M
Michael R. Green
Researcher at University of Texas MD Anderson Cancer Center
Publications - 597
Citations - 65007
Michael R. Green is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: RNA splicing & RNA. The author has an hindex of 126, co-authored 537 publications receiving 57447 citations. Previous affiliations of Michael R. Green include Eppley Institute for Research in Cancer and Allied Diseases & United States University.
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Book ChapterDOI
Interaction of Gal4p with Components of Transcription Machinery In Vivo
TL;DR: In vitro protein–protein interaction experiments, such as GST pulldown assays that have been widely used to identify potential targets for a number of activators, including three well-characterized activators: yeast Gal4p, human p53, and viral VP16 are explored.
Journal ArticleDOI
The cAMP response element binding protein, CREB, is a potent inhibitor of diverse transcriptional activators.
TL;DR: It is shown that CREB and the highly related protein ATF-1 are also potent transcription inhibitors, and CREB inhibits transcription of multiple activators, whose DNA-binding domains and activation regions are unrelated to one another.
Journal ArticleDOI
U2AF65 adapts to diverse pre-mRNA splice sites through conformational selection of specific and promiscuous RNA recognition motifs
TL;DR: Small-angle X-ray scattering analyses demonstrated that Py tract variations select distinct inter-RRM spacings from a pre-existing ensemble of U2AF65 conformations, highlighting both local and global conformational selection as a means for universal 3′ splice site recognition by U2 AF65.
Journal ArticleDOI
Oncogenic RAS directs silencing of tumor suppressor genes through ordered recruitment of transcriptional repressors.
Narendra Wajapeyee,Sunil K. Malonia,Sunil K. Malonia,Rajendra Kumar Palakurthy,Rajendra Kumar Palakurthy,Michael R. Green,Michael R. Green +6 more
TL;DR: RNAi and pharmacological inhibition experiments reveal that silencing requires continuous function of RAS and its cofactors and can be rapidly reversed, which may have therapeutic implications for reactivation of silenced TSGs in RAS-positive cancers.
Journal ArticleDOI
Profound misregulation of muscle-specific gene expression in facioscapulohumeral muscular dystrophy.
TL;DR: It is suggested that a global misregulation of gene expression is the underlying basis for FSHD, distinguishing it from other forms of muscular dystrophy.