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Peter K. Rogan

Researcher at University of Western Ontario

Publications -  186
Citations -  5605

Peter K. Rogan is an academic researcher from University of Western Ontario. The author has contributed to research in topics: Gene & RNA splicing. The author has an hindex of 41, co-authored 186 publications receiving 5253 citations. Previous affiliations of Peter K. Rogan include Allegheny General Hospital & Agricultural Research Service.

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Hepatic CYP2B6 expression: gender and ethnic differences and relationship to CYP2B6 genotype and CAR (constitutive androstane receptor) expression.

TL;DR: The 1459C>T SNP, which resulted in the Arg487Cys substitution, was associated with the lowest level of CYP2B6 activity in livers of females, and several common SNPs that are associated with polymorphic CYP 2B6 expression were found.
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Chromosome breakage in the Prader-Willi and Angelman syndromes involves recombination between large, transcribed repeats at proximal and distal breakpoints.

TL;DR: It is postulate that the END repeats flanking 15q11-q13 mediate homologous recombination resulting in deletion and proposed that active transcription of these repeats in male and female germ cells may facilitate the homologously recombination process.
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Imprinting-Mutation Mechanisms in Prader-Willi Syndrome

TL;DR: It is suggested that promoter elements at SNRPN play a key role in the initiation of imprint switching during spermatogenesis, since the epigenetic effect of an IM in the parental germ line determines the phenotypic effect in the patient.
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The frequency of uniparental disomy in Prader-Willi syndrome. Implications for molecular diagnosis.

TL;DR: In this article, the frequency of maternal uniparental disomy in Prader-Willi syndrome was determined using molecular genetic techniques, using DNA markers within 15q11q13 and elsewhere on chromosome 15 in 30 patients who had no cytogenetically visible deletion.
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Information analysis of human splice site mutations.

TL;DR: Comparison between normal and mutant splice site Ri values distinguishes substitutions that impair splicing from those which do not, distinguishes null alleles from those that are partially functional, and detects activated cryptic splice sites.