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LGI1 is rearranged as a result of translocations in glioblastoma cell lines. Zusätzlich bieten wir Ihnen Leucine-Rich, Glioma Inactivated 1 Proteine (5) und Leucine-Rich, Glioma Inactivated 1 Kits (3) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal LGI1 Primary Antibody für IHC, ELISA - ABIN1002722
Gu, Gibert, Wirth, Elischer, Bloch, Meyer, Steinlein, Begemann: Using gene-history and expression analyses to assess the involvement of LGI genes in human disorders. in Molecular biology and evolution 2005
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Human Polyclonal LGI1 Primary Antibody für ELISA, WB - ABIN1002723
Chernova, Somerville, Cowell: A novel gene, LGI1, from 10q24 is rearranged and downregulated in malignant brain tumors. in Oncogene 1999
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LGI1 has a role in regulating cortical development, which is increasingly becoming recognized as one of the causes of idiopathic epilepsy.
LGI1 and ADAM22 (zeige ADAM22 Antikörper) form an essential synaptic organizing complex that coordinates the maturation of excitatory synapses by regulating the functional incorporation of PSD-95 (zeige DLG4 Antikörper)
Review article demonstrating that LGI1 may be an essential player in the development of the brain
Glutamatergic neuron-targeted loss of Lgi1 causes a severe epileptic phenotype; Lgi1 displays an essential role in brain during the whole life.
Lgi1 contains nuclear localization signal that mediates Lgi1 localization to cytoplasm and nucleus in CNS embryonic neurons.
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.
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
LGI1(+/-) and LGI1(-/-) mice may provide useful models for lateral temporal lobe epilepsy, and more generally idiopathic focal epilepsy.
Lgi1 null mutant mice exhibit myoclonic seizures and CA1 (zeige CA1 Antikörper) neuronal hyperexcitability.
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 (zeige CA3 Antikörper) field of the hippocampus.
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 (zeige ADAM22 Antikörper) and ADAM23 (zeige Adam23 Antikörper) 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 (zeige SLC12A4 Antikörper).
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 (zeige AURKA Antikörper) and one visual aura (zeige AURKA Antikörper); 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.
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.
leucine-rich glioma-inactivated protein 1
, leucine-rich, glioma inactivated 1
, leucine-rich glioma-inactivated protein 1-like
, polymorphic marker clone YB07
, leucine-rich repeat LGI family, member 1
, putative leucine-rich glioma inactivated 1