ArticleMolecular vision2012
Evaluation of NTF4 as a causative gene for primary open-angle glaucoma.
Article in Molecular vision, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Recent developments of neuroprotective agents for degenerative retinal disorders.Neural regeneration research · 2022Review
- Asian Race and Primary Open-Angle Glaucoma: Where Do We Stand?Journal of clinical medicine · 2022Review
- Exploration of the Immune-Related Signatures and Immune Infiltration Analysis in Melanoma.Analytical cellular pathology (Amsterdam) · 2021Article
- Research progress on human genes involved in the pathogenesis of glaucoma (Review).Molecular medicine reports · 2018Review
- Detection of mutations in MYOC, OPTN, NTF4, WDR36 and CYP1B1 in Chinese juvenile onset open-angle glaucoma using exome sequencing.Scientific reports · 2018Article
- Glaucoma Pathogenesis and Neurotrophins: Focus on the Molecular and Genetic Basis for Therapeutic Prospects.Current neuropharmacology · 2018Review
- Major review: Molecular genetics of primary open-angle glaucoma.Experimental eye research · 2017Review
- An Updated Review on the Genetics of Primary Open Angle Glaucoma.International journal of molecular sciences · 2015Review
- Genetics of primary open angle glaucoma.Japanese journal of ophthalmology · 2014Review
- Association of apolipoprotein E-219T>G promoter polymorphism with primary open angle glaucoma in Turkish population.International journal of ophthalmology · 2014Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe neurotrophin-4 (NTF4) gene has been recently implicated in primary open-angle glaucoma (POAG). In this study, we investigated the implication of NTF4 in POAG among three Chinese cohorts.
methodsThe coding regions and exon-intron boundaries of NTF4 was sequenced in 950 unrelated Chinese subjects, including a Hong Kong cohort of 390 patients and 230 controls, a Shantou cohort of 130 patients, and a Beijing cohort of 200 patients. Constructs carrying the detected variants were generated using site-directed mutagenesis and transfected into HeLa cells, followed by solubility and migration analyses.
resultsThree variants were identified. p.Pro151Pro was detected in three POAG patients and one control subject. Two novel missense variants, p.Gly157Ala and p.Ala182Val, were identified each in one POAG patient from the Hong Kong cohort, but not in controls. Functional assays showed that the p.Gly157Ala mutant protein was less soluble in Triton X-100, and that migration of HeLa cells transfected with either mutant construct was less than cells transfected with the wildtype.
conclusionsThe NTF4 variants p.Gly157Ala and p.Ala182Val have been shown to be functional mutations, occurring in 2 of a total of 720 Chinese POAG patients. NTF4 is functionally related to POAG pathogenesis but its mutation frequency is low. Therefore, NTF4 does not have a major contribution in the molecular genetics of POAG.
Indexed as
Identifiers
22815630PMC3398503W1567799071What OpenQuestion holds
Registered trials
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