D
David E. Levy
Researcher at New York University
Publications - 242
Citations - 38178
David E. Levy is an academic researcher from New York University. The author has contributed to research in topics: Transcription factor & Interferon. The author has an hindex of 97, co-authored 241 publications receiving 35917 citations. Previous affiliations of David E. Levy include National Taiwan University & Spanish National Research Council.
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Journal ArticleDOI
Malignant transformation but not normal cell growth depends on signal transducer and activator of transcription 3.
Karni Schlessinger,David E. Levy +1 more
TL;DR: The data suggest that STAT3 mediates the maintenance of focal adhesion kinase activity in the absence of cell adhesion by suppressing the action of an inhibitory phosphatase.
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The MEK-ERK pathway is necessary for serine phosphorylation of mitochondrial STAT3 and Ras-mediated transformation.
TL;DR: It is shown that the MEK-ERK pathway is required for activated Ras-induced phosphorylation of STAT3 on S727, that inhibition ofSTAT3 S727 phosphorylated contributes to the anti-oncogenic potential of MEK inhibitors, and that mitochondrial STAT3 is one of the critical substrates of the Ras-MEK- ERK- axis during cellular transformation.
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Nuclear and cytoplasmic mRNA quantification by SYBR green based real-time RT-PCR.
TL;DR: This method provides an accurate and efficient procedure for estimating the relative ratios of nuclear and cytoplasmic RNA concentrations and DNA binding dyes such as SYBR Green I are simple, versatile, and yet highly reliable and least expensive.
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Divergent roles of STAT1 and STAT5 in malignancy as revealed by gene disruptions in mice
David E. Levy,D. G. Gilliland +1 more
TL;DR: Investigation of cell growth and malignancy in the absence of particular Stat proteins using targeted gene disruptions in transgenic mice shows that Stat1 primarily mediates growth inhibitory signals and contributes to the host rejection of tumors, and that its activation in transformed cells is not necessary for malignancies.
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Differentiation of monocytes to macrophages switches the Mycobacterium tuberculosis effect on HIV-1 replication from stimulation to inhibition: modulation of interferon response and CCAAT/enhancer binding protein beta expression.
Michael D. Weiden,Naohiko Tanaka,Yaming Qiao,Ben Yang Zhao,Yoshihiro Honda,Koh Nakata,Antony Canova,David E. Levy,William N. Rom,Richard Pine +9 more
TL;DR: Results show that induction of ISGF-3, expression of the inhibitory 16-kDa C/EBPβ, and suppression of HIV-1 replication via a transcriptional mechanism are macrophage-specific responses to infection with M. tuberculosis.