Genomes and Genes
Affiliation: University of Wisconsin
- A REST derived gene signature stratifies glioblastomas into chemotherapy resistant and responsive diseaseMatthew P Wagoner
Department of Neuroscience, University of Wisconsin at Madison, Madison, WI 53706, USA
BMC Genomics 13:686. 2012..Recent work has highlighted the role of the transcription factor RE1 Silencing Transcription Factor, REST in glioblastoma but how REST function correlates with disease outcome has not been described...
- Epigenetics and epilepsyAvtar Roopra
Department of Neuroscience, University of Wisconsin Madison, Madison, Wisconsin 53706, USA
Epilepsia 53:2-10. 2012..Finally we highlight possible future directions in the field of epigenetics and epilepsy...
- 2-Deoxy-D-glucose reduces epilepsy progression by NRSF-CtBP-dependent metabolic regulation of chromatin structureMireia Garriga-Canut
Department of Neurology, Medical Science Center, Room 1715, University of Wisconsin Madison, 1300 University Avenue, Madison, Wisconsin 53706, USA
Nat Neurosci 9:1382-7. 2006..The metabolic regulation of neuronal genes by CtBP will open avenues of therapy for neurological disorders and cancer...
- Induction of the RNA regulator LIN28A is required for the growth and pathogenesis of RESTless breast tumorsKearney T W Gunsalus
Graduate Program in Cellular and Molecular Biology, Department of Neuroscience, University of Wisconsin Madison, Madison, Wisconsin 53706, USA
Cancer Res 72:3207-16. 2012..Our findings therefore show a critical role for the REST-LIN28A axis in tumor aggression and suggest a causative relationship between REST loss and tumorigenicity in vivo...
- Seizure suppression via glycolysis inhibition with 2-deoxy-D-glucose (2DG)Carl E Stafstrom
Department of Neurology, University of Wisconsin, Madison, Wisconsin 53792, USA
Epilepsia 49:97-100. 2008..Finally, 2DG has a favorable preliminary toxicity profile. These factors support the possibility that 2DG or other modifiers of glycolysis can be used as novel treatments for epilepsy...
- The transcription factor REST is lost in aggressive breast cancerMatthew P Wagoner
Department of Neurology, University of Wisconsin Madison, Madison, Wisconsin, USA
PLoS Genet 6:e1000979. 2010..Additionally, the alternative splicing observed in REST-less breast cancer is an attractive therapeutic target...
- Metabolic regulation of neuronal plasticity by the energy sensor AMPKWyatt B Potter
Department of Neurology, University of Wisconsin Madison, Madison, Wisconsin, United States of America
PLoS ONE 5:e8996. 2010..Our work opens up the possibility of using modulators of energy metabolism to control neuronal plasticity in diseases and conditions of aberrant plasticity such as epilepsy...
- Reduced Juvenile Long-Term Depression in Tuberous Sclerosis Complex Is Mitigated in Adults by Compensatory Recruitment of mGluR5 and Erk SignalingWyatt B Potter
Department of Neuroscience, Medical Science Center, University of Wisconsin Madison, Madison, Wisconsin, United States of America Neuroscience Training Program, University of Wisconsin Madison, Madison, Wisconsin, United States of America
PLoS Biol 11:e1001627. 2013..These findings highlight the potential of modulating the mGluR5-Erk pathway in a developmental stage-specific manner to treat TSC. ..
- Anticonvulsant and antiepileptic actions of 2-deoxy-D-glucose in epilepsy modelsCarl E Stafstrom
Department of Neurology, University of Wisconsin, Madison, WI 53792, USA
Ann Neurol 65:435-47. 2009....
- Localized domains of G9a-mediated histone methylation are required for silencing of neuronal genesAvtar Roopra
Department of Neurology, University of Wisconsin Madison, 1300 University Avenue, Madison, WI 53706, USA
Mol Cell 14:727-38. 2004..Finally, we demonstrate that dominant-negative G9a abrogates silencing of chromosomal neuronal genes. These findings implicate a role for histone methylation in targeting neuronal gene expression to the nervous system...
- Up-regulation of the mitotic checkpoint component Mad1 causes chromosomal instability and resistance to microtubule poisonsSean D Ryan
Department of Cell and Regenerative Biology, University of Wisconsin, Madison, WI 53705, USA
Proc Natl Acad Sci U S A 109:E2205-14. 2012..These results suggest that levels of Mad1 must be tightly regulated to prevent aneuploidy and transformation and that Mad1 up-regulation may promote tumors and cause resistance to current therapies...