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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Leucine-rich, glioma inactivated 1

EPT, LGI1, leucine-rich, glioma-inactivated 1, ET-LI
This gene is rearranged as a result of translocations in glioblastoma cell lines. The protein contains a hydrophobic segment representing a putative transmembrane domain with the amino terminus located outside the cell. It also contains leucine-rich repeats with conserved cysteine-rich flanking sequences. This gene is predominantly expressed in neural tissues and its expression is reduced in low grade brain tumors and significantly reduced or absent in malignant gliomas. Mutations in this gene result in autosomal dominant lateral temporal epilepsy. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: HAD, CAN, AGE, ACID, endothelin-1
Papers on EPT
Mechanisms of Change in Written Exposure Treatment of Posttraumatic Stress Disorder.
Sloan et al., Boston, United States. In Behav Ther, Jan 2016
Emotional processing theory (EPT) posits that fear reduction within and between sessions creates new learning, but evidence is limited by self-report assessments and inclusion of treatment components other than exposure.
The Treatment and Follow-Up of Anti-LGI1 Limbic Encephalitis.
Lin et al., Changchun, China. In Eur Neurol, Jan 2016
OBJECTIVE: This study aims to retrospectively study clinical characteristics, diagnosis, treatment and follow-up visits in patients with anti-leucine-rich glioma inactivated-1 (LGI1) limbic encephalitis (LE) for prompting the early diagnosis and efficacious treatment of this disease.
Screening LGI1 in a cohort of 26 lateral temporal lobe epilepsy patients with auditory aura from Turkey detects a novel de novo mutation.
Baykan et al., İstanbul, Turkey. In Epilepsy Res, Jan 2016
Heterozygous mutations in LGI1 account for up to 50% of ADLTE families and only rarely observed in IPEAF cases.
Pathologically confirmed autoimmune encephalitis in suspected Creutzfeldt-Jakob disease.
Sillevis Smitt et al., Utrecht, Netherlands. In Neurol Neuroimmunol Neuroinflamm, Dec 2015
Antineuronal antibodies were tested in CSF obtained postmortem by immunohistochemistry on fresh frozen rat brain sections, by Luminex assay for the presence of well-characterized onconeural antibodies, and by cell-based assays for antibodies against NMDAR, GABABR1/2, GABAAR GLUR1/2, LGI1, Caspr2, and DPPX.
Tolerance of the foodborne pathogen Listeria monocytogenes to quaternary ammonium sanitizers is mediated by a novel efflux pump encoded by emrELm.
Gilmour et al., Winnipeg, Canada. In Appl Environ Microbiol, Dec 2015
UNASSIGNED: A novel genomic island (LGI1) was discovered in Listeria monocytogenes isolates responsible for the deadliest listeriosis outbreak in Canada, in 2008.
Imaging of autoimmune encephalitis - Relevance for clinical practice and hippocampal function.
Finke et al., Berlin, Germany. In Neuroscience, Dec 2015
Here, we review the neuroimaging characteristics of autoimmune encephalitides, including N-methyl-d-aspartate (NMDA) receptor, leucine-rich glioma inactivated 1 (LGI1), contactin-associated protein-like 2 (CASPR2) encephalitis as well as more recently discovered and less frequent forms such as dipeptidyl-peptidase-like protein 6 (DPPX) or glycine receptor encephalitis.
Nagy et al., In Ideggyogy Sz, Aug 2015
In the recent years, it has been increasingly recognised that in a group of limbic encephalitis antibodies are directed against the scaffolding protein LGI1 (Leucine-rich glioma inactivated 1), which is part of the voltage gated potassium channel (VGKC) complex on neural synapses.
LGI Proteins and Epilepsy in Human and Animals.
Hasegawa et al., Vienna, Austria. In J Vet Intern Med, Jul 2015
Genetic mutation of LGI1 was confirmed to be the cause of autosomal dominant lateral temporal lobe epilepsy in humans.
Genetic models of focal epilepsies.
Baulac et al., Paris, France. In J Neurosci Methods, Jul 2015
In this article, we provide an update on the mutational spectrum of neuronal nicotinic acetylcholine receptor genes (CHRNA4, CHRNB2, CHRNA2) and KCNT1 causing autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE), and of LGI1 in autosomal dominant epilepsy with auditory features (ADEAF).
The active intrathecal B-cell response in LGI1-antibody encephalitis.
von Büdingen et al., San Francisco, United States. In Lancet, Mar 2015
BACKGROUND: Leucine-rich glioma inactivated 1 (LGI1) is a component of the voltage-gated potassium channel complex.
Chemical corrector treatment ameliorates increased seizure susceptibility in a mouse model of familial epilepsy.
Fukata et al., Okazaki, Japan. In Nat Med, 2015
Mutations in the human gene LGI1, encoding a neuronal secreted protein, cause autosomal dominant lateral temporal lobe epilepsy (ADLTE).
Paving the Way to Understand Autoantibody-Mediated Epilepsy on the Molecular Level.
Strutz-Seebohm et al., Münster, Germany. In Front Neurol, 2014
Recently, autoantibodies targeting receptor or channel complexes like NMDAR, AMPAR, GABA-receptors, glycine receptors, LGI1 or CASPR2 (previously termed as VGKC-complex antibodies) have been discovered.
Immunotherapy-responsive chorea as the presenting feature of LGI1-antibody encephalitis.
Vincent et al., Oxford, United Kingdom. In Neurology, 2012
Antibodies bind to proteins complexed with voltage-gated potassium channel (VGKC) complex in two patients with LG11-antibody encephalitis.
LGI1 microdeletion in autosomal dominant lateral temporal epilepsy.
Nobile et al., Alghero, Italy. In Neurology, 2012
This is the first microdeletion affecting LGI1 identified in autosomal dominant lateral temporal epilepsy.
Domain-dependent clustering and genotype-phenotype analysis of LGI1 mutations in ADPEAF.
Ottman et al., New York City, United States. In Neurology, 2012
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.
Mutant LGI1 inhibits seizure-induced trafficking of Kv4.2 potassium channels.
Anderson et al., Boston, United States. In J Neurochem, 2012
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.
Epilepsy gene LGI1 regulates postnatal developmental remodeling of retinogeniculate synapses.
Anderson et al., Boston, United States. In J Neurosci, 2012
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.
Investigation of LGI1 as the antigen in limbic encephalitis previously attributed to potassium channels: a case series.
Dalmau et al., Philadelphia, United States. In Lancet Neurol, 2010
The target antigen of antibodies in patients with limbic encephalitis previously attributed to voltage-gated potassium channels is in fact LGI1, a secreted neuronal protein that functions as a ligand for two epilepsy-related proteins, ADAM22 and ADAM23.
Concerted proton-electron transfers: electrochemical and related approaches.
Savéant et al., Paris, France. In Acc Chem Res, 2010
The reaction may go through an electron- or proton-transfer intermediate, giving rise to the electron-proton transfer (EPT) and the proton-electron transfer (PET) pathways.
Arrested maturation of excitatory synapses in autosomal dominant lateral temporal lobe epilepsy.
Anderson et al., Boston, United States. In Nat Med, 2009
The normal postnatal maturation of presynaptric and postsynaptic functions was arrested by the 835delC mutant Lgi1.
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