Molecular and cellular biology · 1996
Cyclin A expression is under negative transcriptional control during the cell cycle.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Huet X, Rech J, Plet A, Vié A, Blanchard J M
Аннотация
Transcription of the gene coding for cyclin A, a protein required for S-phase transit, is cell cycle regulated and is restricted to proliferating cells. To further explore transcriptional regulation linked to cell division cycle control, a genomic clone containing 5' flanking sequences of the murine cyclin A gene was isolated. When it was fused to a luciferase reporter gene, it was shown to function as a proliferation-regulated promoter in NIH 3T3 cells. Transcription of the mouse cyclin A gene is negatively regulated by arrest of cell proliferation. A mutation of a GC-rich sequence conserved between mice and humans is sufficient to relieve transcriptional repression, resulting in a promoter with constitutively high activity. In agreement with this result, in vivo footprinting reveals a protection of the cell cycle-responsive element in G0/early G1 cells which is not observed at later stages of the cell cycle. Moreover, the footprint is present in dimethyl sulfoxide-induced differentiating and not in proliferating Friend erythroleukemia cells. Conversely, two other sites, which in vitro bind ATF-1 and NF-Y, respectively, are constitutively occupied throughout cell cycle progression.
Предметные рубрики MeSH
3T3 CellsAnimalsBase CompositionBase SequenceCell CycleCell DivisionConserved SequenceCyclinsDNA FootprintingDNA PrimersDNA ProbesFibroblastsGene Expression RegulationGenomic LibraryHumansLuciferasesMiceMolecular Sequence DataMutagenesis, Site-DirectedPromoter Regions, GeneticRecombinant Fusion ProteinsSequence Homology, Nucleic AcidSkinTranscription, Genetic