Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Research Project (R01)
Project #
1R01GM051219-01
Application #
2189591
Study Section
Molecular Cytology Study Section (CTY)
Project Start
1994-09-01
Project End
1998-08-31
Budget Start
1994-09-01
Budget End
1995-08-31
Support Year
1
Fiscal Year
1994
Total Cost
Indirect Cost
Name
Washington University
Department
Physiology
Type
Schools of Medicine
DUNS #
062761671
City
Saint Louis
State
MO
Country
United States
Zip Code
63130
Glass, Laura; Wente, Susan R (2018) Gle1 mediates stress granule-dependent survival during chemotoxic stress. Adv Biol Regul :
Aditi; Glass, Laura; Dawson, T Renee et al. (2016) An amyotrophic lateral sclerosis-linked mutation in GLE1 alters the cellular pool of human Gle1 functional isoforms. Adv Biol Regul 62:25-36
Burns, Laura T; Wente, Susan R (2014) Casein kinase II regulation of the Hot1 transcription factor promotes stochastic gene expression. J Biol Chem 289:17668-79
Burns, Laura T; Wente, Susan R (2014) From hypothesis to mechanism: uncovering nuclear pore complex links to gene expression. Mol Cell Biol 34:2114-20
Folkmann, Andrew W; Dawson, T Renee; Wente, Susan R (2014) Insights into mRNA export-linked molecular mechanisms of human disease through a Gle1 structure-function analysis. Adv Biol Regul 54:74-91
Adams, Rebecca L; Terry, Laura J; Wente, Susan R (2014) Nucleoporin FG domains facilitate mRNP remodeling at the cytoplasmic face of the nuclear pore complex. Genetics 197:1213-24
Natalizio, Barbara J; Wente, Susan R (2013) Postage for the messenger: designating routes for nuclear mRNA export. Trends Cell Biol 23:365-73
Casey, Amanda K; Wente, Susan R (2012) Nuclear transport: shifting gears in fungal nuclear and cytoplasmic organization. Curr Biol 22:R846-8
Wente, Susan R; Rout, Michael P (2010) The nuclear pore complex and nuclear transport. Cold Spring Harb Perspect Biol 2:a000562
Alcázar-Román, Abel R; Bolger, Timothy A; Wente, Susan R (2010) Control of mRNA export and translation termination by inositol hexakisphosphate requires specific interaction with Gle1. J Biol Chem 285:16683-92

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