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GLE1 Gle1p

Gle1, Gle1p, LCCS, hGle1
This gene encodes a predicted 75-kDa polypeptide with high sequence and structure homology to yeast Gle1p, which is nuclear protein with a leucine-rich nuclear export sequence essential for poly(A)+RNA export. Inhibition of human GLE1L by microinjection of antibodies against GLE1L in HeLa cells resulted in inhibition of poly(A)+RNA export. Immunoflourescence studies show that GLE1L is localized at the nuclear pore complexes. This localization suggests that GLE1L may act at a terminal step in the export of mature RNA messages to the cytoplasm. Two alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
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Top mentioned proteins: Dbp5, Nucleoporin, ACID, STEP, CAN
Papers on Gle1
Restoration of miR-127-3p and miR-376a-3p counteracts the neoplastic phenotype of giant cell tumor of bone derived stromal cells by targeting COA1, GLE1 and PDIA6.
New
Herr et al., Heidelberg, Germany. In Cancer Lett, Mar 2016
Luciferase reporter assays demonstrated direct interactions of miR-127-3p with COA1 and direct interaction of miR-376a-3p with GLE1 and PDIA6, suggesting a pivotal role of these genes in the molecular etiology of GTCB.
An amyotrophic lateral sclerosis-linked mutation in GLE1 alters the cellular pool of human Gle1 functional isoforms.
New
Wente et al., Nashville, United States. In Adv Biol Regul, Dec 2015
In prior studies, two deleterious heterozygous mutations in the gene encoding human (h)Gle1 were identified in ALS patients.
Systematic DNA methylation analysis of multiple cell lines reveals common and specific patterns within and across tissues of origin.
New
Zhang et al., Xi'an, China. In Hum Mol Genet, Sep 2015
We constructed an LCCS co-methylation network and investigated the common DNA methylation patterns across all cell lines, which reveal two distinct groups in terms of their methylation level and genomic characteristics.
Cytoplasmic hGle1A regulates stress granules by modulation of translation.
New
Wente et al., Nashville, United States. In Mol Biol Cell, May 2015
We document that human Gle1 (hGle1) is a critical regulator of translation during stress.
Deleterious mutations in the essential mRNA metabolism factor, hGle1, in amyotrophic lateral sclerosis.
New
Dion et al., Nashville, United States. In Hum Mol Genet, Apr 2015
Lethal congenital contracture syndrome 1 and lethal arthrogryposis with anterior horn cell disease are autosomal recessive fetal motor neuron diseases that are caused by mutations in another global RNA-processing protein, hGle1.
An exome sequencing strategy to diagnose lethal autosomal recessive disorders.
New
Lango Allen et al., Exeter, United Kingdom. In Eur J Hum Genet, Mar 2015
The first couple were each heterozygous for a previously reported GLE1 variant, p.Arg569His or p.Val617Met; both were inherited by their two affected fetuses.
ZBTB42 mutation defines a novel lethal congenital contracture syndrome (LCCS6).
Alkuraya et al., Riyadh, Saudi Arabia. In Hum Mol Genet, 2015
Lethal congenital contracture syndrome (LCCS) is a lethal autosomal recessive form of arthrogryposis multiplex congenita (AMC).
Nucleoporin FG domains facilitate mRNP remodeling at the cytoplasmic face of the nuclear pore complex.
Wente et al., Nashville, United States. In Genetics, 2014
In Saccharomyces cerevisiae, the NPC proteins Nup159 and Nup42 are asymmetrically localized to the cytoplasmic face and have distinct functional domains: a phenylalanine-glycine (FG) repeat domain that docks mRNP transport receptors and domains that bind the DEAD-box ATPase Dbp5 and its activating cofactor Gle1, respectively.
Insights into mRNA export-linked molecular mechanisms of human disease through a Gle1 structure-function analysis.
Review
Wente et al., Nashville, United States. In Adv Biol Regul, 2014
GLE1 mutations are causally linked to the human diseases lethal congenital contracture syndrome 1 (LCCS-1) and lethal arthrogryposis with anterior horn cell disease (LAAHD).
Gle1 functions during mRNA export in an oligomeric complex that is altered in human disease.
Impact
Wente et al., Nashville, United States. In Cell, 2013
A GLE1 mutation (FinMajor) is causally linked to human lethal congenital contracture syndrome-1 (LCCS1); however, the resulting perturbations on Gle1 molecular function were unknown.
[Screening of differential proteins binding to Nox1 promoter in A549 cell model of inflammation and oxidative stress].
Huang et al., Guangzhou, China. In Nan Fang Yi Ke Da Xue Xue Bao, 2013
RESULTS: Seven differentially expressed protein spots (all upregulated in the cell model) were obtained, among which GLE1, DDX19A, KRT1 and KRT10 were identified by mass spectrometry.
A zebrafish model of lethal congenital contracture syndrome 1 reveals Gle1 function in spinal neural precursor survival and motor axon arborization.
GeneRIF
Wente et al., Nashville, United States. In Development, 2012
defective zebrafish GLE1 function in human LCCS1 results in both neurogenic and non-neurogenic defects linked to the apoptosis of proliferative organ precursors
Gle1 is a multifunctional DEAD-box protein regulator that modulates Ded1 in translation initiation.
GeneRIF
Wente et al., Nashville, United States. In J Biol Chem, 2011
Gle1 is a multifunctional DEAD-box protein regulator that modulates Ded1 in translation initiation.
Dbp5, Gle1-IP6 and Nup159: a working model for mRNP export.
GeneRIF
Wente et al., Nashville, United States. In Nucleus, 2011
Dbp5, Gle1-IP6 and Nup159: a working model for mRNP export.
Control of mRNA export and translation termination by inositol hexakisphosphate requires specific interaction with Gle1.
GeneRIF
Wente et al., Nashville, United States. In J Biol Chem, 2010
Gle1 specifically binds IP(6); this interaction is required for the full potentiation of Dbp5 ATPase activity during both mRNA export and translation termination
Structure of the C-terminus of the mRNA export factor Dbp5 reveals the interaction surface for the ATPase activator Gle1.
GeneRIF
Weis et al., Berkeley, United States. In Proc Natl Acad Sci U S A, 2009
Study identified several charged surface residues that, when mutated, weaken the binding of Gle1 and inhibit the ability of Gle1 to stimulate Dbp5's ATPase activity.
The mRNA export factor Gle1 and inositol hexakisphosphate regulate distinct stages of translation.
Impact
GeneRIF
Wente et al., Nashville, United States. In Cell, 2008
Study shows that Gle1 and inositol hexakisphosphate are required for efficient translation termination, in addition, Gle1 has a conserved physical association with the initiation factor eIF3.
Mutations in mRNA export mediator GLE1 result in a fetal motoneuron disease.
Impact
GeneRIF
Peltonen et al., Helsinki, Finland. In Nat Genet, 2008
Mutations in mRNA export mediator GLE1 result in fetal motoneuron disease.
Activation of the DExD/H-box protein Dbp5 by the nuclear-pore protein Gle1 and its coactivator InsP6 is required for mRNA export.
Impact
GeneRIF
Weis et al., Berkeley, United States. In Nat Cell Biol, 2006
Our results define specific functions for Gle1 and InsP6 in mRNA export and suggest that local activation of Dbp5 at the nuclear pore is critical for mRNA export.
A phospholipase C-dependent inositol polyphosphate kinase pathway required for efficient messenger RNA export.
Impact
Wente et al., Durham, United States. In Science, 1999
In order to identify additional factors required for nuclear export of messenger RNA, a genetic screen was conducted with a yeast mutant deficient in a factor Gle1p, which associates with the nuclear pore complex (NPC).
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