The effects of soy supplementation on gene expression in breast cancer: a randomized placebo-controlled study.
Kettering, United Kingdom. In J Natl Cancer Inst, 2014
This signature was characterized by overexpression (>2-fold) of cell cycle transcripts, including those that promote cell proliferation, such as FGFR2, E2F5, BUB1, CCNB2, MYBL2, CDK1, and CDC20 (P < .01).
Multicilin drives centriole biogenesis via E2f proteins.
Los Angeles, United States. In Genes Dev, 2014
Here we show that Multicilin acts by forming a ternary complex with E2f4 or E2f5 and Dp1 that binds and activates most of the genes required for centriole biogenesis, while other cell cycle genes remain off.
Promising roles of mammalian E2Fs in hepatocellular carcinoma.
Hefei, China. In Cell Signal, 2014
Eight members, E2F1 E2F8 have been recognized of this family so far, and the members of this family are generally divided into activator E2F (E2F1--E2F3a), repressor E2F (E2F3b--E2F5) and inhibitor E2F (E2F6--E2F8) subclasses based on their structur-e and function.
A multi-resource data integration approach: identification of candidate genes regulating cell proliferation during neocortical development.
Tallahassee, United States. In Front Neurosci, 2013
We used a mouse in situ hybridization dataset (The Allen Institute for Brain Science) to identify 13 genes (Cdon, Celsr1, Dbi, E2f5, Eomes, Hmgn2, Neurog2, Notch1, Pcnt, Sox3, Ssrp1, Tead2, Tgif2) with high correlation of expression in the proliferating cells of the VZ of the neocortex at early stages of development (E15.5).
Role of skeletal muscle in palate development.
Halifax, Canada. In Histol Histopathol, 2013
A cDNA microarray analysis revealed differentially expressed genes in the cleft palate of amyogenic mouse fetuses and suggested candidate molecules with a novel function in palatogenesis (e.g., Tgfbr2, Bmp7, Trim71, E2f5, Ddx5, Gfap, Sema3f).
Tumor suppression by ARF: gatekeeper and caretaker.
Chicago, United States. In Cell Cycle, 2010
While the regulation of the activator E2Fs is related to cell cycle arrest, there is evidence that the regulation of the repressors, E2F4 and E2F5, is significant in maintaining genomic stability.
Inactivation of E2F3 results in centrosome amplification.
Columbus, United States. In Cancer Cell, 2003
Loss of E2F3, but not E2F1, E2F2, E2F4, or E2F5 results in unregulated cyclin E-dependent kinase activity, defects in nucleophosmin B association with centrosomes, and premature centriole separation and duplication.