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Disease Info Card
External Ophthalmoplegia
Information about External Ophthalmoplegia: characteristics, related genes and pathways, plus antibodies you can use for research. This page is being enriched constantly, if you see some information you would like this page to include please send your suggestions to us.
Overview of External Ophthalmoplegia
Most recent studies have shown that External Ophthalmoplegia shares some biological mechanisms with acidosis, acidosis-lactic, ataxia, atrophy, blepharoptosis, chronic-progressive-external-ophthalmoplegia, encephalopathies, epilepsy, kearns-sayre-syndrome, melas-syndrome, mitochondrial-diseases, mitochondrial-encephalomyopathies, mitochondrial-myopathies, muscle-weakness, myopathy, ophthalmoplegia, retinal-diseases, retinitis-pigmentosa, weakness.
Among the many pathways, these few ones have gauged particular interests from scientists studying External Ophthalmoplegia, and have been seen in publications frequently: Aging, Cardiac Conduction, Cell Death, Dna Replication, Electron Transport, Electron Transport Chain, Excretion, Innervation, Lipid Storage, Localization, Mitochondrial Dna Replication, Mitochondrial Translation, Muscle Atrophy, Oxidative Phosphorylation, Pathogenesis, Pigmentation, Reflex, Regeneration, Translation, Transport
Quite a number of genes have been found to play important roles in External Ophthalmoplegia, such as CHMP1B, COX5A, COX8A, CPOX, CSF2, CYCS, LAMC2, MRRF, POLG, POLG2, PRPF6, RYR1, SLC25A4, TYMP. See what Boster has to offer for the research of these genes by clicking the gene name links below and view a more detailed info card/product listing for that gene.
In a later update, we will include information such as current drugs and therapy solutions as well as on-going and past clinical trials for this disease. Plesae stay updated.