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James E. Hopper

Researcher at Pennsylvania State University

Publications -  38
Citations -  2529

James E. Hopper is an academic researcher from Pennsylvania State University. The author has contributed to research in topics: Saccharomyces cerevisiae & Gene. The author has an hindex of 27, co-authored 38 publications receiving 2485 citations. Previous affiliations of James E. Hopper include Penn State Milton S. Hershey Medical Center & Duke University.

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Isolation of the yeast regulatory gene GAL4 and analysis of its dosage effects on the galactose/melibiose regulon.

TL;DR: Yeast transformed with GAL4-bearing plasmid become constitutive for expression of the galactose/melibiose genes, even in normally repressing (glucose) medium, indicating that the repressing effects of glucose, at least in part, are mediated by the product of the negative regulatory gene GAL80.
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Breast cancer metastasis suppressor 1 (BRMS1) forms complexes with retinoblastoma-binding protein 1 (RBP1) and the mSin3 histone deacetylase complex and represses transcription.

TL;DR: Deletion analyses show that the carboxyl-terminal 42 amino acids of BRMS1 are not critical for interaction with much of the mSin3 complex and that BR MS1 appears to have more than one binding point to the complex, and suggest a novel mechanism by whichBRMS1 might suppress cancer metastasis.
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Translation of the L-species dsRNA genome of the killer-associated virus-like particles of Saccharomyces cerevisiae.

TL;DR: In this paper, the translational activity of the virus-like particle-derived double-stranded RNA (dsRNA) was analyzed in the wheat germ cell-free system and denaturation of the dsRNA immediately prior to in vitro translation resulted in the synthesis of one major and at least three minor polypeptides.
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Disruption of regulatory gene GAL80 in Saccharomyces cerevisiae: effects on carbon-controlled regulation of the galactose/melibiose pathway genes.

TL;DR: The data demonstrate that the G AL80 protein is a purely negative regulator, the GAL80 protein does not mediate carbon catabolite repression, and theGAL4 protein is not simply an antagonizer of GAL 80-mediated repression.
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Overproduction of the GAL1 or GAL3 protein causes galactose-independent activation of the GAL4 protein: evidence for a new model of induction for the yeast GAL/MEL regulon.

TL;DR: It is reported that overproduction of the GAL3 protein causes constitutive expression of GAL/MEL genes in the absence of exogenous galactose, consistent with the observations that GAL1 is strikingly similar in amino acid sequence to GAL2 and has GAL4-like induction activity.