Leucine-Rich, Glioma Inactivated 1 (LGI1) ELISA Kits

Human Leucine-Rich, Glioma Inactivated 1 (LGI1) Interaktionspartner

1. Study shows that hippocampal dentate gyrus atrophy predicts pattern separation impairment in patients with LGI1 encephalitis.

2. the LGI1-ADAM22 complex functions as the trans-synaptic machinery for precise synaptic transmission

3. The data obtained strongly suggest the possibility of gene LGL1 inactivation by epigenetic mechanism: modified <>.

4. 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}

5. 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

6. Autosomal dominant epilepsy with auditory features family due to a novel LGI1 mutation.

7. Clinical analysis of a lateral temporal lobe epilepsy cohort from Turkey and genetic contribution of LGI1 to autosomal dominant lateral temporal lobe epilepsy phenotype

8. 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

9. 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

10. 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.

11. A new LGI1 missense mutation is identified in a large Korean family with autosomal dominant lateral temporal lobe epilepsy.

12. Seven LGI1-affected individuals report auditory aura and one visual aura; three families with autosomal dominant epilepsy and auditory features have novel LGI1 mutations.

13. Downregulation of LGI1 promotes tumor metastasis in esophageal squamous cell carcinoma.

14. 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.

15. The LGI1-ADAM22 interaction is neutralized by autoantibodies to epilepsy-related LGI1 in limbic encephalitis.

16. This study demonistrated that Low penetrance of autosomal dominant lateral temporal epilepsy in Italian families without LGI1 mutations.

17. Cerebrocortical manifestations are recorded in 76% of patients with LGI1 immunoglobulin G (IgG) seropositivity.

18. Antibodies bind to proteins complexed with voltage-gated potassium channel (VGKC) complex in two patients with LG11-antibody encephalitis.

19. This is the first microdeletion affecting LGI1 identified in autosomal dominant lateral temporal epilepsy.

20. 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.

Mouse (Murine) Leucine-Rich, Glioma Inactivated 1 (LGI1) Interaktionspartner

1. Neural stem cell specific inactivation of LGI1 results in cortical dysplasia.

2. LGI1 is expressed at the axonal initial segment and regulates action potential firing by setting the density of the axonal Kv1.1 channels.

3. LGI1 has a role in regulating cortical development, which is increasingly becoming recognized as one of the causes of idiopathic epilepsy.

4. LGI1 and ADAM22 form an essential synaptic organizing complex that coordinates the maturation of excitatory synapses by regulating the functional incorporation of PSD-95

5. Review article demonstrating that LGI1 may be an essential player in the development of the brain

6. Glutamatergic neuron-targeted loss of Lgi1 causes a severe epileptic phenotype; Lgi1 displays an essential role in brain during the whole life.

7. Lgi1 contains nuclear localization signal that mediates Lgi1 localization to cytoplasm and nucleus in CNS embryonic neurons.

8. This study demonistrated that LGI1 plays a critical role in both dendritic and axonal pruning, we identify a novel molecular pathway in synapse and circuit remodeling.

9. Lgi1 may have a role in establishing normal brain architecture and neuronal functions during brain development suggesting that it may be involved in neurogenesis and neuronal plasticity

10. LGI1(+/-) and LGI1(-/-) mice may provide useful models for lateral temporal lobe epilepsy, and more generally idiopathic focal epilepsy.

11. Lgi1 null mutant mice exhibit myoclonic seizures and CA1 neuronal hyperexcitability.

12. in the brain of C57BL/6J adult mice by in situ hybridization. We found that the LGI1 transcript is mainly expressed in the dentate gyrus and CA3 field of the hippocampus.

13. Reduce levels of secreted LGI1 is associated with autosomal dominant partial epilepsy with auditory features

14. Two protein isoforms encoded by LGI1/epitempin are differentially expressed in mouse brain: the 60-kDa form is detected in the microsomal fraction, while the 65-kDa product is found in the cytosolic fraction.

15. This study was the first to determine a specific profile of Lgi1 gene expression during central nervous system development, which suggests a possible inhibitory function in latter stages of development.

16. study identified LGI1 as a specific binding partner of ADAM22 protein from mouse brain, and demonstrated the specific interaction between LGI1 and ADAM22

17. The normal postnatal maturation of presynaptric and postsynaptic functions was arrested by the 835delC mutant Lgi1.

Zebrafish Leucine-Rich, Glioma Inactivated 1 (LGI1) Interaktionspartner

1. Knockdown of zebrafish Lgi1a results in abnormal development, brain defects and a seizure-like behavioral phenotype.