Genomes and Genes
Hsin Sheng Yang
Affiliation: National Cancer Institute
- The transformation suppressor Pdcd4 is a novel eukaryotic translation initiation factor 4A binding protein that inhibits translationHsin Sheng Yang
Gene Regulation Section, Center for Cancer Research, National Cancer Institute, Frederick, Maryland 21702, USA
Mol Cell Biol 23:26-37. 2003..Pdcd4 binding to eIF4A is linked to its transformation-suppressing activity, as Pdcd4-eIF4A binding and consequent inhibition of translation are required for Pdcd4 transrepression of AP-1...
- Pdcd4 suppresses tumor phenotype in JB6 cells by inhibiting AP-1 transactivationHsin Sheng Yang
Gene Regulation Section, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA
Oncogene 22:3712-20. 2003..Thus, Pdcd4 suppresses tumor phenotype by inhibiting AP-1-dependent transcription, possibly through inhibiting c-Jun and c-Fos activation...
- A novel function of the MA-3 domains in transformation and translation suppressor Pdcd4 is essential for its binding to eukaryotic translation initiation factor 4AHsin Sheng Yang
Gene Regulation Section, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, Maryland 21702, USA
Mol Cell Biol 24:3894-906. 2004..Together, these results indicate that not only binding to eIF4A but also prevention of eIF4A binding to the MA-3 domain of eIF4Gc contributes to the mechanism by which Pdcd4 inhibits translation...
- Promising molecular targets for cancer prevention: AP-1, NF-kappa B and Pdcd4Matthew R Young
The Gene Regulation Section, Basic Research Laboratory, National Cancer Institute Frederick, National Institutes of Health, Frederick, MD 21702, USA
Trends Mol Med 9:36-41. 2003..A protein known as programmed-cell-death-4 is a new potential molecular target that has a surprising mode of action...
- Mutational analysis of the DEAD-box RNA helicase eIF4AII characterizes its interaction with transformation suppressor Pdcd4 and eIF4GIHalina Zakowicz
Laboratory of Cancer Prevention, Bldg 576, Rm 101, National Cancer Institute, Frederick, MD 21702, USA
RNA 11:261-74. 2005..A competition experiment revealed that Pdcd4 competes with C-terminal eIF4G for binding to eIF4A. In summary, the Pdcd4-binding domains on eIF4A impact both binding to eIF4G and translation initiation in cells...
- Tumorigenesis suppressor Pdcd4 down-regulates mitogen-activated protein kinase kinase kinase kinase 1 expression to suppress colon carcinoma cell invasionHsin Sheng Yang
Laboratory of Cancer Prevention, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA
Mol Cell Biol 26:1297-306. 2006..Thus, Pdcd4 suppresses tumor progression in human colon carcinoma cells by the novel mechanism of down-regulating MAP4K1 transcription, with consequent inhibition of c-Jun activation and AP-1-dependent transcription...
- Aerosol delivery of urocanic acid-modified chitosan/programmed cell death 4 complex regulated apoptosis, cell cycle, and angiogenesis in lungs of K-ras null miceHua Jin
Laboratory of Toxicology, College of Veterinary Medicine, Seoul National University, Seoul 151 742, Korea
Mol Cancer Ther 5:1041-9. 2006....
- Phenethyl isothiocyanate, a cancer chemopreventive constituent of cruciferous vegetables, inhibits cap-dependent translation by regulating the level and phosphorylation of 4E-BP1Jing Hu
Department of Pharmacology and University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, Hillman Cancer Center Research Pavilion, 5117 Centre Avenue, Pittsburgh, PA 15213, USA
Cancer Res 67:3569-73. 2007..The present study also suggests that inhibition of cap-dependent translation may be an important mechanism in PEITC-induced apoptosis...
- Interactions between SIRT1 and AP-1 reveal a mechanistic insight into the growth promoting properties of alumina (Al2O3) nanoparticles in mouse skin epithelial cellsSwatee Dey
Graduate Center for Toxicology, University of Kentucky, 1095 VA Drive, Health Sciences Research Building 454, Lexington, KY 40536 0298, USA
Carcinogenesis 29:1920-9. 2008..The results identify SIRT1 as an AP-1 modulator and suggest a novel mechanism by which alumina nanoparticles may function as a potential carcinogen...