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Roger White

Researcher at Imperial College London

Publications -  71
Citations -  10429

Roger White is an academic researcher from Imperial College London. The author has contributed to research in topics: Nuclear receptor & Receptor. The author has an hindex of 40, co-authored 70 publications receiving 10158 citations. Previous affiliations of Roger White include New York University & Lincoln's Inn.

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Cognitive impairments in adult mice with constitutive inactivation of RIP140 gene expression.

TL;DR: Observations showed that RIP140 gene depletion results in learning and memory deficits as well as stress response, bringing to light a major role for this transcriptional coregulator in the neurophysiological developmental mechanisms underlying cognitive functions.
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1,4-Bis[2-(3,5-dichloropyridyloxy)]benzene, an extremely potent modulator of mouse hepatic cytochrome P-450 gene expression.

TL;DR: The findings demonstrate that TCPOBOP is one of the most potent modulators of cytochrome P-450 gene expression described to date, and it is not inconceivable that a single dose of this compound may alter hepatic gene expression for the majority of the lifespan of a mouse.
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Identification of phosphorylation sites in the mouse oestrogen receptor

TL;DR: A region of AF-1 that encompasses Ser-122 appears to interact with AF-2 in the full-length receptor, and a reduction of transcriptional activity was observed when Ser- 122 was mutated in the context of mutations in a putative amphipathic alpha-helix involved in AF- 2 activity.
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Multiple signaling defects in the absence of RIP140 impair both cumulus expansion and follicle rupture.

TL;DR: It is proposed that widespread gene dysregulation in ovarian tissues in the absence of RIP140 leads to the anovulatory phenotype, and an important role for RIP140 in the regulation of multiple processes leading to ovulation is defined.
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Elevated expression of the metabolic regulator receptor-interacting protein 140 results in cardiac hypertrophy and impaired cardiac function

TL;DR: This study demonstrates that RIP140 is an important cofactor in postnatal cardiac function and that inhibition of the action of RIP140 may provide a model system to investigate specific interventions designed to prevent or delay the onset of cardiac disease.