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Times Cited: 191
Times Cited: 191
Times Cited
Times Co-cited
Similarity
Identification of a gene that causes primary open angle glaucoma.
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The number of people with glaucoma worldwide in 2010 and 2020.
H A Quigley, A T Broman. Br J Ophthalmol 2006
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Accumulation of mutant myocilins in ER leads to ER stress and potential cytotoxicity in human trabecular meshwork cells.
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Non-secretion of mutant proteins of the glaucoma gene myocilin in cultured trabecular meshwork cells and in aqueous humor.
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Topical ocular sodium 4-phenylbutyrate rescues glaucoma in a myocilin mouse model of primary open-angle glaucoma.
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Ocular-specific ER stress reduction rescues glaucoma in murine glucocorticoid-induced glaucoma.
Gulab S Zode, Arti B Sharma, Xiaolei Lin, Charles C Searby, Kevin Bugge, Gun Hee Kim, Abbot F Clark, Val C Sheffield. J Clin Invest 2014
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Trabecular meshwork cellularity in primary open-angle glaucoma and nonglaucomatous normals.
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The pathophysiology and treatment of glaucoma: a review.
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Aggregated myocilin induces russell bodies and causes apoptosis: implications for the pathogenesis of myocilin-caused primary open-angle glaucoma.
Gary Hin-Fai Yam, Katarina Gaplovska-Kysela, Christian Zuber, Jürgen Roth. Am J Pathol 2007
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Increased Endoplasmic Reticulum Stress in Human Glaucomatous Trabecular Meshwork Cells and Tissues.
Joseph C Peters, Sanjoy Bhattacharya, Abbot F Clark, Gulab S Zode. Invest Ophthalmol Vis Sci 2015
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Analysis of myocilin mutations in 1703 glaucoma patients from five different populations.
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Clinical features associated with mutations in the chromosome 1 open-angle glaucoma gene (GLC1A)
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Global prevalence of glaucoma and projections of glaucoma burden through 2040: a systematic review and meta-analysis.
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Expression of Mutant Myocilin Induces Abnormal Intracellular Accumulation of Selected Extracellular Matrix Proteins in the Trabecular Meshwork.
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Targeted Disruption of the Myocilin Gene (Myoc) Suggests that Human Glaucoma-Causing Mutations Are Gain of Function.
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Extracellular matrix in the trabecular meshwork: intraocular pressure regulation and dysregulation in glaucoma.
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Mutant human myocilin induces strain specific differences in ocular hypertension and optic nerve damage in mice.
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Dexamethasone-Induced Ocular Hypertension in Mice: Effects of Myocilin and Route of Administration.
Gaurang C Patel, Tien N Phan, Prabhavathi Maddineni, Ramesh B Kasetti, J Cameron Millar, Abbot F Clark, Gulab S Zode. Am J Pathol 2017
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CRISPR-Cas9-based treatment of myocilin-associated glaucoma.
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Glucose-regulated protein 94 triage of mutant myocilin through endoplasmic reticulum-associated degradation subverts a more efficient autophagic clearance mechanism.
Amirthaa Suntharalingam, Jose F Abisambra, John C O'Leary, John Koren, Bo Zhang, Myung Kuk Joe, Laura J Blair, Shannon E Hill, Umesh K Jinwal, Matthew Cockman,[...]. J Biol Chem 2012
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A molecular mechanism for glaucoma: endoplasmic reticulum stress and the unfolded protein response.
Robert R H Anholt, Mary Anna Carbone. Trends Mol Med 2013
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Transplantation of iPSC-derived TM cells rescues glaucoma phenotypes in vivo.
Wei Zhu, Oliver W Gramlich, Lauren Laboissonniere, Ankur Jain, Val C Sheffield, Jeffrey M Trimarchi, Budd A Tucker, Markus H Kuehn. Proc Natl Acad Sci U S A 2016
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Expression of mutated mouse myocilin induces open-angle glaucoma in transgenic mice.
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Adult-onset primary open-angle glaucoma caused by mutations in optineurin.
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Prevalence of mutations in TIGR/Myocilin in patients with adult and juvenile primary open-angle glaucoma.
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Induced pluripotent stem cells restore function in a human cell loss model of open-angle glaucoma.
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Transgenic mice expressing the Tyr437His mutant of human myocilin protein develop glaucoma.
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Myocilin allele-specific glaucoma phenotype database.
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Functional analysis of the glaucoma-causing TIGR/myocilin protein: integrity of amino-terminal coiled-coil regions and olfactomedin homology domain is essential for extracellular adhesion and secretion.
Stéphane Gobeil, Laurence Letartre, Vincent Raymond. Exp Eye Res 2006
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Genetically increasing Myoc expression supports a necessary pathologic role of abnormal proteins in glaucoma.
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Age-dependent prevalence of mutations at the GLC1A locus in primary open-angle glaucoma.
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Sodium 4-phenylbutyrate acts as a chemical chaperone on misfolded myocilin to rescue cells from endoplasmic reticulum stress and apoptosis.
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Targeting the ER-autophagy system in the trabecular meshwork to treat glaucoma.
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Copy number variations on chromosome 12q14 in patients with normal tension glaucoma.
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Intraocular pressure homeostasis: maintaining balance in a high-pressure environment.
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Consensus recommendations for trabecular meshwork cell isolation, characterization and culture.
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Stem cells from trabecular meshwork home to TM tissue in vivo.
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Gene structure and properties of TIGR, an olfactomedin-related glycoprotein cloned from glucocorticoid-induced trabecular meshwork cells.
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The stability of myocilin olfactomedin domain variants provides new insight into glaucoma as a protein misfolding disorder.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.