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Taken together, ASF1A is aberrantly over-expressed in GIC tumors and plays key roles in GIC development and progression by stimulating the transcription of β-catenin target genes.
Hypoxia-inducible factor (HIF) is a main heterodimeric transcription factor that regulates the cellular adaptive response to hypoxia by stimulating the transcription of a series of hypoxia-inducible genes.
The β-Ca2SiO4/PHBV composite scaffolds containing 2.5 or 5%β-Ca2SiO4β-Ca2SiO4ticlenhanceificanthe enhance the proliferation of MG-63 cells by stimulating the transcription of the transforming growth factor-β1 (TGF-β1) and bone morphogenetic protein-7 (BMP-7) genes.
In addition to the above-mentioned roles of its inactivation in cancer cell metabolism, TP53 is central in the orchestration of cell death pathways upon cellular stress such as DNA damage by stimulating the transcription of pro-apoptotic proteins (PUMA, BAX), autophagy and cell-cycle arrest.
However, TNFα stimulation did not significantly alter the stability of p110δ transcripts in ActD-treated HUVECs or EA.hy926 cells, demonstrating that TNFα induces p110δ expression by stimulating the transcription of PIK3CD.
Importantly, β-catenin is able to interact with the FoxO family of transcription factors, which defend against oxidative stress by stimulating the transcription of oxidant scavenging enzymes such as superoxide dismutase and catalase [ 37].
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Estrogen exerts its effect by simultaneously stimulating the transcription of genes, via the estrogen receptor, necessary for cell proliferation and by causing DNA damage via their catechol estrogen metabolites [ 1, 2].
Trimethylation of H3K4 selectively enhances p53-dependent transcription by stimulating the rate of pre-initiation complex (PIC) formation at the promoter.
Estrogens enhance transcription of target genes by stimulating the association of the estrogen receptor (ER) and related coactivators to estrogen response elements or to transcription complexes formed at activator protein (AP -1 or specificity protein (Sp)-binding sites.
When the tumour suppressor p53 is activated by DNA damage, it stimulates the transcription of its target genes, which then induce cell cycle arrest or apoptosis.
CSB is a DNA-dependent ATPase that participates in transcription by stimulating transcription elongation (Selby and Sancar, 1997) and transcription initiation of some genes after UV-damage (Proietti-De-Santis et al., 2006).
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