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Reduction of plasma glutathione in psychosis associated with schizophrenia and bipolar disorder in translational psychiatry

Translational psychiatry, 2017-08, Vol.7 (8), p.e1215-e1215

2017

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Interference by Huntingtin and Atrophin-1 with CBP-Mediated Transcription Leading to Cellular Toxicity

Science (American Association for the Advancement of Science), 2001-03, Vol.291 (5512), p.2423-2428

2001

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A huntingtin-associated protein enriched in brain with implications for pathology

Nature (London), 1995-11, Vol.378 (6555), p.398-402

1995

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Differential cellular expression of isoforms of inositol 1,4,5-triphosphate receptors in neurons and glia in brain

Journal of comparative neurology (1911), 1999-04, Vol.406 (2), p.207-220

1999

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Nuclear Targeting of Mutant Huntingtin Increases Toxicity

Molecular and cellular neuroscience, 1999-08, Vol.14 (2), p.121-128

1999

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FKBP12 Binds the Inositol 1,4,5-Trisphosphate Receptor at Leucine-Proline (1400–1401) and Anchors Calcineurin to this FK506-like Domain

The Journal of biological chemistry, 1997-10, Vol.272 (44), p.27582-27588

1997

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Atrophin-1, the Dentato-Rubral and Pallido-Luysian Atrophy Gene Product, Interacts with ETO/MTG8 in the Nuclear Matrix and Represses Transcription

The Journal of cell biology, 2000-09, Vol.150 (5), p.939-948

2000

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A mutation in NPAS3 segregates with mental illness in a small family

Molecular psychiatry, 2014-01, Vol.19 (1), p.7-8

2014

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Inositol 1,4,5-trisphosphate receptors in endocrine cells: localization and association in hetero- and homotetramers

Molecular biology of the cell, 1996-06, Vol.7 (6), p.949-960

1996

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Nuclear Localization of a Non-caspase Truncation Product of Atrophin-1, with an Expanded Polyglutamine Repeat, Increases Cellular Toxicity

The Journal of biological chemistry, 2003-04, Vol.278 (15), p.13047-13055

2003

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Polyglutamine pathogenesis

Philosophical transactions of the Royal Society of London. Series B. Biological sciences, 1999-06, Vol.354 (1386), p.1005-1011

1999

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Molecular cloning of a cDNA for the human inositol 1,4,5-trisphosphate receptor type 1, and the identification of a third alternatively spliced variant

Brain research. Molecular brain research., 1995-09, Vol.32 (2), p.291-296

1995

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Cell death triggered by polyglutamine-expanded huntingtin in a neuronal cell line is associated with degradation of CREB-binding protein

Human molecular genetics, 2003-01, Vol.12 (1), p.1-12

2003

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A quantitative expression of resiliency in the workplace: an odds ratio analysis

International journal of emergency mental health, 2008, Vol.10 (3), p.169

2008

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Reduction of plasma glutathione in psychosis associated with schizophrenia and bipolar disorder in translational psychiatry

Interference by Huntingtin and Atrophin-1 with CBP-Mediated Transcription Leading to Cellular Toxicity

A huntingtin-associated protein enriched in brain with implications for pathology

Differential cellular expression of isoforms of inositol 1,4,5-triphosphate receptors in neurons and glia in brain

Nuclear Targeting of Mutant Huntingtin Increases Toxicity

FKBP12 Binds the Inositol 1,4,5-Trisphosphate Receptor at Leucine-Proline (1400–1401) and Anchors Calcineurin to this FK506-like Domain

Atrophin-1, the Dentato-Rubral and Pallido-Luysian Atrophy Gene Product, Interacts with ETO/MTG8 in the Nuclear Matrix and Represses Transcription

A mutation in NPAS3 segregates with mental illness in a small family

Inositol 1,4,5-trisphosphate receptors in endocrine cells: localization and association in hetero- and homotetramers

Nuclear Localization of a Non-caspase Truncation Product of Atrophin-1, with an Expanded Polyglutamine Repeat, Increases Cellular Toxicity

Polyglutamine pathogenesis

Molecular cloning of a cDNA for the human inositol 1,4,5-trisphosphate receptor type 1, and the identification of a third alternatively spliced variant

Cell death triggered by polyglutamine-expanded huntingtin in a neuronal cell line is associated with degradation of CREB-binding protein

A quantitative expression of resiliency in the workplace: an odds ratio analysis

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