Topic
USF2
About: USF2 is a research topic. Over the lifetime, 131 publications have been published within this topic receiving 5674 citations. The topic is also known as: FIP & bHLHb12.
Papers published on a yearly basis
Papers
TL;DR: The complete purification and identification of USF from HeLa cell nuclei is reported, showing that two major forms of the USF protein can be distinguished both by their slightly different mobilities in sodium dodecyl sulfate gel electrophoresis and by different electrophoretic mobilities of the corresponding protein-DNA complexes.
267 citations
TL;DR: DNA binding and transcriptional properties of USF purified to near-homogeneity from HeLa cell nuclei showed identical affinities for the major late promoter upstream sequence, indicating that USF can efficiently transfer from one binding site to another by passing through a doubly bound intermediate state.
177 citations
TL;DR: It is demonstrated that upstream stimulatory factor binding to the E-box at −65 is required for insulin regulation of the fatty acid synthase promoter and that USFs are in vivo components of the insulin response complex.
176 citations
TL;DR: Chromatin immunoprecipitations showed that a repressive complex containing USF1 and USF2 is present in normal cells with little or no telomerase activity, and in E6 keratinocytes, this repressive complex is replaced by c-Myc, which corresponds to higher levels of TERT transcription and consequently, telomersase activity.
Abstract: Human papillomavirus type 16 (HPV-16), a DNA tumor virus, has a causal role in cervical cancer, and the viral oncoproteins E6 and E7 contribute to oncogenesis in multiple ways. E6 increases telomerase activity in keratinocytes through increased transcription of the telomerase catalytic subunit gene (TERT), but the factors involved in this have been elusive. We have found that mutation of the proximal E box in the TERT promoter has an activating effect in luciferase assays. This suggested that a repressive complex might be present at this site. HPV-16 E6 activated the TERT promoter predominantly through the proximal E box, and thus, might be acting on this repressive complex. This site is specific for the Myc/Mad/Max transcription factors as well as USF1 and USF2. Addition of exogenous USF1 or USF2 repressed activation of the TERT promoter by E6, dependent on the proximal E box. Using siRNA against USF1 or USF2 allowed for greater activation of the TERT promoter by E6. Conversely, loss of c-Myc function, through a dominant-negative Myc molecule, reduced activation by E6. Chromatin immunoprecipitations showed that in the presence of E6, there was a reduction in binding of USF1 and USF2 at the TERT promoter proximal E box, and a concomitant increase in c-Myc bound to this site. This shows that a repressive complex containing USF1 and USF2 is present in normal cells with little or no telomerase activity. In E6 keratinocytes, this repressive complex is replaced by c-Myc, which corresponds to higher levels of TERT transcription and consequently, telomerase activity.
169 citations
TL;DR: USF transactivators, and especially USF1/USF2 heterodimers, seem to be essential to sustain the dietary induction of the FAS gene in the liver.
147 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2021 | 2 |
| 2020 | 2 |
| 2019 | 2 |
| 2018 | 3 |
| 2017 | 1 |
| 2016 | 2 |