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Arnold J. Levine
Researcher at Institute for Advanced Study
Publications - 493
Citations - 122094
Arnold J. Levine is an academic researcher from Institute for Advanced Study. The author has contributed to research in topics: Gene & Mutant. The author has an hindex of 139, co-authored 485 publications receiving 116005 citations. Previous affiliations of Arnold J. Levine include Harvard University & Affymetrix.
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Adenovirus early region 1B 58,000-dalton tumor antigen is physically associated with an early region 4 25,000-dalton protein in productively infected cells.
TL;DR: In this paper, an analysis of tryptic peptides derived from this 25K protein demonstrated that it was unrelated to the E1B-58K protein, which is the same protein that was previously shown to be associated with the cellular p53 antigen in adenovirus transformed cells.
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Tissue-specific codon usage and the expression of human genes
TL;DR: Systematic differences in synonymous codon usage between genes selectively expressed in six adult human tissues suggest that codon-mediated translational control may play an important role in the differentiation and regulation of tissue-specific gene products in humans.
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A functionally inactive p53 protein in teratocarcinoma cells is activated by either DNA damage or cellular differentiation.
TL;DR: The hypothesis that the p53 protein in undifferentiated teratocarcinoma cells is transcriptionally inactive and accounts for the lack of selection for p53 gene mutations in this tumor type is supported.
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Regulation of transcription functions of the p53 tumor suppressor by the mdm-2 oncogene
TL;DR: All three functions of the p53 protein—transcriptional activation, repression and mutant protein activation—require the p 53 amino terminal domain functions and are regulated by the mdm-2 protein in a cell.
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Essential role for p53-mediated transcription in E1A-induced apoptosis.
TL;DR: The activity of p53 as a transcription factor is directly correlated with the ability of E1A to induce apoptosis, and there may exist at least two different mechanisms by which p53 can suppress cell-cycle progression, only one of which is dependent on p53-mediated transcription.