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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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Journal ArticleDOI
The Spectrum of Mutations at the p53 Locus
Arnold J. Levine,Michael C. Wu,Anwell Chang,Abigail L Silver,Edward F. Attiyeh,Jiayuh Lin,Charles B. Epstein +6 more
TL;DR: It has been suggested that the p53 protein acts as a checkpoint in the cell cycle, permitting time for the repair of DNA damage prior to entry into S-phase or killing the cell that has too much DNA damage.
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Gene Amplifications in Well-Differentiated Pancreatic Neuroendocrine Tumors Inactivate the p53 Pathway
Wenwei Hu,Zhaohui Feng,Ippolito Modica,David S. Klimstra,Lin Song,Peter J. Allen,Murray F. Brennan,Arnold J. Levine,Laura H. Tang +8 more
TL;DR: The findings suggest that the negative regulation of p53 function could be an important mechanism for the initiation and/or progression of pancreatic NETs, and reactivation of p 53 could be a potential therapeutic strategy for patients with this disease.
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Structure-function relationships of the adenovirus DNA-binding protein.
TL;DR: The degree of phosphorylation of the M, = 72,000 protein in the NHz-terminal domain affected the quality of the binding to single-stranded DNA by the COOH-terminals of this protein.
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Overexpression of WISP-1 Down-regulated Motility and Invasion of Lung Cancer Cells through Inhibition of Rac Activation
TL;DR: It is demonstrated that overexpression of WISP-1 in H460 lung cancer cells inhibited lung metastasis and in vitro cell invasion and motility and illustrates a negatively regulated pathway by WISp-1 involving integrins and Rac in the down-regulation of invasion.
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Isolation and characterization of polyoma host range mutants that replicate in nullipotential embryonal carcinoma cells.
Kenji Sekikawa,Arnold J. Levine +1 more
TL;DR: Polyoma wild-type virus replicates in most murine differentiated cells but fails to produce virus in murine embryonal carcinoma cells, and this type of mutation suggests several models to explain the polyoma host range restriction in embryonal cancer cells.