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Heidi G. Sutherland

Researcher at Queensland University of Technology

Publications -  94
Citations -  4788

Heidi G. Sutherland is an academic researcher from Queensland University of Technology. The author has contributed to research in topics: Migraine & Population. The author has an hindex of 24, co-authored 85 publications receiving 4282 citations. Previous affiliations of Heidi G. Sutherland include University of Sydney & Griffith University.

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Epigenetic inheritance at the agouti locus in the mouse.

TL;DR: It is demonstrated here that this maternal epigenetic effect is not the result of a maternally contributed environment, and results from incomplete erasure of an epigenetic modification when a silenced Avy allele is passed through the female germ line, with consequent inheritance of the epigenetic modified.
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Transcription factories: gene expression in unions?

TL;DR: In this article, the experimental evidence in support of the transcription factory model and the evidence that argues against such a spatially structured view of transcription are discussed. But, this concept is not universally accepted.
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Psip1/Ledgf p52 Binds Methylated Histone H3K36 and Splicing Factors and Contributes to the Regulation of Alternative Splicing

TL;DR: The PWWP domain of the chromatin-associated protein Psip1/Ledgf can specifically recognize tri-methylated H3K36 and that, like this histone modification, thePsip1 short (p52) isoform is enriched at active genes.
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Localization of a putative transcriptional regulator (atrx) at pericentromeric heterochromatin and the short arms of acrocentric chromosomes

TL;DR: The unexpected association of a putative transcriptional regulator with highly repetitive DNA provides a potential explanation for the variability in phenotype of patients with identical mutations in the ATRX gene.
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Role of PSIP1/LEDGF/p75 in lentiviral infectivity and integration targeting.

TL;DR: Reductions were seen in lentiviral infectivity compared to controls and the frequency of integration in transcription units was correlated with the cell-type specific levels of PSIP1/LEDGF/p75 expression.