-
the LGI1-ADAM22 complex functions as the trans-synaptic machinery for precise synaptic transmission
-
The data obtained strongly suggest the possibility of gene LGL1 inactivation by epigenetic mechanism: modified <>.
-
The clinical phenotypes of anti-LGI1 encephalitis and anti-Caspr2 encephalitis have been described in more detail including data on treatment and long-term follow-up. Lumping patients with anti-LGI1, anti-Caspr2 antibodies or lacking both, should be considered obsolete--{REVIEW}
-
these results support the existence of a second mechanism, alternative to inhibition of protein secretion, by which ADLTE-causing LGI1 mutations exert their loss-of-function effect extracellularly, and suggest that interactions of LGI1 with both ADAM22 and ADAM23 play an important role in the molecular mechanisms leading to utosomal dominant lateral temporal epilepsy
-
Autosomal dominant epilepsy with auditory features family due to a novel LGI1 mutation.
-
Clinical analysis of a lateral temporal lobe epilepsy cohort from Turkey and genetic contribution of LGI1 to autosomal dominant lateral temporal lobe epilepsy phenotype
-
Report of three novel LGI1 mutations, a microdeletion of exon 2 and two missense mutations in exon 8, occurring in two autosomal dominant lateral temporal epilepsy families and in one sporadic patient with lateral temporal epilepsy
-
study found no cryptic imbalances were in LGI1 in partial epilepsy with auditory features (PEAF) patients, suggesting that LGI1 microdeletions are not a frequent cause of PEAF
-
The Multiplex ligation-dependent probe amplifications analysis did not reveal any pathogenic changes in the LGI1 gene. Chromosomal rearrangements involving the LGI1 gene were not identified in our series of familial or sporadic LTE.
-
A new LGI1 missense mutation is identified in a large Korean family with autosomal dominant lateral temporal lobe epilepsy.
-
Seven LGI1-affected individuals report auditory aura and one visual aura; three families with autosomal dominant epilepsy and auditory features have novel LGI1 mutations.
-
Downregulation of LGI1 promotes tumor metastasis in esophageal squamous cell carcinoma.
-
This study expands the phenotypic spectrum associated with Autosomal dominant lateral temporal lobe epilepsy due to LGI1 mutation and underlines the need for more systematic evaluation of Attention-deficit hyperactivity disorder and related symptoms.
-
The LGI1-ADAM22 interaction is neutralized by autoantibodies to epilepsy-related LGI1 in limbic encephalitis.
-
This study demonistrated that Low penetrance of autosomal dominant lateral temporal epilepsy in Italian families without LGI1 mutations.
-
Cerebrocortical manifestations are recorded in 76% of patients with LGI1 immunoglobulin G (IgG) seropositivity.
-
Antibodies bind to proteins complexed with voltage-gated potassium channel (VGKC) complex in two patients with LG11-antibody encephalitis.
-
This is the first microdeletion affecting LGI1 identified in autosomal dominant lateral temporal epilepsy.
-
The N-terminal leucine-rich repeat region of the LGI1 gene is likely to play a major role in pathogenesis of autosomal dominant partial epilepsy with auditory features.
-
LGI1, a secreted synaptic protein mutated to cause human partial epilepsy, regulates a seizure-induced circuit response by redistributing Kv4.2 channels to the neuronal surface in a transgenic mouse model.
