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Stat3 as an Oncogene
Stat3 as an Oncogene
The cyclin D1 gene is a target of the beta-catenin/LEF-1 pathway.
- M. Shtutman, J. Zhurinsky, A. Ben-Ze’ev
- BiologyProceedings of the National Academy of Sciences…
- 11 May 1999
Increased beta-catenin levels may promote neoplastic conversion by triggering cyclin D1 gene expression and, consequently, uncontrolled progression into the cell cycle through a LEF-1 binding site in the cyclinD1 promoter.
NF-κB Controls Cell Growth and Differentiation through Transcriptional Regulation of Cyclin D1
- D. Guttridge, C. Albanese, J. Reuther, R. Pestell, A. Baldwin
- BiologyMolecular and Cellular Biology
- 1 August 1999
It is shown that NF-κB also promotes cell growth in embryonic fibroblasts, correlating with its regulation of cyclin D1, and is identified as an important transcriptional target of NF-α, revealing a mechanism to explain how NF-β is involved in the early phases of the cell cycle to regulate cell growth and differentiation.
ROCK inhibitor and feeder cells induce the conditional reprogramming of epithelial cells.
Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)
There continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes, so it is important to update guidelines for monitoring autophagic activity in different organisms.
Transforming p21ras Mutants and c-Ets-2 Activate the Cyclin D1 Promoter through Distinguishable Regions (*)
- C. Albanese, J. Johnson, R. Pestell
- Biology, MedicineThe Journal of Biological Chemistry
- 6 October 1995
It is demonstrated that transforming mutants of p21ras induce the cyclin D1 promoter in human trophoblasts, mink lung epithelial cells, and in Chinese hamster ovary fibroblast cell lines, providing evidence for cross-talk between the p 21ras and cell cycle regulatory pathways.
Direct Acetylation of the Estrogen Receptor α Hinge Region by p300 Regulates Transactivation and Hormone Sensitivity*
It is shown that the estrogen receptor (ERα) is acetylated in vivo, and the conservation of the ERα acetylation motif in a phylogenetic subset of nuclear receptors suggests that direct acetylators may contribute to additional signaling pathways involved in metabolism and development.
Arsenic trioxide inhibits human cancer cell growth and tumor development in mice by blocking Hedgehog/GLI pathway.
- E. Beauchamp, Lymor Ringer, A. Uren
- Biology, MedicineThe Journal of clinical investigation
- 4 January 2011
Evidence that arsenic trioxide (ATO) suppresses human cancer cell growth and tumor development in mice by inhibiting GLI1 is presented, establishing ATO as a Hh pathway inhibitor acting at the level ofGLI1 both in vitro and in vivo.
Conditional reprogramming and long-term expansion of normal and tumor cells from human biospecimens
Conditional reprogramming (CR) is described, which involves coculture of irradiated mouse fibroblast feeder cells with normal and tumor human epithelial cells in the presence of a Rho kinase inhibitor (Y-27632).