ArticleThe Journal of biological chemistry2011
Gle1 is a multifunctional DEAD-box protein regulator that modulates Ded1 in translation initiation.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 47 citations in OpenAlex.
- Medulloblastoma-associated mutations in the RNA helicase DDX3X/DED1 cause defects in the translational response to TORC1 inhibition.The Journal of biological chemistry · 2026Article
- Development and validation of liquid-liquid phase separation-associated prognostic biomarkers in gastric cancer.Discover oncology · 2025Article
- Phosphorylation impacts GLE1 nuclear localization and association with DDX1.Advances in biological regulation · 2023Article
- Nuclear pore complexes - a doorway to neural injury in neurodegeneration.Nature reviews. Neurology · 2022Review
- The RNA Helicase Ded1 Regulates Translation and Granule Formation during Multiple Phases of Cellular Stress Responses.Molecular and cellular biology · 2022Article
- Translational control by helicases during cellular stress.Methods in enzymology · 2022Article
- Snx4-assisted vacuolar targeting of transcription factors defines a new autophagy pathway for controllingAutophagy · 2021Article
- Functions of Gle1 are governed by two distinct modes of self-association.The Journal of biological chemistry · 2020Article
- Extension of the phenotypic spectrum of GLE1-related disorders to a mild congenital form resembling congenital myopathy.Molecular genetics & genomic medicine · 2020Article
- Dbp5/DDX19 between Translational Readthrough and Nonsense Mediated Decay.International journal of molecular sciences · 2020Review
- Mechanisms of nuclear mRNA export: A structural perspective.Traffic (Copenhagen, Denmark) · 2019Review
- The DEAD-box RNA helicase Ded1 has a role in the translational response to TORC1 inhibition.Molecular biology of the cell · 2019Article
- Metabolic stress activates an ERK/hnRNPK/DDX3X pathway in pancreatic β cells.Molecular metabolism · 2019Article
- MAPK- and glycogen synthase kinase 3-mediated phosphorylation regulates the DEAD-box protein modulator Gle1 for control of stress granule dynamics.The Journal of biological chemistry · 2019Article
- Gle1 mediates stress granule-dependent survival during chemotoxic stress.Advances in biological regulation · 2019Article
- Structural and functional analysis of mRNA export regulation by the nuclear pore complex.Nature communications · 2018Article
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- Nup42 and IPTraffic (Copenhagen, Denmark) · 2017Article
- Gle1 Regulates RNA Binding of the DEAD-Box Helicase Ded1 in Its Complex Role in Translation Initiation.Molecular and cellular biology · 2017Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
DEAD-box protein (Dbp) family members are essential for gene expression; however, their precise roles and regulation are not fully defined. During messenger (m)RNA export, Gle1 bound to inositol hexakisphosphate (IP(6)) acts via Dbp5 to facilitate remodeling of mRNA-protein complexes. In contrast, here we define a novel Gle1 role in translation initiation through regulation of a different DEAD-box protein, the initiation factor Ded1. We find that Gle1 physically and genetically interacts with Ded1. Surprisingly, whereas Gle1 stimulates Dbp5, it inhibits Ded1 ATPase activity in vitro, and IP(6) does not affect this inhibition. Functionally, a gle1-4 mutant specifically suppresses initiation defects in a ded1-120 mutant, and ded1 and gle1 mutants have complementary perturbations in AUG start site recognition. Consistent with this role in initiation, Gle1 inhibits translation in vitro in competent extracts. These results indicate that Gle1 has a direct role in initiation and negatively regulates Ded1. Together, the differential regulation of two distinct DEAD-box proteins by a common factor (Gle1) establishes a new paradigm for controlling gene expression and coupling translation with mRNA export.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.