddv082
PMCID: PMC4447889

Genes

MYOC
SOD2

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Mutated myocilin and heterozygous Sod2 deficiency act synergistically in a mouse model of open-angle glaucoma.PMID 25740847Read ↗

Expression of myocilin mutants sensitizes cells to oxidative stress-induced apoptosis: implication for glaucoma pathogenesis.Semantic proximity Read ↗

Reduction of ER stress via a chemical chaperone prevents disease phenotypes in a mouse model of primary open angle glaucoma.Semantic proximity Read ↗

Somatic Mutations within Myocilin due to Aging May Be a Potential Risk Factor for Glaucoma.Semantic proximity Read ↗

Serine to proline mutation at position 341 of MYOC impairs trabecular meshwork function by causing autophagy deregulationSemantic proximity Read ↗

Serine to proline mutation at position 341 of MYOC impairs trabecular meshwork function by causing autophagy deregulationSemantic proximity Read ↗

Cystatin a, a potential common link for mutant myocilin causative glaucoma.Semantic proximity Read ↗

Somatic Mutations within Myocilin due to Aging may be a Potential Risk Factor for Glaucoma.Semantic proximity Read ↗

Cross-talk between MYOC p. Y437H mutation and TGF-β2 in the pathology of glaucoma.Semantic proximity Read ↗

Disease modeling of myocilin mutation-dependent normal tension glaucoma: human retinal ganglion cell susceptibility to unfolded protein response and mTOR signaling.Semantic proximity Read ↗

Human Pro370Leu Mutant Myocilin Induces the Phenotype of Open-Angle Glaucoma in Transgenic Mice.Semantic proximity Read ↗

Binding of a glaucoma-associated myocilin variant to the αB-crystallin chaperone impedes protein clearance in trabecular meshwork cellsSemantic proximity Read ↗

Stem cell transplantation rescued a primary open-angle glaucoma mouse modelSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.