W
W. Douglas Cress
Researcher at University of South Florida
Publications - 72
Citations - 5272
W. Douglas Cress is an academic researcher from University of South Florida. The author has contributed to research in topics: Lung cancer & Cancer. The author has an hindex of 32, co-authored 64 publications receiving 4899 citations. Previous affiliations of W. Douglas Cress include Duke University.
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Expression of transcription factor E2F1 induces quiescent cells to enter S phase
TL;DR: It is demonstrated that overexpression of the E2F1 complementary DNA can activate DNA synthesis in cells that would otherwise growth-arrest, with an efficiency that is similar to that achieved by the expression of the adenovirus El A gene.
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Histone deacetylases, transcriptional control, and cancer.
W. Douglas Cress,Edward Seto +1 more
TL;DR: A key event in the regulation of eukaryotic gene expression is the posttranslational modification of nucleosomal histones, which converts regions of chromosomes into transcriptionally active or inactive chromatin.
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Interactions between E2F1 and SirT1 regulate apoptotic response to DNA damage.
Chuangui Wang,Lihong Chen,Xinghua Hou,Zhenyu Li,Neha Kabra,Yihong Ma,Shino Nemoto,Toren Finkel,Wei Gu,W. Douglas Cress,Jiandong Chen +10 more
TL;DR: It is shown that the cell-cycle and apoptosis regulator E2F1 induces SirT1 expression at the transcriptional level and knockdown ofSirT1 by small interference RNA increases E1F1 transcriptional and apoptotic functions.
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Role of Stat3 in Regulating p53 Expression and Function
Guilian Niu,Kenneth L. Wright,Yihong Ma,Gabriela Wright,Mei Huang,Rosalyn B. Irby,Jon Briggs,James G. Karras,W. Douglas Cress,Drew M. Pardoll,Richard Jove,Jiangdong Chen,Hua Yu +12 more
TL;DR: In this article, the p53 gene transcription rate was inhibited by the Stat3 DNA-binding site in the P53 promoter in a wide diversity of cancers and is a promising molecular target for cancer therapy.
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Mcl-1 regulates survival and sensitivity to diverse apoptotic stimuli in human non-small cell lung cancer cells.
TL;DR: Mcl-1 protein is overexpressed in a subset of human NSCLC and enhanced levels of M cl-1 may protect lung cancer cells from death induced by a variety of pro-apoptotic stimuli, and epidermal growth factor (EGF) can enhance Mcl- 1 protein levels in an ERK-dependent manner.