This website uses cookies to ensure you get the best experience on our website.
- Table of Contents
Information about Late-infantile Neuronal Ceroid Lipfuscinosis: 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.
Most recent studies have shown that Late-infantile Neuronal Ceroid Lipfuscinosis shares some biological mechanisms with ataxia, atrophy, blind-vision, brain-diseases, ceroid-lipofuscinosis-neuronal-5, encephalopathies, epilepsies-myoclonic, epilepsy, hereditary-diseases, infantile-neuronal-ceroid-lipofuscinosis, juvenile-neuronal-ceroid-lipfuscinosis, lysosomal-storage-diseases, nerve-degeneration, nervousness, neurodegenerative-disorders, neuronal-ceroid-lipofuscinoses, storage-disease, visual-impairment.
Among the many pathways, these few ones have gauged particular interests from scientists studying Late-infantile Neuronal Ceroid Lipfuscinosis, and have been seen in publications frequently: Aging, Cardiac Conduction, Cell Death, Circadian Rhythm, Clathrin-mediated Endocytosis, Cognition, Endocytosis, Glycosylation, Immune Response, Localization, Meiosis, Meiosis Ii, Mitosis, Muscle Atrophy, Pathogenesis, Proteolysis, Receptor-mediated Endocytosis, Translation, Transport, Visual Behavior
Quite a number of genes have been found to play important roles in Late-infantile Neuronal Ceroid Lipfuscinosis, such as ACD, CLN3, CLN5, CLN6, CLN8, CTSC, CTSD, DNAJC5, MFSD8, NCL, PPP5C, PPT1, TAC1, TPP1, TTPA. 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.