ArticlePloS one2011
A computational model of the LGI1 protein suggests a common binding site for ADAM proteins.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 38 citations in OpenAlex.
- The LGI1 protein: molecular structure, physiological functions and disruption-related seizures.Cellular and molecular life sciences : CMLS · 2021Review
- Insights into the mechanisms of epilepsy from structural biology of LGI1-ADAM22.Cellular and molecular life sciences : CMLS · 2020Review
- Functions of 'A disintegrin and metalloproteases (ADAMs)' in the mammalian nervous system.Cellular and molecular life sciences : CMLS · 2019Review
- Structural basis of epilepsy-related ligand-receptor complex LGI1-ADAM22.Nature communications · 2018Article
- Dynamic scaffolds for neuronal signaling: in silico analysis of the TANC protein family.Scientific reports · 2017Article
- ADAM23 promotes neuronal differentiation of human neural progenitor cells.Cellular & molecular biology letters · 2017Article
- Secretion-Positive LGI1 Mutations Linked to Lateral Temporal Epilepsy Impair Binding to ADAM22 and ADAM23 Receptors.PLoS genetics · 2016Article
- Homozygous Deletion of the LGI1 Gene in Mice Leads to Developmental Abnormalities Resulting in Cortical Dysplasia.Brain pathology (Zurich, Switzerland) · 2015Article
- The LGI1-ADAM22 protein complex directs synapse maturation through regulation of PSD-95 function.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Essential roles of leucine-rich glioma inactivated 1 in the development of embryonic and postnatal cerebellum.Scientific reports · 2015Article
- Glutamatergic neuron-targeted loss of LGI1 epilepsy gene results in seizures.Brain : a journal of neurology · 2014Article
- LGI proteins in the nervous system.ASN neuro · 2013Review
- Genetics of epilepsy and relevance to current practice.Current neurology and neuroscience reports · 2012Review
- Domain-dependent clustering and genotype-phenotype analysis of LGI1 mutations in ADPEAF.Neurology · 2012Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations of human leucine-rich glioma inactivated (LGI1) gene encoding the epitempin protein cause autosomal dominant temporal lateral epilepsy (ADTLE), a rare familial partial epileptic syndrome. The LGI1 gene seems to have a role on the transmission of neuronal messages but the exact molecular mechanism remains unclear. In contrast to other genes involved in epileptic disorders, epitempin shows no homology with known ion channel genes but contains two domains, composed of repeated structural units, known to mediate protein-protein interactions.A three dimensional in silico model of the two epitempin domains was built to predict the structure-function relationship and propose a functional model integrating previous experimental findings. Conserved and electrostatic charged regions of the model surface suggest a possible arrangement between the two domains and identifies a possible ADAM protein binding site in the β-propeller domain and another protein binding site in the leucine-rich repeat domain. The functional model indicates that epitempin could mediate the interaction between proteins localized to different synaptic sides in a static way, by forming a dimer, or in a dynamic way, by binding proteins at different times.The model was also used to predict effects of known disease-causing missense mutations. Most of the variants are predicted to alter protein folding while several other map to functional surface regions. In agreement with experimental evidence, this suggests that non-secreted LGI1 mutants could be retained within the cell by quality control mechanisms or by altering interactions required for the secretion process.
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