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Tish Hockenberry

Researcher at Schering-Plough

Publications -  6
Citations -  1828

Tish Hockenberry is an academic researcher from Schering-Plough. The author has contributed to research in topics: Gene & Chromatin immunoprecipitation. The author has an hindex of 5, co-authored 6 publications receiving 1759 citations.

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K- and N-Ras Are Geranylgeranylated in Cells Treated with Farnesyl Protein Transferase Inhibitors *

TL;DR: In the presence of potent farnesyl protein transferase inhibitors, Ras proteins in the human colon carcinoma cell line DLD-1 were alternatively prenylated by geranylgeranyl transferase-1 and N- and K-Ras proteins incorporated the geranyl Geranyl isoprene group and remained associated with the membrane fraction.
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Human survivin is negatively regulated by wild-type p53 and participates in p53-dependent apoptotic pathway

TL;DR: It is shown that wild-type p53 represses survivin expression at both mRNA and protein levels, suggesting that loss of survivin mediates, at least, in part the p53-dependent apoptotic pathway.
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Global transcriptional program of p53 target genes during the process of apoptosis and cell cycle progression

TL;DR: A small-scale quantitative chromatin immunoprecipitation analysis indicated that in vivo p53–DNA interaction was detected in eight out of 10 genes, suggesting that a portion of p53 target genes in the human genome could be negatively regulated by p53 via sequence-specific DNA binding.
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Contribution of the ERK5/MEK5 Pathway to Ras/Raf Signaling and Growth Control

TL;DR: It is demonstrated that the ERK5/MEK5 pathway is required for Raf-dependent cellular transformation and that a constitutively active form of MEK5, MEk5DD, synergizes with Raf to transform NIH 3T3 cells, suggesting that ERk5 plays a large role in Raf-1-mediated signal transduction.
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Transcriptional regulation during p21WAF1/CIP1-induced apoptosis in human ovarian cancer cells.

TL;DR: Quantitative reverse transcription-PCR analysis revealed that the differential expression of BAX, BCL2, and caspase 3 genes was not altered in rAd-p21-induced apoptotic cells, suggesting p21 WAF1/CIP1 -induced apoptosis through a pathway distinguishable from p53- induced apoptosis.