Molecular cell · 2002
ALL-1 is a histone methyltransferase that assembles a supercomplex of proteins involved in transcriptional regulation.
СтатьяПоддержка исследования: вне правительства СШАПоддержка правительства СШАПоддержка службы здравоохранения 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.
Nakamura Tatsuya, Mori Toshiki, Tada Shinichiro, Krajewski Wladyslaw, Rozovskaia Tanya, Wassell Richard, Dubois Garrett, Mazo Alexander, Croce Carlo M, Canaani Eli
Аннотация
ALL-1 is a member of the human trithorax/Polycomb gene family and is also involved in acute leukemia. ALL-1 is present within a stable, very large multiprotein supercomplex composed of > or =29 proteins. The majority of the latter are components of the human transcription complexes TFIID (including TBP), SWI/SNF, NuRD, hSNF2H, and Sin3A. Other components are involved in RNA processing or in histone methylation. The complex remodels, acetylates, deacetylates, and methylates nucleosomes and/or free histones. The complex's H3-K4 methylation activity is conferred by the ALL-1 SET domain. Chromatin immunoprecipitations show that ALL-1 and other complex components examined are bound at the promoter of an active ALL-1-dependent Hox a9 gene. In parallel, H3-K4 is methylated, and histones H3 and H4 are acetylated at this promoter.
Предметные рубрики MeSH
Blotting, WesternCell NucleusChromatinDNA-Binding ProteinsHeLa CellsHistone MethyltransferasesHistone-Lysine N-MethyltransferaseHistonesHomeodomain ProteinsHumansK562 CellsMass SpectrometryMethylationMethyltransferasesMyeloid-Lymphoid Leukemia ProteinPrecipitin TestsProtein BindingProtein MethyltransferasesProtein Processing, Post-TranslationalProtein Structure, TertiaryProto-OncogenesSilver StainingTranscription FactorsTranscription, Genetic